Case Studies in Cardiothoracic Medicine

CASES STUDIES IN
CARDIOTHORACIC MEDICINE
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Warning:
Veterinary science is constantly evolving, as are pharmacology and the other sciences. Inevitably, it is
therefore the responsibility of the veterinary surgeon to determine and verify the dosage, the method
of administration, the duration of treatment and any possible contraindications to the treatments given
to each individual patient, based on his or her professional experience. Neither the publisher nor the
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from the correct or incorrect application of the information contained in this book.
To my inspirational mentors and colleagues (VLF, DC, AB, JRP),
who taught me the importance of clinical research in day-to-day case
management
and that sometimes it is OK not to know the answer.
And to my patients and their owners,

who inspire me daily to work hard,
develop my skills, and be kind.
Kieran Borgeat
To my veterinary colleagues and my mentors

Michael Herrtage and Victoria Johnson,
without whom I wouldn’t be a radiologist.
And to my family, friends, and partner for always being there.
Raquel Salgüero Fernández

ACKNOWLEDGEMENTS
Kieran Borgeat wishes to thank:
I would like to acknowledge the support and training of my residency
supervisors; without their patience and tutoring, I would not have become a
cardiologist.
I would also like to acknowledge my colleagues over the years, who have
put up with my sometimes overenthusiastic appreciation for the heart and
cardiorespiratory diseases, and the team at Zetland Vets in helping me begin
my cardiology journey, and colleagues since then—Luca, Rosie, Kate. My
life would be far less interesting without the residents I train, of whom I am
incredibly proud and challenged daily into being a better clinician.
And finally, I must acknowledge the patients with whom I work every
day, and their carers who bring them to see me. The gentle nature and
kindness of animals keeps me focused on why I became a vet in the first
place—to help improve animal welfare—and reminds me that every student
I teach, paper I publish, or sentence in a textbook makes a contribution to
helping animals all over the world; much more impact than I could ever
have as a clinician alone.
Raquel Salgüero Fernández wishes to thank:

I would like to acknowledge the help and support I received from all the
residents, residency supervisors, and veterinary colleagues, including
nurses, receptionists, and veterinarians, from all disciplines, especially the
imaging teams, I have worked with during the years. They were my main
support and family during the time I spent abroad and have become great
friends afterwards.
I would also like to acknowledge all the veterinarians that have passed
through my life after I became a radiologist. It is an honour to have been
invited to give talks, courses, etc. and teach what I know to the rest of my
colleagues and learn from them. Special thanks to Jordi López–Álvarez,
friend and cardiologist colleague, who had the idea of this project and
started it with us; this book would not have been possible without him.
And, of course, I must acknowledge my family, friends, and partner for
understanding my passion for the veterinary world and for believing in me
and motivating me to always pursue my goals in life.
THE AUTHORS
KIERAN BORGEAT
BSc (Hons) BVSc MVetMed CertVC FHEA MRCVS DipACVIM
DipECVIM-CA (Cardiology)
Kieran is an American, European, and RCVS recognised specialist in

veterinary cardiology. After graduating from the University of Bristol, UK,
with an intercalated degree in Veterinary Science, he worked in general
practice and achieved the RCVS Certificate in Veterinary Cardiology. He
went on to complete his specialist training at the Royal Veterinary College
in London.
Kieran is currently clinical lead in cardiology at Langford Vets,
University of Bristol. He also works as a cardiology consultant for the
VetCT Telemedicine Hospital and is examiner for the cardiology modules
of the RCVS Cert-AVP at the Royal Veterinary College. He is a past
member of the Veterinary Cardiovascular Society committee, past chair of
the ACVIM Cardiology Research Committee, and a current member of the
ECVIM Credentials Committee.
Kieran has spoken internationally on cardiology and interventional
radiology and is actively involved in a number of continuing education
initiatives. He has pioneered the use of transpulmonic stents in complex
congenital heart disease and was lead author of the first veterinary case
report to be published by the American Society of Echocardiography. He
has a strong interest in feline heart disease, inherited heart disease, and
congenital heart disease in both dogs and cats.
RAQUEL SALGÜERO FERNÁNDEZ

LdaVet MA DipECVDI MRCVS
Raquel is a Diplomate of the European College of Veterinary Diagnostic

Imaging and a recognised specialist in Diagnostic Imaging by the RCVS.
She is also a recognised specialist in diagnostic imaging by the Spanish
Small Animal Veterinary Association (Asociación de Veterinarios
Españoles Especialistas en Pequeños Animales, AVEPA).
Raquel graduated in veterinary medicine from the Complutense
University of Madrid, Spain, in 2006 and worked for 4 years in private
practice in Spain and the UK. She did two internships in referral hospitals
in the UK (VRCC Veterinary Referrals and University of Cambridge) and a
master’s degree in veterinary education and teaching. From 2012 to 2015,
she undertook a residency in diagnostic imaging at the University of
Cambridge under the supervision of Michael Herrtage, obtaining her
diploma of the European College of Veterinary Diagnostic Imaging in 2015.
After working as a radiologist in several referral hospitals in the UK, she
moved to Spain in 2017 and was in charge of the diagnostic imaging
department at the Puchol veterinary hospital in Madrid.
Raquel is now an assistant professor at the Complutense University of
Madrid, collaborates with Puchol veterinary hospital, and is a consultant
teleradiologist. She is a member of the European Association of Veterinary
Diagnostic Imaging and the AVEPA Working Group of Specialists in
Diagnostic Imaging (Grupo de Especialistas en Diagnóstico por Imagen).
Raquel has written several publications in national and international
journals and has participated in several imaging courses. She has experience
in all the diagnostic imaging modalities in small animals and has special
interest in neuroimaging, thoracic and abdominal ultrasound, and CT
angiography.
FOREWORD
Small animal medicine has advanced by leaps and bounds in the last 40
years, particularly in diagnosis and well-founded therapy. In the 1970s and
1980s, cardiac diagnoses were based mainly on the combination of history,
clinical examination, radiology, and electrocardiography. Treatment for
congestive heart failure at that time consisted mainly of diuresis, xanthine
derivatives such as theophylline, sometimes cardiac glycosides (digoxin),
and—in the hands of some practitioners—the legendary backstop of “heart
tonic and stimulant tablets”; a last resort of doubtful efficacy! In those years
before the evidence-based veterinary medicine revolution, the efficacy of
each of these standard therapies was unproven.
One of the first properly conducted veterinary drug trials took place in
the 1990s in a placebo-controlled trial in canine cardiology, with the
successful evaluation of the angiotensin converting enzyme inhibitor
enalapril for the treatment of congestive heart failure. Since this successful
evaluation of a new agent for cardiac therapy, several other successful
clinical trials have made available further agents such as pimobendan, in
both preclinical and overt heart disease. Drug therapy with these and other
agents has since been shown to both prolong life and improve quality of life
in cardiac patients. When I published The Color Atlas of Veterinary
Cardiology (alongside Professors John Bonagura and Don Kelly) in 1995,
our aim was to bring together theoretical knowledge of veterinary
cardiology with clinical images, to help veterinarians in the diagnosis and
management of cardiac disease. In the 25 years since then, there have been
many advances in clinical practice.
In the twenty-first century, cardiac pacemakers have become reasonably
routine therapy for some arrhythmias, and minimally invasive heart surgery
has become the standard of care for some congenital heart diseases. The gap
between human and veterinary cardiology has decreased and, in some areas,
veterinary cardiology helps to inform researchers in human medicine. High-
quality ultrasound machines have become available at a more accessible
price to clinics, and the use of computed tomography imaging for
cardiovascular and respiratory disorders has become more widespread. The
authors of this book, which has a similar scope to our “Color Atlas”, have
put together an updated series of cases, covering a specialist and modern
approach to cardiorespiratory diseases in dogs and cats.
Sadly, the evidence base underpinning our approach to respiratory
medicine in small animals seems to have lagged. Challenges in obtaining
funding for large-scale trials using drugs that are widely available and
considered of low importance by the pharmaceutical industry have perhaps
held back the development of pulmonology as a subspecialty. However,
techniques such as bronchoscopy, bronchoalveolar lavage, and computed
tomography imaging have evolved, and these techniques are well illustrated
in this book as critical components of best practice. Here, respiratory
diagnoses encompass several recently described disorders that have
undergone rigorous study, such as Angiostrongylus vasorum infection,
eosinophilic bronchopneumopathy, and idiopathic pulmonary fibrosis in
dogs. Our understanding of these illnesses has grown hugely in the last two
decades, but even these diseases are usually treated somewhat empirically.
Clearly, small animal pulmonary medicine is an area ripe for further study.
Dr Borgeat, Diplomate of the ACVIM and ECVIM-CA, and Dr Salgüero,
Diplomate of the ECVDI, have managed cardiorespiratory cases in a variety
of environments: general practice, academic teaching hospitals, and private
referral centres. They are regarded as enthusiastic and engaging teachers,
and this book will demonstrate these characteristics, alongside their
commitment to clinical excellence. In addition to advanced cross-sectional
imaging and interventional techniques, the continued importance of thoracic
radiography and electrocardiography in managing cardiorespiratory disease
is also illustrated here. These cornerstones remain of vital utility to
clinicians at all levels of veterinary practice, and familiarity with them is
crucial to obtaining a diagnosis and also in monitoring cardiorespiratory
patients.
This book is not intended to be a classic veterinary medical text, some of
which attempt to address every known disease. Rather, it presents a good
selection of well-recognised cardiac and respiratory disorders in dogs and
cats with logical case studies of genuine patients. These should be of
considerable assistance to both established veterinary surgeons with an
interest in cardiorespiratory medicine and vets who feel this may be a
weakness and wish to develop their knowledge in a practical way. Complex
cases should help postgraduate students to gain perspective on uncommon
diseases whilst studying at internship or residency level. Each case
presented here is very well illustrated by advanced clinical diagnostic
techniques, and I imagine that keen undergraduates will also find that this
book should interest them, and possibly stimulate further curiosity in small
animal cardiorespiratory medicine. I hope that these future generations of
clinicians gain the same reward and thrill from working with veterinary
cardiorespiratory medicine as I have done.
Dr Peter Darke BVSc PhD DVR DVC MRCVS DipACVIM

DipECVIM-CA
Former head of cardiopulmonary services, Royal (Dick) School of
Veterinary Studies, University of Edinburgh, UK
Former lecturer in small animal medicine, School of Veterinary Science,
University of Bristol, UK
Founding member, Veterinary Cardiovascular Society
Bicknoller, Somerset, UK, December 2020
PREFACE
When we think of learning about animal diseases, we often remember
lectures at vet school or continuing education courses which have presented
information through the eyes of the disease—here is how the disease looks,
here is how to make its diagnosis, here is how to treat it. Or we think of lists
of differential diagnoses associated with various presenting signs or
physical examination findings. This method of learning information has the
benefit of being efficient and comprehensive, but it lacks the benefit of
being attached to a memorable story. People often learn best when there is a
story to tell. Veterinary medicine lends itself to learning through the stories
of our patients—the animals for whom we are advocates, giving a voice to
their silence.
Learning from a case helps to contextualise complex information and
provides authenticity to the experience. As learners, if we put our minds in
the position they will be in when we need the information—the clinic
environment, in front of a panel of blood results, for example—then we will
be better able to recall the information we need when we need it. Learning
from the story of the animal itself will maximise the chances that we will be
able to bring benefit to our own patients in the future. This is the aim which
underpins our whole job as veterinarians.
With that in mind we have written this book, which acts as a guide to
clinical cardiorespiratory medicine, divided into a series of journeys taken
by genuine patients. This is not a book of differential diagnoses, but a book
of stories. The backbone of each case is thoracic imaging, helping us not
only to obtain a diagnosis, but to assess prognosis and guide therapy. Our
experience and opinion will be presented, alongside crucial points from
scientific literature to back up decision-making along the way. We hope that
reading bite-sized cases from our book is like seeing practice—being able
to review key discussion points from each case, with top tips and advice
given along the way. We hope that what we have learnt through
postgraduate training and experience on the clinic floor can help you to feel
more confident in approaching cardiothoracic cases in your own jobs, and
to better help the animals under your care.
Thank you for reading!
The authors
TABLE OF CONTENTS
01 CARDIAC CASE STUDIES

Acquired heart disease
Case 1. Myxomatous mitral valve disease
Case 2. Dilated cardiomyopathy
Case 3. Hypertrophic cardiomyopathy
Case 4. Arrhythmogenic right ventricular cardiomyopathy
Case 5. Cardiac haemangiosarcoma
Case 6. Heart base tumour
Case 7. Infective endocarditis
Arrhythmias
Case 8. Ventricular tachycardia
Case 9. Supraventricular tachycardia
Case 10. Third-degree atrioventricular block
Case 11. Sick sinus syndrome
Congenital heart disease

Case 12. Pulmonic stenosis
Case 13. Subaortic stenosis
Case 14. Patent ductus arteriosus
Case 15. Ventricular septal defect
Case 16. Tricuspid valve dysplasia
Case 17. Mitral valve dysplasia
Case 18. Tetralogy of Fallot
Case 19. Atrioventricular septal defect
Case 20. Cor triatriatum dexter
Case 21. Divided left atrium
02 RESPIRATORY CASE STUDIES

Pulmonary disease
Case 22. Feline asthma
Case 23. Bronchial foreign body
Case 24. Aspiration pneumonia
Case 25. Eosinophilic bronchopneumopathy
Case 26. Idiopathic pulmonary fibrosis
Case 27. Pneumocystic pneumonia. Pneumocystis carinii
Case 28. Parasitic pneumonia. Angiostrongylus vasorum
Pleural disease
Case 29. Spontaneous pneumothorax
Case 30. Idiopathic chylothorax
Mediastinal disease
Case 31. Thymoma
Case 32. Vascular ring anomalies. Persistent right aortic arch
BIBLIOGRAPHY
ACQUIRED HEART DISEASE
Case 4. Arrhythmogenic right ventricular cardiomyopathy
ARRHYTHMIAS
CONGENITAL HEART DISEASE

Heart disease affects approximately one in ten dogs and one in seven cats
presenting to primary care practice. The overwhelming majority of them are
patients with acquired heart disease. In dogs, the most common diseases are
myxomatous mitral valve disease (MVD), dilated cardiomyopathy (DCM),
and arrhythmogenic right ventricular cardiomyopathy (ARVC). These
diseases are most likely genetic in origin, with age-dependent penetrance,
so that particular breeds (even families within breeds) are overrepresented.
In cats, hypertrophic cardiomyopathy (HCM) is the most common heart
disease, although some cats with cardiomyopathy are classified as having
slightly different diseases (e.g. restrictive cardiomyopathy). Feline DCM is
almost always nutritional in origin, owing to taurine deficiency. Cats fed
modern commercial diets with adequate taurine supplementation may still
develop a DCM phenotype, but this is rare and represents either end-stage
HCM, with wall ischaemia and reduced systolic function, or a particular
genetic cardiomyopathy.
Most dogs with MVD present with an asymptomatic left apical systolic
heart murmur. Considering this as a reasonable diagnostic feature, the
prevalence of MVD in primary care practice was estimated at 3.5 % in a
UK population. In this study, male dogs were more at risk, and dogs
weighing over 20 kg had approximately half the risk of developing MVD.
Higher heart rate and increased murmur intensity were associated with a
greater risk of death due to MVD. On echocardiography, MVD can be
identified by mitral valve prolapse, distortion, and regurgitation. One study
reported a 97 % prevalence of prolapse in Cavalier King Charles Spaniels
over 3 years old, and more severe valve prolapse is associated with shorter
survival time. This emphasises the importance of echocardiography in not
only diagnosis, but also assessment of disease. A Danish breeding
programme based on echocardiographic measurement of mitral prolapse in
Cavaliers has been shown to reduce the risk of mitral murmurs by 73 % in
the progeny of screened dogs.
A 2019 consensus statement on the assessment and treatment of MVD in

dogs describes MVD to have four key stages:
■ Stage A. At-risk population.
■ Stage B. Dogs with MVD but no clinical signs or history of congestive
heart failure.
■ Stage C. Current or previous signs of congestive heart failure (pulmonary
oedema) responsive to standard therapy.
■ Stage D. Refractory signs of heart failure with diuretic resistance (8
mg/kg/day furosemide, or more).
Stage B is subdivided into B1, dogs with no cardiomegaly, and B2, dogs
with cardiomegaly (left atrium-to-aortic root ratio >1.6 and left ventricular
internal dimension in diastole normalised for body weight >1.7 on
echocardiography, and vertebral heart score >11.5 on thoracic radiography).
Dogs with stage B2 MVD benefit from treatment with pimobendan, as
described by the EPIC study in 2016, so staging of MVD in dogs is vital to
quality of life, even when no overt clinical signs are present.
The most common primary heart muscle disease in dogs is DCM.
Differences in the disease course between breeds are well identified and
may reflect different genetic mechanisms, or even different inciting causes.
Dobermanns, Boxers, and Great Danes have a more aggressive disease
course, characterised by frequent ventricular arrhythmias and a high
incidence of sudden death. Newfoundlands and Irish Wolfhounds have a
slower disease progression, with a higher prevalence of atrial fibrillation
and a lower incidence of sudden death. The severity of arrhythmias in DCM
can be evaluated using ambulatory Holter ECG recording. This is
recommended as part of breed screening for DCM in Dobermanns: more
than 300 ventricular premature complexes in 24 hours is suggestive of a
DCM diagnosis even in the absence of any echocardiographic changes.
A DCM phenotype is defined by left ventricular dilation and reduced
systolic function in the absence of other causes. Some dogs with a DCM
phenotype may have tachycardia-induced cardiomyopathy (reversible
disease in which excessive tachycardia activates remodelling), an
arteriovenous shunt causing high-output heart failure, or previous
myocardial insult which has caused fibrosis and functional abnormalities
(e.g. previous myocarditis). These inciting causes should be excluded
before a final diagnosis of DCM is made. This is challenging, particularly
for chronic myocarditis because diagnosis relies upon endomyocardial
biopsy and results may overlap with findings in dogs with primary DCM.
Where significant left ventricular dilation is present, altered ventricular
geometry leads to mitral annular stretch, causing mitral regurgitation which
further reduces output and contributes to disease progression. Despite this,
the majority of dogs presenting with DCM do not have an audible heart
murmur, which—in contrast to MVD, where 100 % of dogs with clinically
significant disease have an audible heart murmur—presents a challenge for
practitioners to screen for early disease in asymptomatic patients. Affected
dogs can present with left-sided heart failure (pulmonary oedema), or with
bilateral signs due to both ventricles being affected. Prospective clinical
data suggests that Dobermanns with occult DCM benefit from treatment
with pimobendan: heart size reduces, and the asymptomatic phase is
prolonged. This should be extrapolated to other breeds of dogs with DCM
but not yet displaying clinical signs of heart failure.
Recent concerns have been raised about a possible association between
grain-free diets and the development of a nutritional secondary DCM in
dogs. To date, there is no convincing published evidence, but a large
amount of anecdotal evidence exists, and it appears to be a global concern.
The absence of grain seems unlikely, in itself, to cause a problem, but the
large quantities of legumes or pulses (peas, lentils) used to balance the
nutrition in vitro may cause alterations to bile acid metabolism which limit
taurine supply and cause DCM. The current tendency is to obtain a full diet
history for all dogs presented with heart disease and advise switching to a
non–grain free diet if the dog is fed grain-free, home-cooked, or raw diets;
owners who do not wish to feed a complete commercial diet should see a
board-certified veterinary nutritionist to obtain a balanced series of recipes
around which to base their dog’s diet.
Although rarely diagnosed in dogs, HCM is commonplace in cats. Large
epidemiological studies in a shelter population of cats suggest that 15 % of
all cats have HCM, regardless of the presence of an audible heart murmur.
HCM is more common in older cats (30 % prevalence in a group of cats
over 9 years of age). Heart murmurs had, at best, less than a 50 % positive
predictive value for heart disease in all cats. However, increased murmur
intensity (grade III or above), male sex, older age, and body condition score
6/9 or more were factors associated with an increased likelihood of HCM
on echocardiography.
Consensus guidelines on the diagnosis and management of cardiomyopathy

in cats outlined a staging system:
■ Stage A. At risk of cardiomyopathy.
■ Stage B. With preclinical cardiomyopathy.
■ Stage C. With congestive heart failure signs (left- or right-sided).
■ Stage D. With refractory heart failure signs.
Stage B is divided in B1, cats with no left atrial dilation on

echocardiography, and B2, cats with left atrial dilation, in which clopidogrel
should be prescribed to reduce the risk of arterial thromboembolism (ATE).
An HCM phenotype may be caused by primary factors, such as
hyperthyroidism, systemic hypertension, myocardial infiltration,
acromegaly, or transient myocardial thickening (a disorder which may
represent a deleterious effect of catecholamines on the heart). These
diseases should be excluded before a final diagnosis of HCM is made.
In addition to heart failure signs, cats with cardiomyopathy may develop
ATE (caused by poor atrial function, blood stasis, and endothelial
dysfunction) or may suffer sudden cardiac death, presumably associated
with ventricular arrhythmias. Identifying cats most at risk of ATE is
challenging, but it is a disease with high morbidity and mortality. Cats with
ATE almost always have underlying cardiomyopathy, and a prevalence of
0.25 % has been reported in general practice. Prognosis is poor and
recurrence affects up to 50 % of cats, but long-term survival is possible.
With the era of molecular cardiology on the horizon for humans, where
genetic therapy may be able to counteract the disease-causing genetic
abnormalities underlying acquired heart diseases, veterinary cardiology has
become a vitally important research area. Here, animal disease acts as a
naturally occurring model of human disease, providing an area in which to
better understand prognostic factors and biochemical changes associated
with disease progression, or even in which to test novel therapeutic agents.
CASE 1. MYXOMATOUS
MITRAL VALVE DISEASE
SIGNALMENT
Breed: Cavalier King Charles Spaniel
Age: 9 years, 11 months old
Sex: Female, intact
Presenting complaint: Incidental heart murmur detected 2 years
previously. Increased intensity of murmur grade detected recently at routine
vaccination
CLINICAL EXAMINATION
Auscultation revealed a grade IV/VI systolic heart murmur, loudest at the
left apex, with even intensity during systole (band profile). The murmur
extended through to, and partially obscured, the second heart sound (S2).
The patient’s heart rate was 90–100 bpm, and a respiratory sinus arrhythmia
was present. Pulmonary auscultation was normal, as was the remainder of
the physical examination. She weighed 9.5 kg and had a body condition
score of 6/9.
DIAGNOSTIC INVESTIGATION
ECHOCARDIOGRAPHY
The mitral valve appeared thickened and distorted. Severe mitral valve
prolapse was evident in systole (Fig. 1). Wall motion appeared
hyperdynamic (fractional shortening 60 %, normal 25–40 %), and left
ventricular internal diameter in diastole (LVIDd) was enlarged (Fig. 2). Left
atrial dilation was also present (Fig. 3). Left apical views confirmed severe
prolapse (Fig. 4), and Doppler interrogation of transmitral flow pattern
showed increased E wave maximum velocity, suggestive of moderate to
severe mitral regurgitation (Fig. 5).
Findings were consistent with myxomatous mitral valve disease
(MMVD), stage B2: no clinical signs of congestive heart failure but
meeting echocardiographic criteria for cardiomegaly.
Echocardiographic findings of left atrium-to-aortic root ratio >1.6 and

left ventricular internal dimension in diastole corrected for body weight
>1.7, or radiographic identification of vertebral heart score >11.5 or
vertebral left atrial size >3, should prompt treatment with pimobendan to
reduce heart size and slow disease progress.
FIGURE 1. Right parasternal long-axis four-chamber echocardiographic views optimised for the
mitral valve apparatus. In late diastole (a), the mitral valve leaflets (arrows) appear clearly thickened.
In early systole (b), valve prolapse (arrows) is present. A high-resolution zoom image of the valve (c)
shows severe valve prolapse (arrows) in peak systole. Prolapse is defined when the valve leaflets
cross beyond a horizontal line drawn across the mitral annulus between the valve hinge points
(arrowheads). A greater degree of prolapse is associated with a more rapid disease progression, but
mild prolapse may be identified as an incidental finding in dogs, years prior to the onset of a mitral
valve murmur. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 2. Right parasternal short-axis M-mode echocardiographic view of the left ventricle at the
level of the chordae tendineae. Left ventricular internal dimensions in diastole and systole (LVIDd
and LVIDs, respectively) are shown, and an impression of wall motion is provided. When assessing
preclinical mitral valve disease, consensus recommendation is to normalise LVIDd for body weight
(LVIDd-N) using the formula LVIDd (cm)/body weight (kg)0.294. If this measurement exceeds 1.7,
haemodynamically significant chamber enlargement is present. Here, the LVIDd measures 35 mm, so
the LVIDd-N is 1.81.
FIGURE 3. Right parasternal short-axis echocardiographic view for measurement of the left atrium-
to-aortic root (LA:Ao) ratio. Measurement timing is important to standardise. Despite the lack of
consensus amongst cardiologists, many recommend using the first frame of aortic valve closure.
Here, the left atrium is at its largest, and the aortic valve cusps are easy to see and ensure correct
timing. The aorta is measured inner edge to inner edge, from the mid-point of the right coronary cusp
to the commissure between the noncoronary and left coronary cusps (1 o’clock to 7 o’clock if a clock
face analogy is used). The left atrium is also measured inner edge to inner edge, almost as a
continuation of the line used for the aortic root; care must be taken to avoid entering a pulmonary
vein (PV). The LA:Ao ratio measures 1.8 (normal <1.5, enlarged >1.6), identifying that the mitral
regurgitation was haemodynamically significant.
FIGURE 4. Systolic echocardiographic images from a left apical four-chamber view, optimised for
the mitral valve. In the wide-angle image (a), taken in early systole, marked mitral valve prolapse can
be identified. A high-resolution zoom image (b), taken in mid-systole, shows that the prolapse is
predominantly affecting the anterior (septal) mitral valve leaflet (arrows; the point of coaptation
between the anterior and posterior leaflets is indicated by a dashed arrow). Colour flow Doppler (c)
shows at least two jets of mitral regurgitation, with a green mosaic pattern highlighting the largest
regurgitant flow.
FIGURE 5. Pulse wave Doppler echocardiographic trace showing mitral inflow, obtained from a left
apical four-chamber view optimised for flow using colour Doppler. Early (E wave) and late (A wave)
diastolic flow through the mitral valve is visible. Mitral inflow pattern is identified by timing with the
simultaneous electrocardiogram. Early inflow is at the beginning of diastole, just after the T wave
and associated with mitral valve opening as the ventricular pressure drops during relaxation. Late
(atrial) inflow occurs after atrial contraction, so it is timed just after the P wave. Because larger
volumes of mitral regurgitation are associated with a greater atrial pressure at end-systole, an
increase in maximum E wave velocity is associated with worse mitral regurgitation (“what goes
backwards must come forwards”) and more rapid disease progression. In this case, Emax measured
1.24 m/s, which is considered to represent a worse prognosis than lower velocities.
TREATMENT
Pimobendan was prescribed at 0.26 mg/kg PO every 12 h, as recommended
by the 2019 ACVIM consensus statement due to published benefits in
reducing heart size, improving quality of life scores, and prolonging the
time before the onset of heart failure signs in dogs with stage B2 MMVD.
Re-examination for patients in stage B2 on treatment tends to be
scheduled every 6 months, with no strong recommendation for additional
treatment unless the dog develops clinical signs of pulmonary oedema
(when standard treatment with furosemide, spironolactone, and an
angiotensin-converting enzyme [ACE] inhibitor is indicated in addition to
pimobendan).
DISCUSSION
MMVD has several names, which are often used interchangeably, including
degenerative atrioventricular valve disease and endocardiosis. Most
clinicians avoid the term endocardiosis because of possible confusion with
endocarditis, a completely different disease.
Small-breed dogs (<14 kg) are at greater risk of MMVD: Cavalier King
Charles Spaniel, Miniature Dachshund, Chihuahua, Yorkshire Terrier,
Norfolk Terrier, Cocker Spaniel, and Whippet. Small crossbred dogs are
also commonly represented. Large-breed dogs are not free of MMVD; it is
also well described in the Border Collie, German Shepherd Dog, and Great
Dane. Older dogs are more likely to be affected by the disease, presumably
because of an age-dependent penetrance of causative genes and the effect of
epigenetic factors. Male dogs appear to be affected younger or have a more
progressive disease course than females.
Although dogs with MMVD have mitral prolapse prior to the
development of an audible heart murmur, it is reasonable to presume that all
dogs with clinically significant MMVD have an easily audible left apical
heart murmur on auscultation. Murmur grade has been shown to increase as
the severity of MMVD increases (until the weeks before the onset of heart
failure signs, when the murmur grade often reduces because of changes in
pressure gradients and systolic function). A grade I to II/VI heart murmur is
likely to represent early disease, and heart size is probably normal. In
contrast, a grade III or louder murmur is much more likely to indicate
haemodynamically significant disease (causing cardiac remodelling) and
therefore should be prioritised for investigation. Whilst this association is a
fair guideline to use in clinical practice, even dogs with a palpable grade
V/VI murmur can have a normal heart size. Echocardiography is the gold
standard for detecting cardiomegaly, in addition to confirming MMVD as
the diagnosis.
Screening for dogs likely to be affected by myxomatous mitral valve

disease simply relies upon demonstration of a typical heart murmur:
grade II or louder, located at the left apex. Louder murmurs (grade III or
above) should be investigated for cardiomegaly, even in the absence of
overt clinical signs.
Pimobendan has been proven to benefit dogs in stage B2 MMVD. Since

around 60 % of dogs in stage B1 never develop heart failure signs in their
natural lifespan, treatment of all dogs with a mitral murmur is unnecessary,
and—even when owner finances may be limited—some sort of imaging to
determine heart size is vital to make treatment decisions. Where
echocardiography is not an option, radiography to evaluate heart size may
detect more severe left atrial dilation, using either vertebral heart score or
vertebral left atrial size (Fig. 6).
Most dogs in stage B2 develop left-sided congestive heart failure (stage
C). As MMVD progresses with time, patients develop diuretic resistance,
become refractory to standard therapy, and require adjustments to treatment
(stage D). In advanced cases of MMVD, valve apparatus may rupture and
cause a sudden increase in mitral regurgitation severity, leading to severe,
acute pulmonary oedema. In other cases, jet lesions on the atrial
endocardium may become endocardial tears, leading to atrial rupture (often
resulting in sudden cardiac death) or an acquired interatrial communication.
Sudden death is not uncommon in dogs with myxomatous mitral valve

disease, likely associated with a full-thickness endocardial tear, rupture
of a major chorda tendinea, or fatal arrhythmias.
FIGURE 6. Examples of suitable radiographic measures to determine cardiomegaly in dogs with
mitral valve disease. Vertebral heart score (VHS) is measured using both the long and short axis of
the cardiac silhouette (a). The long axis should be measured from the dorsal border, just below the
bifurcation of the trachea, to the apex of the heart. The short axis should be measured at 90° to this,
starting at the dorsal intersection of the caudal vena cava with the cardiac silhouette and extending
cranially. Each of these measurements is taken in vertebral lengths, from the cranial margin of the T4
vertebra, and added in a sum to give the VHS. Median VHS across all dog breeds is 10.7, but >11.5
is considered to be definitely enlarged in dogs predisposed to MMVD. Vertebral left atrial size
(VLAS) is measured similarly (b), but a single measurement of left atrial width is taken across the
caudodorsal margin of the cardiac silhouette (from the bifurcation of the trachea to the dorsal margin
of the caudal vena cava). Normal is <2.5, but a measurement of 3 vertebrae is considered definitely
enlarged. Although echocardiography is the most sensitive method for detecting cardiac remodelling,
radiographic techniques such as this may be more accessible and cost-effective.
CASE 2. DILATED
CARDIOMYOPATHY
SIGNALMENT
Breed: Cocker Spaniel
Age: 8 years old
Sex: Male, neutered
Presenting complaint: Heart murmur detected incidentally at vaccination.
Normal exercise tolerance and no overt clinical signs. One episode of
collapse 9 weeks earlier
Physical examination was unremarkable aside from a grade II/VI left apical
systolic murmur that had a soft quality. The patient’s heart rate was 80 bpm,
with a patterned irregularity typical of sinus arrhythmia. Pulmonary
auscultation and abdominal palpation were normal, and jugular veins were
not distended. Pulse quality, mucous membrane colour, and capillary refill
time were also normal. He weighed 11.6 kg and had a body condition score
of 6/9.
Cardiac troponin I (cTnI) levels were mildly elevated at 0.29 ng/ml
(reference <0.1 ng/ml), and whole blood taurine levels were 382 nmol/ml
(reference >250 nmol/ml).
ECHOCARDIOGRAPHY
Two-dimensional measurements of left ventricular dimensions were
enlarged in both diastole (LVIDd) (Fig. 1) and systole (LVIDs) when
normalised for body weight (LVIDd-N 2.54, reference 1.15–1.55; LVIDs-N
1.95, reference 0.68–1.09). M-mode showed reduced wall excursion (Fig.
2), and planimetric measurements of ejection fraction showed subnormal
systolic function (Fig. 3). Left atrium-to-aortic root ratio was severely
enlarged (Fig. 4). Colour flow Doppler showed a medium-sized, centrally
located jet of mitral regurgitation (Fig. 5). No prolapse or distortion of the
mitral valve was detected. Simultaneous electrocardiography (ECG)
showed a left bundle branch block (wide QRS complex morphology).
FIGURE 1. Echocardiographic 2D images of the heart. Subjectively, wall motion appears to be

reduced. The right parasternal long-axis view shows dilation of the left heart chambers (a). The right
parasternal short-axis view at the level of the papillary muscles (PM) supports these findings (b). Left
ventricular internal diameter in diastole (LVIDd) measurement is indicated in both planes; this should
be performed using a leading edge to leading edge method in the first frame of mitral valve closure
(long-axis) or the onset of the QRS complex (short-axis). LA, left atrium; RA, right atrium; RV, right
ventricle.
FIGURE 2. Echocardiographic M-mode image of the left ventricle acquired at the level of the
chordae tendineae. Wall motion is reduced (fractional shortening 20 %). The positions used to
measure left ventricular internal dimensions in diastole and systole (LVIDd and LVIDs, respectively)
are indicated. LVIDd measurement should be timed to the start of the QRS complex on simultaneous
electrocardiography. Although LVIDs is often measured at the nadir of interventricular septum
motion, there is poor consensus amongst cardiologists owing to different timing between maximal
septum and left ventricular free wall motion when using M-mode. Many cardiologists recommend
using the minimum left ventricular diameter measured between the nadir of septal motion and the
maximal excursion of the free wall, as seen in this figure. This avoids underestimation but may
overestimate wall motion (and therefore systolic function). Because M-mode is a one-dimensional
measurement of a complex 3D movement of the ventricular myocardium, fractional shortening
should not be the sole method used to estimate systolic function. Fractional shortening is calculated
as the difference between end-diastolic and end-systolic diameter, expressed as a percentage of the
end-diastolic diameter.
FIGURE 3. Two-dimensional, planimetric method for estimating ejection fraction using
echocardiography, based on Simpson’s method of discs. The outline of the ventricular endocardium
is traced in two dimensions. Then, computer software splits the left ventricle into 20 segments (discs)
along its length and estimates the volume of each segment based on the diameters indicated from the
manual trace. In the past, this was often performed using a left apical window and a biplane method
(using a four-chamber and a two-chamber view, at right angles to one another) to average out minor
errors in measurement. However, owing to challenges in acquiring the views and accurately tracing
the endocardium from a left apical view, the right parasternal long-axis view is now preferred and has
been shown to correlate well with 3D volumes. The ejection fraction is calculated as the difference
between the end-diastolic volume (a) and the end-systolic volume (b), expressed as a percentage of
the end-diastolic volume. In this case, it measures 30 % (normal >40–50 %).
FIGURE 4. Measurement of left atrium-to-aortic root (LA:Ao) ratio using echocardiography from
the right parasternal short-axis view at the level of the heart base. LA:Ao ratio measures 2.8 (normal
<1.5), suggesting severe left atrial dilation.
FIGURE 5. Colour flow Doppler image taken over the mitral valve from the right parasternal long-
axis view (orientated obliquely to better image regurgitation). A moderately sized jet of mitral
regurgitation is visible as a green mosaic pattern amongst red and blue flow. The central location of
this jet in dogs with left ventricular dilation contrasts with the large, eccentric jet almost always
present in dogs with myxomatous mitral valve disease, which tends to run along the free wall of the
left atrium (LA). Colour settings can be adjusted to make jets appear larger (increasing gain) or
smaller (decreasing gain). To ensure repeatability, the operator should set the level of gain
appropriately prior to recording images by increasing the Doppler gain until the colour image appears
to be covered in speckles, then slowly reducing the gain until the speckles disappear and colour is
seen as clearly uniform flow occurring at appropriate times during the heart cycle. LV, left ventricle.
TWENTY-FOUR-HOUR HOLTER
ELECTROCARDIOGRAPHY
A background sinus rhythm was present throughout. Two isolated
monomorphic ventricular premature complexes (VPCs) were detected and
considered to be normal.
Findings were consistent with primary idiopathic dilated cardiomyopathy
(DCM).
A range of accurate echocardiographic measurements, compared to
weight-indexed or breed-specific reference values, are vital for making a
diagnosis of dilated cardiomyopathy, especially in the preclinical phase
of the disease.
TREATMENT
In order to increase systolic function, pimobendan was prescribed at 0.22
mg/kg PO every 12 h. Re-evaluation of echocardiographic measurements
and 24-hour Holter ECG were planned 6 months after presentation to
monitor for any evidence of disease progression. The owners were
instructed to monitor clinical signs at home and return the dog for re-
evaluation if any concerns arose beforehand.
Pimobendan helps to reduce heart size and prolong symptom-free

survival time in dogs with preclinical dilated cardiomyopathy.
DISCUSSION
DCM is the second most common heart disease in dogs, representing
approximately 10–15 % of all acquired heart diseases identified in practice.
However, this figure is based on historical data which likely
underrepresented preclinical DCM. In reality, many more dogs may be
suffering from preclinical DCM than have been reported in the literature, so
the true prevalence may be higher. In case series evaluating dogs with
DCM, less than half of affected dogs present with a heart murmur, which is
often low grade. This is because mitral regurgitation, which is not a primary
feature of the disease, only occurs secondary to annular stretch, physically
pulling the valve leaflets apart and preventing normal coaptation. The mitral
valve is not thickened or distorted early in the disease, although secondary
myxomatous changes may occur after months or years of a leaking valve
putting the tissue under abnormal strain.
The absence of a heart murmur in most dogs presents a problem: how do
we know which dogs are affected without large-scale screening
programmes to detect occult DCM? Physical examination is of little use,
and echocardiography is the most accurate diagnostic technique. The use of
cardiac biomarker measurement in screening is unknown but the subject of
ongoing research. Increased cTnI and N-terminal pro-brain natriuretic
peptide (NT-proBNP) may be useful to trigger echocardiography, but false
positives and negatives will occur. The combination of both biomarkers
together is likely to be more useful than either alone. Since DCM is an
adult-onset disease in almost all breeds, younger dogs are less likely to
require screening. In addition, a family history of DCM or suspected sudden
cardiac death would be a strong indicator for screening of an individual.
When family history is unclear (as in most dogs), breed predispositions are
important: Dobermanns, Great Danes, and Boxers seem to have an early-
onset, progressive form of DCM, with ventricular arrhythmias and sudden
death occurring frequently. In the Dobermann, a negative echocardiogram
does not exclude the possibility of arrhythmia-only DCM, so 24-h Holter
ECG should be routinely performed as part of screening in this breed. In
contrast, Irish Wolfhounds and Newfoundlands tend to have a more slowly
progressive phenotype of DCM, in which atrial fibrillation predominates
and sudden death is relatively rare. Cocker Spaniels (one of the only non-
large/giant breeds affected by DCM) have been reported to have a longer
disease course and a more benign progression, but severe DCM in this
breed is possible.
Presumably, genetic mutations predispose most dogs to DCM. Only one
causative mutation is currently available for commercial testing (PDK4
gene in the Dobermann in the USA but not in Europe). Inheritance patterns
have been identified in certain breeds (mostly autosomal dominant, but
autosomal recessive in the Portuguese Water Dog juvenile DCM, and
potentially X-linked in some populations of Great Dane). Genetics of DCM
in humans has been proven to be highly complex, suggesting that the
identification of single mutations in dogs is a small part of a much more
complex genetic background, so screening for disease based on a single
genetic test is likely to be highly inaccurate.
In addition, the DCM phenotype may not in fact be caused by a genetic
mutation; it may be another problem masquerading as a primary
cardiomyopathy or “phenocopy” of DCM. For example, in cases with
tachycardia-induced cardiomyopathy (TICM), a persistent tachyarrhythmia
causes systolic dysfunction and chamber dilation which may be
indistinguishable from primary DCM on echocardiography. If the
arrhythmia is identified and treated appropriately, the changes are likely to
be entirely reversible. In the case reported here, a 24-hour Holter was
performed to exclude significant arrhythmias, which may be intermittent
and not detected in-hospital. Less than 50 VPCs/day is considered normal
in dogs, and no tachyarrhythmias were detected, so TICM was ruled out.
Another example of a DCM phenocopy is the development of systolic
dysfunction and chamber dilation which may occur after myocarditis,
because of extensive myocardial damage and fibrosis. A number of dogs
diagnosed with DCM may have in fact a chronic myocarditis underlying the
echocardiographic changes. Identifying which of these diseases is present is
almost impossible, even with endomyocardial biopsy techniques.
Histopathological changes in primary DCM involve fibrosis and other
similarities to chronic myocarditis, and microbiological or molecular
techniques may not detect an infectious agent in a chronic case. In the
present case, cTnI levels were measured to exclude an acute myocarditis
(>5–8 ng/ml would be indicative, a 50- to 80-fold increase above
reference). The mild to moderate elevation detected in the patient was likely
secondary to chronic myocardial disease.
Dilated cardiomyopathy (DCM) in dogs is mostly caused by primary

genetic mutations, but there are other causes of the DCM phenotype,
including tachycardia-induced cardiomyopathy and chronic myocarditis.
In dogs with DCM, treatment with pimobendan in the preclinical phase

has been shown to prolong the symptom-free survival time. Before
prescribing any long-term medication, it is important to be as sure about the
diagnosis as possible and to exclude any reversible problems, such as
TICM. If primary DCM is suspected, screening close family relatives is
recommended, especially breeding individuals. Most dogs with DCM will
develop heart failure or arrhythmias in time, but many have a good quality
of life on treatment for some years.
CASE 3. HYPERTROPHIC
CARDIOMYOPATHY
SIGNALMENT
Breed: Domestic shorthair cat
Age: 11 years old
Sex: Male, neutered
Presenting complaint: 24-hour history of tachypnoea. Progressive lethargy
and inappetence over 7–10 days. A heart murmur had been reported in the
past
The cat was quiet but alert and responsive. His mucous membranes were
pink and moist, with a prolonged capillary refill time (>2 seconds). The
respiratory rate was increased at 56 breaths per minute with a restrictive
(rapid and shallow) respiratory pattern. The heart rate was 180 bpm, and
auscultation revealed a gallop sound. Occasional premature beats were
heard. No heart murmurs were detected, but lung sounds were muffled in
the ventral half of the thorax. The patient weighed 5.01 kg and had a body
condition score of 4/9, with mild muscle wastage over the dorsum. The
femoral pulse was normal bilaterally.
After cage rest and oxygen therapy, noninvasive systolic blood pressure
was measured by Doppler ultrasound at 80 mmHg (reference 120–160
mmHg).
The results of the complete blood cell count and serum biochemical profile
were unremarkable, including total thyroxine measurement.
Sedation with intramuscular butorphanol (0.2 mg/kg) facilitated
diagnostic testing.
THORACIC ULTRASONOGRAPHY AND

THORACOCENTESIS
A focused thoracic ultrasound revealed a moderate amount of anechoic
pleural fluid. Thoracocentesis was performed and 210 ml of pink-tinged,
translucent fluid was drained using a butterfly needle. Fluid analysis
identified a modified transudate.
Focused ultrasonographic assessment is preferable over thoracic

radiography in the patient with respiratory distress, especially when
pleural effusion is included in the differential diagnosis.
ECHOCARDIOGRAPHY
Asymmetric diastolic left ventricular hypertrophy was present. The free
wall measured 8.0 mm and the interventricular septum measured 6.2 mm
(reference <5.5 mm) (Fig. 1). The left atrium (LA) was severely dilated
(maximum LA diameter was 24 mm, reference <16 mm; left atrium-to-
aortic root ratio was 2.3, reference <1.5) (Fig. 2) with poor function (poor
left atrial motion in M-mode and low LA appendage flow velocity of up to
0.2 m/s, reference >0.4 m/s) (Fig. 3). Spontaneous echocontrast was visible
in the left auricular appendage. No left ventricular outflow tract obstruction
was detected. Doppler interrogation of mitral (Fig. 4) and pulmonary
venous inflows showed a restrictive diastolic flow pattern, suggestive of
increased left atrial pressure and most likely congestive heart failure, given
the concurrent respiratory pattern.
Left atrial size is a crucial part in the echocardiographic assessment in

cats with respiratory distress.
FIGURE 1. Echocardiographic images of the left ventricle showing asymmetric hypertrophy, with a
thicker free wall (asterisk) than the interventricular septum (double asterisk). LA, left atrium; LV, left
ventricle.
FIGURE 2. Echocardiographic images showing severe left atrial dilation, measured both in the long-
axis (a), timed at maximum left atrial diameter (LAD) in the image frame prior to mitral valve
opening, and in the short-axis (b), timed in the first frame in which the aortic valve appears closed.
An enlarged left auricular appendage (LAA) can be seen clearly in the short-axis view. Ao, aorta;
LA, left atrium.
FIGURE 3. Echocardiographic images showing depressed left atrial function. Left atrial motion
measured by fractional shortening was subnormal (a). Left auricular appendage (LAA) flow velocity
was low (cursor placement within the dilated auricle is shown in b; a flow velocity of up to 0.2 m/s is
demonstrated in c). LA, left atrium; LV, left ventricle.
FIGURE 4. Continuous wave Doppler interrogation demonstrating the restrictive pattern identified
to mitral inflow. Timing of the various flow patterns can be associated with simultaneous ECG.
ELECTROCARDIOGRAPHY
A background sinus rhythm was present, with frequent atrial and ventricular
premature complexes, likely secondary to atrial dilation.
Findings were consistent with hypertrophic cardiomyopathy (HCM) with
a severe increase in left atrial pressure. In the context of a pleural effusion
and ascites, and suspected increased filling pressures, a diagnosis of
congestive heart failure was made. Due to the impaired atrial function with
severe left atrial dilation, the patient was also considered at risk of arterial
thromboembolism (ATE). Based on the 2020 ACVIM consensus statement
on feline cardiomyopathy, this case was in stage C: overt clinical signs.
TREATMENT
After an initial injection of intramuscular furosemide (2 mg/kg), oral
furosemide was administered at a dose of 2 mg/kg every 12 h using a liquid
preparation to help control congestive signs of fluid accumulation.
Resting/sleeping respiratory rate monitoring was advised to check that the
patient’s clinical signs were under control, and furosemide dose was titrated
to effect. The target respiratory rate was set below 30 breaths per minute.
To reduce the ATE risk, clopidogrel was prescribed at 18.75 mg PO every
24 h. Although clopidogrel is not licensed in cats, research shows safety as
well as clinical benefit by reducing ATE recurrence in at-risk cats. In
addition, pimobendan was prescribed at a total dose of 1.25 mg per cat PO
every 12 h. Again, this medication is currently off-label, but studies suggest
that this drug is also safe in cats and may be beneficial in cats with HCM.
After 24 hours of treatment, the patient had significantly improved, had a
normal systolic blood pressure (140 mmHg), and was eating well. He was
discharged from the hospital that day. The body weight had reduced to 4.6
kg, suggesting loss of total body water. Two weeks after initiating
treatment, the sleeping respiratory rate was well controlled at 24 breaths per
minute, and the dose of furosemide was reduced to 1 mg/kg every 12 h.
After 2 months of treatment, the respiratory rate was observed to have
increased acutely to 44 breaths per minute with increased effort at rest, and
the patient was presented out-of-hours to an emergency clinic. After
stabilisation, thoracic radiography showed cardiomegaly (vertebral heart
score [VHS] 8.5, reference: 7–7.5), marked pulmonary vascular congestion,
a mixed (interstitial and alveolar) lung pattern with predominantly
caudodorsal distribution, small bilateral pleural effusion with retraction of
the lungs from the thoracic wall, and mild hepatomegaly (Fig. 5). These
abnormalities were diagnostic of a heart failure relapse. The dose of
furosemide was increased to 2 mg/kg every 12 h, and the respiratory rate
normalised once again. The patient’s overall quality of life was good; he
remained active and continued to eat well for some months.
Sadly, 11 months after initial presentation, the cat was brought to the
clinic as an emergency by staff from a boarding kennel, who had found the
patient acutely distressed and unable to use the hindlimbs. On examination,
femoral pulse was absent bilaterally and ATE was suspected. Euthanasia
was elected at this time.
FIGURE 5. Thoracic radiographs (dorsoventral [a] and right lateral [b] projections) obtained by the
emergency clinic 2 months after initial presentation, exhibiting a small pleural effusion,
cardiomegaly (best seen in the dorsoventral view), pulmonary vascular congestion (arrowheads), and
marked pulmonary infiltrates. Findings were indicative of left-sided congestive heart failure.
DISCUSSION
Hypertrophic cardiomyopathy (HCM) is a common feline disease, affecting
15 % of cats across all ages, and 30–40 % in older age-groups. It is a
diagnosis of exclusion, where characteristic left ventricular concentric
hypertrophy is detected in the absence of inciting systemic disease (e.g.
hyperthyroidism) or altered loading conditions (e.g. systemic hypertension
or aortic stenosis). It is an idiopathic disease, which presumably has a
genetic basis in cats as it does in humans, although no commercially
available genetic tests for HCM in nonpedigree cats are currently available.
Around 30 % of cats with HCM go on to develop heart failure or ATE,
and a smaller proportion are at risk of sudden cardiac death, presumably
caused by arrhythmias. A 2020 consensus statement on cardiomyopathy in
cats describes a staging system similar to that used for mitral valve disease
in dogs (A–D), where stage B2 reflects cats with moderate to severe left
atrial dilation but no overt clinical signs. These cats are likely to benefit
from treatment with clopidogrel to reduce their risk of ATE.
In advanced cases of HCM, left ventricular remodelling leads to
increased left atrial pressure and poses a risk of left-sided heart failure. In
cats, this most commonly presents as pulmonary oedema, pleural effusion,
or both. In the case presented here, the presence of pulmonary oedema at
the time of initial presentation was never confirmed, but a pleural effusion
in the presence of severe cardiac remodelling and Doppler estimates of high
left atrial pressure were highly suggestive of heart failure. This was also
supported by a response to furosemide therapy.
A thoracic ultrasound was then performed in sternal recumbency before
stabilisation. It was sufficient to detect a clinically significant pleural
effusion and facilitated thoracocentesis before handling the patient any
further. This method of assessing patients with respiratory distress is
preferred over thoracic radiography as it minimises patient stress whilst
maximising diagnostic yield, allowing the operator to also look for left
atrial dilation and B lines (evidence of increased lung water, suggesting
pulmonary oedema). Once respiratory distress was relieved in this patient,
echocardiography was possible and confirmed the diagnosis of HCM.
In this case, the echocardiographic findings of severe left atrial dilation
and poor atrial function suggested an increased risk of ATE. Determining
which cats are more likely to die because of ATE or heart failure is not
possible using current clinical or echocardiographic measures. Spontaneous
echocontrast represents aggregation of platelets and erythrocytes in vivo
and is associated with reduced atrial function in cats with HCM. Preventive
treatment with clopidogrel is indicated for at-risk patients, but some cats
sadly succumb to ATE despite this.
Cats with reduced left atrial function have a shorter survival time and a
greater risk of arterial thromboembolism. Clopidogrel is indicated in
these cases to reduce the risk and prolong survival.
It is possible that combining clopidogrel with low-dose aspirin, or the use

of novel, oral anti-Xa agents (e.g. apixaban) may provide better
antithrombotic potential, but clinical trials are needed in this area.
The off-licence use of pimobendan in cats is an area of growing interest
amongst cardiologists. In patients without significant outflow tract
obstruction, it may provide benefits by improving left ventricular and left
atrial function, improving cardiac output without greatly increasing
myocardial oxygen demand.
The median survival time in cats with HCM after the onset of clinical
signs of heart failure has been estimated to be approximately 1 year. Poor
atrial function and a lack of outflow tract obstruction (as described in this
case) may represent negative prognostic indicators.
CASE 4. ARRHYTHMOGENIC
RIGHT VENTRICULAR
CARDIOMYOPATHY
SIGNALMENT
Breed: Boxer
Sex: Female, neutered
Presenting complaint: Episodic collapse with transient loss of
consciousness and postural tone (typical syncope events)
On presentation, the dog was active but appeared somewhat depressed. The
mucous membrane colour was normal, but the capillary refill time was
prolonged (3 seconds). The patient’s body condition score was reduced
(4/9). A possible hepatomegaly and fluid thrill were detected on abdominal
ballottement. Jugular distension was present at rest, with a positive
hepatojugular reflux. Auscultation did not reveal any heart murmur, but
frequent premature beats and runs of tachycardia were present. The
background heart rate was approximately of 100 bpm, but runs of
tachycardia were at much higher rates. Femoral pulse quality was normal,
but frequent pulse deficits were associated with periods of arrhythmia.
ELECTROCARDIOGRAPHY
A background sinus rhythm was present, with frequent ventricular
premature complexes (VPCs) (Fig. 1).
FIGURE 1. Six-lead electrocardiogram showing a background sinus rhythm with ventricular

premature complexes. The positive QRS complex of these ventricular beats in lead II suggests a right
ventricular origin. A ventricular couplet (complexes 2 and 3 from the left) and a notched QRS
complex (leads III, aVL, and aVF) suggest the presence of myocardial disease. [50 mm/s, 10
mm/mV].
ECHOCARDIOGRAPHY
Global systolic function was subnormal, with left atrial dilation and a
prominent right heart with dysfunction (Fig. 2, Video 1). Tricuspid annular
plane systolic excursion, an M-mode measurement of longitudinal right
ventricular systolic function, was low (12 mm, reference >15 mm in
Boxers). Focused abdominal assessment showed a small volume of free
fluid around the liver lobes, confirming ascites.
FIGURE 2. Echocardiographic images showing right heart dilation. Left atrial diastolic dimensions
appear relatively normal but the right heart is moderately enlarged (a–c). In M-mode (d), reduced
excursion of the left ventricular walls and increased end-systolic left ventricular diameter are present,
supportive of reduced systolic function.
Video 1
Right parasternal long-axis echocardiographic view showing poor systolic function and right
ventricular prominence.
ELECTROCARDIOGRAPHY
Complex arrhythmias were present over the recording period and 5,077
VPCs occurred, many of which exhibited complex morphology, including
couplets, triplets, runs of ventricular tachycardia, and R-on-T phenomenon
(Fig. 3). The complex ventricular arrhythmias were thought to represent a
risk of worsening of the clinical signs and possibly sudden cardiac death,
despite the fact that no episodes of syncope occurred during the Holter
recording; therefore, anti-arrhythmic treatment was recommended.
The diagnosis was arrhythmogenic right ventricular cardiomyopathy
(ARVC) based on a cutoff of 100 VPCs/24 h with complex arrhythmias,
which caused systolic dysfunction and signs of right-sided heart failure.
Arrhythmogenic right ventricular cardiomyopathy is diagnosed by a

combination of clinical signs and detection of more than 100 ventricular
premature complexes in 24 hours on Holter electrocardiography.
FIGURE 3. Selected electrocardiogram strips from the 24-hour Holter recording illustrating the
range of complex ventricular arrhythmias. Background sinus rhythm with frequent ventricular
premature complexes (VPCs) in an alternating pattern (ventricular bigeminy) (a). Ventricular
couplets occurring frequently (b). Background sinus rhythm with a VPC and a fast run of ventricular
tachycardia, with an instantaneous rate exceeding 300 bpm and R-on-T phenomenon (c). [25 mm/s,
10 mm/mV].
TREATMENT
Furosemide was prescribed at 2 mg/kg every 12 h to control signs of
congestive heart failure. To treat systolic dysfunction, pimobendan was
prescribed at 7.5 mg every 12 h. Anti-arrhythmic therapy with sotalol was
recommended, up-titrated over 10 days to a target dose of 1.5–2 mg/kg.
Repeat echocardiography and Holter electrocardiography were advised after
1 week on the target dose in order to assess anti-arrhythmic treatment
efficacy, and also to re-examine systolic function and left atrial size as the
β-blocking effects of sotalol may worsen function in patients with
myocardial disease.
Sotalol is the first-line anti-arrhythmic drug to control ventricular ectopy,

but may pose a risk of decompensating heart failure owing to its negative
effect on systolic function.
DISCUSSION
ARVC is a primary myocardial disease associated with fibrofatty
infiltration of the right (and possibly left) heart and loss of normal
myocardial cell structure. This change in the tissue causes a syndrome of
complex ventricular and supraventricular arrhythmias and systolic
dysfunction, which leads to clinical signs of poor cardiac output, syncope,
heart failure, or possibly sudden cardiac death. Although histopathology
offers the only definitive diagnosis, the clinical syndrome in at-risk breeds
(e.g. Boxer or English Bulldog) and the detection of >100 VPCs on a 24-
hour Holter recording is highly suggestive of ARVC. In the past, some
controversy has existed over an appropriate Holter criteria for ARVC
diagnosis, ranging from 50 to 300 VPCs/24 h, but recent work in
collaboration with human ARVC experts suggests that >100 VPCs/24 h is a
clinically useful cutoff value.
Dogs with arrhythmogenic right ventricular cardiomyopathy may present

with signs of heart failure, associated with systolic dysfunction and a
dilated cardiomyopathy-like phenotype on echocardiography.
Genetic studies in the USA initially suggested a causative gene (the

striatin mutation) in Boxer dogs. However, larger studies in the UK,
combined with pedigree analyses, proved that the striatin mutation was not
causative in this population and demonstrated linkage with a different,
unknown causative gene. Consequently, the striatin genetic test could
produce false negative results, especially in Boxers tested outside the USA.
ARVC has been described in three stages in the Boxer dog:

■ Stage 1. Detectable arrhythmias but no clinical signs.
■ Stage 2. Presence of arrhythmias and clinical signs of syncope or
episodic weakness but no echocardiographic evidence of myocardial
dysfunction.
■ Stage 3. Presence of arrhythmias with cardiac dilation and systolic
dysfunction on echocardiography and signs of heart failure.
In the case presented here, findings were consistent with a stage 3 ARVC.
The distinction between stage 3 ARVC and dilated cardiomyopathy
(DCM) in Boxer dogs is blurred, as both diseases can present with systolic
dysfunction and arrhythmias. Interestingly, genetic studies evaluating the
effect of striatin mutation genotype on disease phenotype suggest that dogs
with systolic dysfunction tend to be homozygous for the gene. Although no
consensus exists, cardiologists will generally refer to a Boxer dog with
systolic dysfunction and frequent, complex ventricular arrhythmias on
Holter monitoring as having ARVC rather than DCM. Definition does not
affect treatment, which should be tailored to the individual needs of each
case. Herein, pimobendan and furosemide were used to treat the clinical
signs of heart failure, and sotalol to control ventricular arrhythmias.
At low doses, sotalol has predominantly β-blocking effects, with additive
potassium channel blockade at higher doses. It is generally well tolerated by
patients, but clinicians should be aware of the potential negative effects of
β-blockade in dogs at risk for, or with a history of, congestive heart failure.
In patients presenting like this particular case, where arrhythmias are
detrimental to cardiac output and pose a significant risk of sudden death,
but signs of heart failure are evident, treatment choice should be carefully
considered. In the case presented here, sotalol was introduced at a low dose
and up-titrated slowly to minimise the risk of potential adverse events.
Alternative options would be to treat with amiodarone, another potassium
channel blocker with less potent β-blocking effects and additive sodium
channel blocking activity, or to use mexiletine (a class I sodium channel
blocking drug) and atenolol in combination. The latter is a β-blocker, like
sotalol, but as it is a separate preparation to mexiletine, the dose can be kept
low or titrated to a level tolerated by the patient. Follow-up Holter
monitoring is useful to assess efficacy of anti-arrhythmic treatment and
titrate drug dose to effect as required. Despite the best intentions, some dogs
with ARVC respond poorly to anti-arrhythmic therapy.
Most dogs with ARVC live for a reasonable time on treatment for their
disease. A proportion of dogs appear to remain relatively free of clinical
signs for some years, but even those with a good response to treatment may
remain at risk for sudden cardiac death and owners should be suitably
informed in order to manage expectations.
CASE 5. CARDIAC
HAEMANGIOSARCOMA
SIGNALMENT
Breed: Border Collie
Sex: Male, neutered
Presenting complaint: Acute onset collapse during exercise that morning,
without prior history. Referring veterinary surgeons detected pale mucous
membranes, tachycardia, and extreme lethargy. A fluid bolus was
administered, and blood tests were performed prior to referral for
emergency assessment (haematology and biochemical profile showed no
significant abnormalities)
The patient’s mucous membranes were pale and moist, with a prolonged
capillary refill time (3 seconds). His heart rate was 152 bpm, and his
respiratory rate was 40 breaths per minute. No murmur was detected on
thoracic auscultation, and his heart sounds were quiet. His pulmonary
sounds were amplified by tachypnoea but normal otherwise. On abdominal
palpation, mild hepatomegaly was detected. Femoral pulse quality was
weak overall and variable (almost absent on inspiration but easier to palpate
on expiration).
ELECTROCARDIOGRAPHY
The electrocardiogram showed a sinus rhythm with electrical alternans (Fig.
1). This is highly suggestive of pericardial effusion (PE), which was
confirmed by a focused thoracic ultrasound scan.
FIGURE 1. Six-lead electrocardiogram showing a sinus rhythm with electrical alternans. QRS
complex amplitude alternates between high (arrowheads) and low (arrows) because of changes in
cardiac axis caused by a swinging motion of the heart within a pericardial effusion. [50 mm/s, 10
mm/mV].
ECHOCARDIOGRAPHY
Echocardiography confirmed a moderate volume of PE (Fig. 2), with raised
intrapericardial pressure evidenced by dynamic right atrial collapse (Fig. 3).
A soft-tissue mass with a cavitary appearance was present on the tip of the
right auricle (Fig. 4, Video 1). The position and echotexture of the mass
were suggestive of a haemangiosarcoma.
Findings were consistent with a haemangiosarcoma, which caused
pericardial haemorrhage.
Cardiac haemangiosarcomas tend to occur in the right heart—especially
the right atrium, auricle, and atrioventricular groove—and have a
cavitated appearance on echocardiography.
FIGURE 2. Right parasternal short-axis echocardiographic view confirming pericardial effusion

(PE), which clearly delineates cardiac structures. LV, left ventricle; RV, right ventricle.
FIGURE 3. Right parasternal long-axis echocardiographic views in diastole (a) and systole (b)
optimised for the right atrium (RA). A small volume of pleural fluid (X) is present and helps to
identify the pericardium containing pericardial effusion (PE). Dynamic change in volume of the RA
was detected: filling of the atrium in late diastole (more on inspiration), and collapse of the atrium
(arrow) in systole (worse on expiration). This finding is crucial, as it determines that the PE is
haemodynamically significant and clinical signs of right heart failure are likely. LA, left atrium; RV,
right ventricle.
FIGURE 4. Left cranial echocardiographic view optimised for the right atrium (RA) and auricular
appendage. A soft-tissue mass (delineated with arrows) surrounded by pericardial effusion (PE) can
be seen at the tip of the auricle.
Video 1
Left cranial echocardiographic view optimised to show the right auricular appendage. An
oscillating, soft-tissue density structure is present associated with the tip of the auricle and
highlighted by a small volume of anechoic pericardial fluid.
TREATMENT
After a discussion with the dog’s owner regarding a possible malignant
tumour, pericardiocentesis was performed to stabilise the patient and obtain
pericardial fluid samples prior to further diagnostics (Fig. 5). Cytological
examination showed reactive mesothelial cells, as expected, but no
evidence of neoplasia, thereby excluding cardiac lymphoma, which
exfoliates well. A CT scan was performed to screen for evidence of
metastasis, but no significant abnormalities were detected (Fig. 6).
Since the mass appeared isolated and located at the tip of the right
auricle, with no evidence of metastasis, surgical treatment was pursued. The
aim of surgery was to prevent further pericardial haemorrhage and obtain a
tissue sample for histopathological confirmation of diagnosis.
Using a right fourth intercostal approach, the thorax was opened and
lungs retracted to expose the heart. After opening the pericardium and
performing a subphrenic pericardiectomy, the mass was clearly visible (Fig.
7, Video 2). It was excised using a surgical stapler, and the chest was closed
routinely. Postoperative recovery was uneventful.
Histopathological results confirmed a haemangiosarcoma (Fig. 8): a
malignant tumour of blood vessels. After a 2-week recovery period, the
patient began a CHOP (cyclophosphamide, doxorubicin, vincristine, and
prednisolone) chemotherapy protocol. Quality of life was good, behaviour
and exercise tolerance were normal, and no complications of chemotherapy
were noted. After 11 months, however, the dog presented with
haemoabdomen, and a splenic mass was confirmed. At this point,
euthanasia was elected.
FIGURE 5. Image of a different patient undergoing pericardiocentesis. The procedure is performed

under sedation with a small-bore chest drain placed using a modified Seldinger technique. An
appropriate window is found using ultrasound guidance on the right hemithorax to reduce the risk of
complications associated with the needle contacting the epicardium. If the needle touches the right
ventricle during pericardiocentesis, ventricular arrhythmias occur but are often self-limiting. If the
needle were to contact the left ventricular epicardium, it could potentially lacerate the left anterior
descending coronary artery and cause fatal haemorrhage. Samples should be obtained for cytology
and possibly bacteriology.
FIGURE 6. Image of the patient undergoing a CT scan to screen for significant thoracic or
abdominal abnormalities. Further imaging to identify possible metastasis of cardiac tumours is
indicated in cases where treatment is considered a reasonable option.
FIGURE 7. Surgical excision of the mass and subtotal pericardiectomy via a right fourth intercostal
thoracotomy. Intraoperatively, the mass (delineated with arrows) was located on a pedicle of tissue
which arose from the tip of the right auricular (RA) appendage (a). A surgical stapler was used to
excise the tip of the auricle (b). After excision, the mass (star) measured 2–3 cm in diameter (c).
Arrowheads indicate the line of staples.
Video 2
Surgical view obtained during right lateral fourth intercostal thoracotomy. The lungs are
retracted, and the right auricle is grasped using atraumatic tissue forceps. A dark red thrombus
surrounds the mass lesions in the tip of the right auricle.
FIGURE 8. Histopathological images of the right auricular mass. At low-power magnification (a), a
large thrombus (asterisk) comprising most of the volume of the mass can be seen, whilst abnormal
cells (stained purple with haematoxylin–eosin) occupy the free wall of the auricle (arrows) and
trabeculae carneae of the internal surface (dashed line). The abnormal cells extend beyond the
surgical margin (solid line). At high-power magnification (b), basophilic cells show features of a
sarcoma, with frequent mitotic figures (arrowheads) and atypical shape and distribution, and form
channels resembling blood vessels (containing erythrocytes). These findings are typical of a
haemangiosarcoma.
DISCUSSION
Approximately half of all dogs presented with PE have an idiopathic
inflammatory pericarditis, and neoplastic causes account for the remainder
of cases. Haemangiosarcoma is a common cause of PE, but heart base
tumours (mostly chemodectomas), mesothelioma, and lymphoma are also
frequently diagnosed. Other types of tumour rarely reported include
myxosarcoma, chondrosarcoma, fibrosarcoma, osteosarcoma, and others.
Heart base tumours are easily diagnosed on echocardiography or cross-
sectional imaging because they invariably occupy a large volume before
causing PE. Lymphoma is easily diagnosed on cytological examination of
PE because of its tendency to exfoliate well (Fig. 9). In contrast,
haemangiosarcoma can be microscopic at the time of haemorrhage (causing
PE) or may be masked by normal cardiac structures (e.g. trabeculae in the
auricles or fat pads in the atrioventricular groove) on echocardiographic
examination. Mesothelioma can also be a diagnostic challenge, as it is not
typically visible on an echocardiogram or CT scan, and may rely on
pericardiectomy to provide tissue samples for histopathological analysis.
Cytological examination of the PE almost always identifies reactive
mesothelial cells, which makes impossible to reliably identify
mesothelioma using only fluid analysis techniques.
The cause of 50 % of all cases of pericardial effusion in dogs is

neoplastic, and haemangiosarcoma is the most common type of tumour
diagnosed
FIGURE 9. Cytological images of pericardial fluid from a dog with cardiac lymphoma. At low-
power magnification (a), high numbers of basophilic, variable-staining round cells can be identified
amongst a background of erythrocytes. At high-power magnification (b), poikilocytosis, abnormal
nuclear morphology, and vacuolar changes are present.
In this case, a haemangiosarcoma was strongly suspected based on

echocardiographic findings (echotexture and position of the lesion were
typical). In the absence of metastasis on thoracic and abdominal CT scan,
mass excision via auriculectomy is a good treatment option for dogs if their
owners are motivated to treat—and finances allow. When a PE is known to
be caused by a right atrial mass, euthanasia is a fair consideration and
should be discussed as an option with owners, given the high index of
suspicion for haemangiosarcoma and the aggressively malignant behaviour
of this tumour. In most cases, micrometastasis has occurred at the time of
diagnosis and pericardiocentesis (and surgery) has increased the risk of the
tumour seeding elsewhere within the thorax. Since, in this case, the mass
appeared isolated, and its location at the tip of the auricle allowed for a
straightforward surgical intervention, surgery was pursued. Postoperative
chemotherapy, either using a metronomic protocol (meloxicam and
cyclophosphamide) or a doxorubicin-based protocol (e.g. CHOP), can be
considered to prolong the time to recurrence. All of these approaches
should be recognised as palliative, as the likelihood of a cure is very low
indeed.
Most cases, like the one described here, have a good quality of life
postoperatively on treatment, but clinical signs associated with
haemangiosarcoma tend to recur within 6–12 months. Without
auriculectomy, most dogs die within days or weeks owing to repeated
haemorrhage.
In dogs with pericardial effusion but no echocardiographic evidence of a

mass, neoplastic causes, such as haemangiosarcoma or mesothelioma,
cannot be excluded.
CASE 6. HEART BASE
TUMOUR
SIGNALMENT
Breed: English Springer Spaniel
Age: 10 years old
Sex: Male, neutered
Presenting complaint: Abdominal effusion, lethargy, and low body
condition score
Although alert, the dog was somewhat quiet and had obvious abdominal
distension. His body condition score was low (3/9). A fluid thrill was
detected on abdominal ballottement. His heart rate was 142 bpm, and his
respiratory rate was 36 breaths per minute. The heart sounds were quiet,
and no heart murmur was audible. His mucous membranes were pink and
moist, but capillary refill time was prolonged (2.5 seconds). Peripheral
pulse quality was poor, and there was no jugular venous distension.
ULTRASONOGRAPHY
Echocardiography revealed a very large soft tissue mass at the heart base,
apparently arising from the heart base (Fig. 1). Right atrial compression was
evident. No pericardial effusion or pleural fluid were present. Aside from
the mass, cardiac structure and function appeared normal. Ultrasonography
confirmed the presence of abdominal fluid, which was determined to be a
modified transudate after performing a fluid tap.
FIGURE 1. Right parasternal echocardiographic views showing the position of the large heart base
mass, which arises from the aortic root, close to the interatrial septum, and appears to obliterate the
right atrium.
CT SCAN
A CT scan of the thorax and abdomen was performed to look for
metastases, as well as a nonselective angiogram via lateral saphenous
injection to assess blood flow dynamics. No evidence of local spread or
distant metastases was identified. The mass measured 5.8 cm × 4.2 cm ×
4.8 cm and entirely obliterated right atrial inflow from the caudal vena
cava. The caudal vena cava appeared distended but not contrast enhancing
(Fig. 2). No contrast could be seen flowing beyond the hepatic parenchyma.
Instead, contrast from the hindlimb injection passed first into the caudal
vena cava, was diverted via collateral flow into a dilated azygous vein and
the vertebral veins, and then entered the right atrium through the cranial
vena cava (Fig. 3).
Fine needle aspirations of the mass were performed under ultrasound
guidance, and cytological examination of the samples showed changes
suggestive of a neuroendocrine tumour.
The diagnosis was a heart base tumour, likely of neuroendocrine origin
(e.g. chemodectoma), which occluded the caudal vena cava and caused
clinical signs of ascites without jugular venous distension (Budd–Chiari-
like syndrome).
FIGURE 2. Transverse (a) and dorsal (b) CT reconstructions of the thorax showing the position of
the heart base mass (star). In the dorsal section, the caudal vena cava can be identified caudal to the
right atrium (RA) but is not contrast enhancing, suggestive of significant blood flow abnormalities.
LA, left atrium; LV, left ventricle; RV, right ventricle.
FIGURE 3. Sagittal CT reconstruction of the thorax showing contrast-enhanced venous return from
the abdomen, via a distended azygous vein (Az) and multiple vertebral veins (arrowheads), to the
heart through the cranial vena cava. Note the mass (star) and the distended, non-contrast-enhanced
caudal vena cava (arrows).
TREATMENT
Furosemide (1 mg/kg PO every 12 h) was prescribed to reduce circulating
volume and therefore alleviate clinical signs of ascites. In addition,
spironolactone (2 mg/kg PO every 24 h) and benazepril (0.5 mg/kg PO
every 24 h) were administered to blunt the activation of the renin–
angiotensin–aldosterone system.
Because caval compression was the cause of ascites, the primary goal of
treatment was to restore normal right atrial inflow. Transatrial stent
placement was preferred over a more invasive surgical approach to
minimise risks of procedural complications.
Palliative treatment for heart base tumours, for example pericardiectomy

(if effusive) or vascular stenting (if compressive), is often associated with
long-term survival, as these masses tend to be slow growing and have a
low potential for metastasis.
The anaesthetised dog was positioned in right lateral recumbency. After

performing a small surgical cutdown to the right femoral vein, vascular
access was achieved using a modified Seldinger technique in the femoral
vein (with an 8 F vascular introducer). The technique was repeated using a
percutaneous approach in the left jugular vein (with a 12 F vascular
introducer). Under fluoroscopic guidance, the caudal vena cava was
accessed from the femoral vein, and contrast was injected at the level of the
diaphragm; trivial contrast flow into the right heart was seen.
From the femoral approach, a 260 cm J-tipped guidewire was advanced
into the right atrium, around the mass. From the jugular approach, a
vascular snare was advanced into the right atrium and used to grab the tip of
the femoral guidewire (Fig. 4a). The femoral guidewire was then
exteriorised through the jugular access sheath to create a “through-and-
through” loop of guidewire from the femoral to the jugular vein that
permitted stable access. Over this wire, serial balloon dilations were
performed using first a 10 mm and then a 14 mm balloon dilation catheter
to stretch the mass away from the walls of the caudal vena cava and right
atrium and to break down any local adhesions and thrombi that may have
been present (Fig. 4b). After removing the balloon catheters, a 16 mm × 8
cm woven metallic stent was advanced through the right atrium, around the
mass, until the distal end was located in the caudal vena cava. The stent was
then deployed so that it spanned the right atrium, from caudal to cranial
vena cava (Fig. 4c). A repeat contrast injection in the caudal vena cava
showed significantly improved blood flow into the right heart. Radiographs
taken after the procedure confirmed an appropriate stent position (Fig. 5).
The patient was rested strictly for 48 hours and then discharged, with
instructions of lead-only exercise for 4 weeks. Ascites had resolved within
7 days of hospital discharge and demeanour had normalised. Medical
treatment was discontinued. At recheck 1 month after discharge,
echocardiography confirmed adequate cranial and caudal vena cava inflow.
No abdominal fluid was present and the patient’s body condition score had
increased to 6/9. Thoracic radiographs showed no alteration in stent
position or conformation. At 6, 12, and 24 months postoperatively, the dog
remained asymptomatic and in good body condition. His exercise tolerance
was normal throughout this time.
FIGURE 4. Still fluoroscopic images showing the minimally invasive transatrial stent procedure.
The vascular snare inserted through the jugular vein can be seen grasping the J-tipped guidewire
passed from femoral vein into the right atrium (a). A balloon dilation catheter pushes the mass away
from the walls of the caudal vena cava and right atrium (b). The stent is deployed in the right atrium
(c).
FIGURE 5. Thoracic radiographs (dorsoventral [a] and right lateral [b] projections) taken after the
transatrial stent procedure showing the stent in an appropriate position. In the dorsoventral view, the
stent can be seen compressed towards its caudal aspect, locating the point of maximum tumour
diameter. Note the abdominal effusion in both images, visible as a loss of abdominal contrast.
DISCUSSION
The most common types of heart base tumour are chemodectomas,
paragangliomas, and ectopic thyroid carcinomas; the first being by far the
most frequent. Chemodectomas, which are relatively common in
brachycephalic dog breeds, arise from the chemoreceptor cells of the wall
of the ascending aorta, near the pulmonary artery and left and right atria.
These masses are often benign and slow growing; therefore, they may be
detected incidentally in dogs with no clinical signs, during
echocardiographic examination for other reasons.
Although heart base tumours are often benign growths, surgical
debulking poses a significant risk due to their inconvenient location.
Although most heart base tumours cause clinical signs of pericardial

effusion, this case presented with evidence of large vessel occlusion.
Typically, ascites associated with right-sided heart failure or pericardial
effusion (cardiac tamponade) is detected concurrently with jugular venous
distension. In the case described above, the unremarkable physical
examination of the jugular veins can be explained by the position of the
mass, which occluded only caudal caval inflow but allowed normal venous
return from the cranial vena cava. This clinical picture is known as the
Budd–Chiari-like syndrome.
Most heart base tumours present with clinical signs owing to pericardial
effusion. However, on occasion, vascular compression is the primary
cause of morbidity.
In this patient, CT imaging illustrated collateral blood flow bypassing the

heart base tumour through multiple vertebral veins and the azygous vein.
Although this adaptation no doubt delayed the onset of the clinical signs,
the capacity of collateral vessels for venous return was likely to be
relatively low, which lead to inadequate return of abdominal blood to the
heart and the development of ascites because of the high hydrostatic
pressure within the hepatic sinusoids. Once normal caval inflow was
restored by the stent procedure, all clinical signs resolved within the
following weeks and no long-term medical management was required.
CASE 7. INFECTIVE
ENDOCARDITIS
SIGNALMENT
Breed: Italian Spinone
Presenting complaint: Four-week history of intermittent pyrexia and
lethargy, with variable response to antibiotic and anti-inflammatory therapy.
Haematology showed neutrophilia and mild nonregenerative anaemia.
Presented very depressed and lethargic, and a heart murmur was detected
A grade II/VI early systolic and a grade III/VI diastolic heart murmur were
detectable, both loudest at the left base. The patient’s heart rate was 120
bpm, with hyperdynamic pulse quality. The mucous membranes were dark
pink, with a prolonged capillary refill time (2.5 seconds). Abdominal
palpation was unremarkable. Mentation was depressed, but she was
responsive and could walk normally when encouraged. Her respiratory rate
was 40 breaths per minute, but pulmonary auscultation was unremarkable.
Her body temperature was 39.9 °C. She weighed 41.6 kg and had a body
condition score of 5/9.
Cardiac troponin I levels were 5.2 ng/ml (reference <0.1 ng/ml), and C-
reactive protein (CRP) levels were 168.4 mg/l (reference <10 mg/l).
ECHOCARDIOGRAPHY
A large, oscillating lesion was present on the ventricular aspect of the aortic
valve (Fig. 1, Video 1), affecting all three leaflets (Fig. 2, Video 2). Aortic
insufficiency was visible on colour and continuous wave Doppler (Fig. 3,
Video 3), with a relatively short pressure half-time, suggesting that it was
haemodynamically significant. The mitral valve appeared unaffected by the
lesion.
FIGURE 1. Right parasternal long-axis echocardiographic view optimised for the left ventricular
outflow tract. The aortic valve is thickened and nodular (arrowheads) with fronds of oscillating tissue
on the ventricular aspect of the valve (arrow). Ao, aorta; LV, left ventricle.
Video 1
Right parasternal long-axis echocardiographic view optimised for left ventricular outflow. The
aortic valve is distorted by oscillating soft-tissue density lesions, affecting both visible cusps.
FIGURE 2. Right parasternal short-axis echocardiographic view taken in mid-systole and optimised
for the aortic valve and left atrium (LA). All three cusps of the aortic valve (arrows) are irregular,
thickened, and incompletely opened. Ao, aorta.
Video 2
Right parasternal short-axis echocardiographic view optimised for the aortic valve. All three
aortic valve cusps appear thickened by the lesion. Left atrial size measurement was at the top
end of the normal range.
FIGURE 3. Aortic regurgitation in diastole. Colour flow Doppler (a) detects multiple jets of aortic
regurgitation which continue flowing throughout diastole (Video 3) and extend far into the
ventricular cavity. Continuous wave Doppler (b) shows a short pressure half-time (significant
reduction in velocity of the regurgitation during the diastolic time interval), suggesting that the
diastolic aortic pressure reduces significantly as a result of the aortic valve regurgitation (i.e. the
valve leak is haemodynamically significant). Ao, aorta. LV, left ventricle.
Video 3
Colour flow Doppler mapping of the right parasternal long-axis outflow tract echocardiographic
view. Severe aortic regurgitation is present, across both visible cusps of the aortic valve, and is
visible throughout diastole.
CT SCAN
Computed tomography of the abdomen and thorax was performed. No
evidence of a site of primary infection was detected, but infarction was
found bilaterally in the renal cortex, suggestive of thromboembolic
consequences of the valve lesions (Fig. 4).
FIGURE 4. CT images showing evidence of infarction of both renal cortices. In arterial phase
postcontrast images (soft-tissue window in transverse plane) (a), loss of the normal contrast uptake
(arrow) in the renal cortex was identified at the lateral aspect of the cranial pole of the right kidney
(RK). In 3D reconstruction (b), the extent of infarction in both kidneys can be seen by a loss of the
normal smooth cortical architecture (arrows). Ao, aorta; LK, left kidney; SI, small intestine; Sp,
spleen.
Clinical and echocardiographic findings were diagnostic of endocarditis,

based on the modified Duke criteria (Table 1). Diagnosis is classified
according to fulfilled criteria as follows:
■ Definitive. Two major criteria, or one major and two minor criteria
■ Possible. One major and one minor criteria, or three minor criteria
■ Rejected. If a firm alternative explanation of clinical signs is made, or if
clinical signs resolve with fewer than 4 days of treatment
Diagnosis of endocarditis should be made using the modified Duke

criteria of major and minor clinical findings.
TABLE 1. Suggested modified Duke criteria for diagnosis of infective endocarditis in dogs (adapted
from MacDonald et al. 2010)
Criteria Findings
■ Echocardiographic valve lesion with typical

characteristics of endocarditis:*
■ Oscillates independently of valve motion
■ Associated with atrial aspect of mitral valve or
ventricular aspect of aortic valve
Major
■ Positive blood cultures:*
■ ≥2 positive blood cultures
■ ≥3 with common skin contaminants
■ Evidence of new valve insufficiency (on
echocardiography or auscultation)
■ Pyrexia of unknown origin*

■ Predisposing factor (e.g. corticosteroid use or subaortic
stenosis)
■ Evidence of embolic signs*
Minor
■ Evidence of systemic immune-mediated disease
■ Medium- to large-breed dog (body weight >15 kg)*
■ Positive blood cultures not meeting major criteria
■ Bartonella spp. serological antibody titre ≥1:1024
* Criteria met in this case (two major and three minor).
BLOOD CULTURE
Blood samples for culture were taken aseptically from three sites at two
different time points. The results were available 48 hours later and revealed
pure growth of Corynebacterium spp. (at all three sites), which was
sensitive to benzylpenicillin, marbofloxacin, and tetracyclines but resistant
in vitro to gentamycin and trimethoprim–sulfamethoxazole. This confirmed
a diagnosis of infective endocarditis.
TREATMENT
Before blood culture results, intravenous antibiotic therapy was initiated
with marbofloxacin (2 mg/kg every 24 h) and clindamycin (10 mg/kg every
24 h). The patient’s demeanour improved markedly and pyrexia resolved.
After receiving blood culture results, clindamycin was discontinued, and
marbofloxacin was administered once daily as before. After 7 days of
intravenous antibiotic therapy, CRP levels had reduced to 32.6 mg/l. The
dog was transitioned to oral marbofloxacin and discharged from the hospital
for an additional 4-week treatment. At this time, CRP remained similarly
elevated. After 8 weeks of treatment, CRP levels were within reference at
3.2 mg/l, and oral antibiotic therapy was stopped. Echocardiography
showed a thickened aortic valve but no oscillating tissue associated with it.
Aortic regurgitation remained present.
Six months after diagnosis, the dog had no clinical signs of disease.
Echocardiography showed that the aortic valve was thickened, but no
vegetative lesions could be seen (Fig. 5). Aortic regurgitation remained
present, and chamber dimensions of the left heart were above weight-scaled
reference intervals; therefore, pimobendan was prescribed.
Echocardiography 2 months later (8 months after diagnosis) demonstrated
further left ventricular enlargement, but the left atrial size had not changed
(Fig. 6).
FIGURE 5. Right parasternal long-axis echocardiographic view of the left ventricular outflow tract
and aortic valve showing no evidence of ongoing vegetative lesions on the valve. The aortic valve
(arrowheads) looks subjectively slightly thickened, and aortic regurgitation remains present. Ao,
aorta; LV, left ventricle.
FIGURE 6. Right parasternal long-axis four-chamber echocardiographic views showing
measurements of left heart chamber dimensions at two different points in time. Left ventricular
dimensions in diastole (a) and systole (b) were enlarged and systolic function subnormal at 6 months
after diagnosis, and this had progressed by 8 months after diagnosis. Left atrial diameter (long-axis,
largest size prior to mitral valve opening) was also above reference but had not altered between the
two time points (c). Reference values: LVIDd-N 1.15–1.55; LVIDs-N 0.68–1.09; LA diameter-N
1.19–1.56. LA, left atrium; LV, left ventricle.
DISCUSSION
Infective endocarditis is an uncommon disease in dogs. The presence of a
predisposing heart disease, especially subaortic stenosis (where high
velocity flow originates below the valve and causes jet lesions and
microfissures on the endocardium of the ventricular aspect of the aortic
valve, allowing bacterial adhesion to the exposed tissue), has led to many
cardiologists recognising the disease in Boxer dogs. In companion species
(dogs, cats, horses), endocarditis occurs almost exclusively on the aortic
and mitral valves, whereas the tricuspid valve is affected in ruminants and
pigs. In camelids, mural endocarditis of either side of the heart seems most
common. The different presentations of this disease are likely to reflect
variable pathophysiology and host immune response.
Endocarditis typically affects the aortic or mitral valve in dogs, cats, and
horses.
Endocarditis is a challenging diagnosis to make, and cases often present

with a chronic history of waxing and waning clinical signs, including
pyrexia and systemic disorders associated with immune complex deposition
or thromboembolic disease. The modified Duke criteria are used to weigh
the likelihood of diagnosis in light of major and minor criteria. Today,
echocardiography is an essential diagnostic tool, but it is theoretically
possible to score a definitive diagnosis with positive blood cultures (one
major criterion), body weight >15 kg, and a history of pyrexia >39.7 °C
(two minor criteria). However, these findings should be contextualised
before making a diagnosis of endocarditis, as they could be explained, for
example, by a para-oesophageal abscess or other septic foci in a dog that
happens to be of large breed. In contrast, if a typical valve lesion is
identified by echocardiography, but blood cultures are negative,
endocarditis should remain a likely differential diagnosis, especially if there
is a history of recent antibiotic use which may reduce circulating
bacteraemia and result in false-negative blood culture results.
Blood cultures may be negative in dogs with endocarditis owing to recent

antibiotic therapy, so accurate echocardiographic assessment is crucial to
diagnosis.
In a number of publications, Bartonella spp. have been implicated in
endocarditis, but there may be geographic differences (e.g. relatively
uncommon in Northern Europe compared to the USA). However,
Bartonella PCR should be considered in dogs with negative blood cultures,
or fluoroquinolone therapy should be considered to provide appropriate
coverage. If blood culture results are negative, but the modified Duke
criteria are met by other means, four-quadrant antibiotic coverage should be
provided intravenously for 7 days, followed by at least 4 weeks of oral
antibiotic therapy. Occasional cases relapse after the change from
intravenous to oral therapy, but a further 7-day course of intravenous
antibiotics might prevent this from happening again. Sadly, some dogs fail
to respond to intravenous antibiotics and may require euthanasia on welfare
grounds in the first week of treatment.
There is no consensus on the optimal duration of oral antibiotic treatment
for endocarditis. Echocardiographic changes are a poor guide to therapy, as
valve tissue may remain inflamed or scarred by fibrous tissue long after the
infective organism has been successfully treated. In addition, layers of
bacteria on the valve may alternate with layers of fibrin and thrombotic
tissue, which protects bacteria from the effects of antibiotics. For this
reason, at least 4 weeks of oral treatment is recommended. Using
circulating inflammatory markers, such as CRP, may be an objective way to
decide on when antibiotics should be discontinued, but there is no published
data to support that this approach is superior to another, and consensus
among experts is lacking.
Even if the acute phase of endocarditis is treated, damage to the affected
valve may remain long-term. Aortic regurgitation is generally poorly
tolerated when clinically significant. Small jets may be present long-term
without significant cardiac remodelling; however, in the case described
here, the relatively short pressure half-time detected on Doppler
interrogation of aortic regurgitation at presentation marked a poorer
prognosis. Follow-up over the months after diagnosis showed progressive
left ventricular dilation and a degree of left atrial enlargement, but the dog
did not show clinical signs of congestive heart failure during this time.
Aortic valve replacement using a transcatheter technique has been reported
in one dog and may represent a future option for similarly affected patients.
ARRHYTHMIAS
Sinus rhythm originates in the sinoatrial node, located at the junction

between the cranial vena cava and the right atrium. The local anatomy is
complex, but in dogs it is connected to the atrioventricular node (AVN) and
the left atrial myocardium by a series of specialised internodal tracts. The
AVN is the only pathway for electrical impulses to pass from atrium to
ventricle in the normal heart, and it is located on the floor of the right
atrium, proximate to the septal leaflet of the tricuspid valve. It is an area of
naturally slow conduction, which temporally separates atrial contraction
from ventricular contraction, allowing the atrial kick to fill the ventricles
and optimise stroke volume. Loss of this normal atrioventricular synchrony
causes approximately a 20 % reduction in cardiac output.
Beyond the AVN, the conduction system travels in the high ventricular
septum (bundle of His) and then splits into the right bundle branch (moving
from the interventricular septum to the right ventricle superficially and
within the moderator band of the right ventricle) and two fascicles of the
left bundle branch, the anterior and posterior fascicles, which split close to
the leaflets of the aortic valve. The conduction system of the left ventricle is
buried deeper within the myocardium than that of the right side. Distally,
the conduction system terminates in a network of Purkinje fibres, most
dense around the papillary muscles and least dense towards the heart base.
Arrhythmias can occur because of four main mechanisms:

■ Abnormal automaticity. Either a nonpacemaker cell gains the ability to
depolarise spontaneously (e.g. ischaemia, inflammation, electrolyte
abnormalities) or a normal pacemaker current is suppressed. Examples
include ventricular tachycardia and focal atrial tachycardia.
■ Enhanced normal automaticity. A normal pacemaker cell becomes
rapid firing. Examples include ventricular tachycardia and focal
junctional tachycardia.
■ Reentrant circuits. Divided into micro reentrant (around small areas of
ischaemic or fibrous tissue) and macro reentrant (around larger structures
such as the right atrium between atria and ventricles). Examples include
ventricular tachycardia and supraventricular tachycardia (micro reentry)
and atrioventricular reciprocating tachycardia and atrial flutter (macro
reentry).
■ Blocks. Termination or attenuation of normal conduction through an
anatomic circuit because of inflammation, ischaemia, fibrosis, or
autonomic imbalance. Examples include left bundle branch block and
third-degree atrioventricular block.
Reading the ECG is an essential skill for veterinary surgeons, but it is often
perceived as intimidating or complex. Sight-reading (pattern recognition) of
ECG abnormalities may be a rapid and effective tool but is prone to
unconscious error. When a logical, simple approach to ECG reading is
adopted and combined with knowledge of the basic anatomy of the
conduction system and pathophysiology of arrhythmias, differentials for
any observed ECG abnormalities can be listed and evaluated in terms of
likelihood, even when the answer may not have been obvious at first look.
Commonly encountered arrhythmias in veterinary practice are:

■ Ventricular premature complex (VPC). Isolated VPCs may be caused
by primary myocardial disease, secondary myocardial damage, an
enhanced physiologic response (stress), or noncardiac diseases. These are
probably as common in critical or anaesthetised patients as in animals
with heart disease. Accelerated idioventricular rhythm is the term given
to runs of VPCs (four or more in a row) with a heart rate up to 160 bpm.
Above this, the term ventricular tachycardia (VT) may be used. At rates
>240 bpm, VT may be electrically unstable and can lead to polymorphic
VT (also called torsade de pointes because the electrical axis of
conduction looks like it twists around a central point) or ventricular
fibrillation, thereby posing a risk of sudden death. In addition, high-rate
ventricular episodes can activate ventricular mechanoreceptors which
lead to reflex bradycardia and vasodilation. This can be one mechanism
of syncope in affected dogs (in addition to tachycardia itself limiting
cardiac output) but has also been reported as a cause of sudden cardiac
death. Instantaneous heart rate of ventricular arrhythmias is usually the
major determinant of treatment requirement, along with complexity and
haemodynamic effect on the patient.
■ Atrial fibrillation (AF). A lack of coordinated atrial activity, leading to
a highly irregular rhythm and no discernible P waves on ECG. Here, the
AVN is bombarded with around 600 impulses per minute, and its slow
conduction and long refractory period prevent ventricular response rate
from matching that (not compatible with life). In cats and small-breed
dogs, AF can only occur with a large atrial mass, so suggests severe heart
disease causing remodelling. In giant-breed dogs, AF may be diagnosed
without underlying heart disease (“lone AF”). In these cases, ventricular
response rate tends to be lower, and treatment may not be required.
However, long-term, irregularity of the heart itself can cause cardiac
remodelling. Assessment of mean 24-hour heart rate using Holter
analysis is important in dogs with AF to make decisions about the need
for rate control medication. Higher rates are associated with a shorter
survival time.
■ Supraventricular premature complexes. Isolated supraventricular
premature complexes (or atrial premature complexes, APCs) can, like
VPCs, be caused by both cardiac disease (atrial dilation) or noncardiac
disease (enhanced physiologic responses to stress and pain). However,
frequent APCs may be a marker of underlying supraventricular
tachycardia (SVT) or a predisposition to AF if the patient would be
considered otherwise at risk. SVT in dogs may have a number of
underlying causes, including focal atrial tachycardia, atrioventricular
reciprocating tachycardia, junctional tachycardia, or atrial flutter.
Determination of which rhythm is present may only be possible using
electrophysiologic mapping techniques (intracardiac ECG). Treatment
requirement depends on rate, and sudden death caused by SVT is rare.
■ Third-degree atrioventricular block. Complete block of
atrioventricular conduction at the level of the AVN, commonly caused by
inflammatory or degenerative changes, and occasionally by drugs,
toxicity, electrolyte abnormalities, or infiltration. Affected dogs are
markedly bradycardic and reliant on normal ventricular escape foci. If
these escape foci fail, asystole results. Medical treatment is rarely
effective, and identifying the underlying cause is almost always
impossible without endomyocardial biopsy techniques (which has
limited accuracy). However, dogs tend to respond well to pacemaker
implantation so that a more normal heart rate can be restored.
Arrhythmias are a common complication of heart disease but may also be

caused by extracardiac diseases. In particular, ventricular arrhythmias can
be caused by systemic inflammation, gastrointestinal disease, neoplasia
(cardiac or noncardiac), structural abdominal disorders (splenic mass
lesions, gastric dilation–volvulus [GDV]), catecholamine excess (stress,
fear, pain), toxicity, heatstroke, or myocardial trauma. In the critical patient,
a number of these factors are often present, so ventricular arrhythmias are
perhaps more common in these cases. The majority of dogs and cats with
secondary arrhythmias are not at high risk of sudden death and, therefore,
do not require specific anti-arrhythmic treatment. However, occasional dogs
with a GDV may require anti-arrhythmic medication to control ventricular
arrhythmias in the days after surgical treatment.
In animals with primary cardiac disease, anti-arrhythmic therapy is
usually lifelong. In the absence of almost any randomised controlled trials,
the choice of antiarrhythmic is often based on knowledge about the drug’s
primary activity and experience of the clinician. Consequently, there is a
lack of consensus or standardisation on choice of anti-arrhythmic agents,
and even on when to treat an arrhythmia. Added to this, a huge day-to-day
variation in arrhythmia frequency can occur, posing other difficulties of
performing treatment trials in veterinary patients. There is a great need for
prospective clinical trials of different anti-arrhythmic protocols for dogs and
cats in order to maximise the best outcomes over the coming decades in
these patients. Until then, expert advice is the best level of evidence on
which to base decision-making.
CASE 8. VENTRICULAR
TACHYCARDIA
SIGNALMENT
Breed: Dalmatian
Sex: Male, neutered
Presenting complaint: Episodic collapse during exertion or excitement: the
dog appears weak for a few paces and then collapses with flaccid limbs,
nonresponsive to owner interaction for 10–30 seconds (sometimes with
opisthotonos or mild limb paddling); then recovers consciousness and
achieves sternal recumbency. After 20–30 seconds, he stands, walks, and
resumes activity. Episodes have occurred five times in the last 2 weeks, and
heavy panting episodes have also been noted at home and during exercise.
Appetite and behaviour are otherwise normal. Episodes were classified as
highly suggestive of syncope
Premature beats were detected on auscultation, on a background of what
sounded like sinus arrhythmia. The patient’s heart rate was 100 bpm.
Pulmonary auscultation and abdominal palpation were normal, and jugular
veins were not distended. Pulse quality, mucous membrane colour, and
capillary refill time were normal, but pulse deficits were associated with
premature beats. He weighed 32 kg and had a body condition score of 7/9.
No abnormalities were detected on haematologic examination or
biochemical profile. Cardiac troponin I (cTnI) levels were mildly elevated
at 0.12 ng/ml (reference <0.1 ng/ml).
ELECTROCARDIOGRAPHY
Background sinus rhythm was present, but frequent ventricular premature
complexes (VPCs) and one episode of ventricular tachycardia (VT) were
detected (Fig. 1).
FIGURE 1. Sixty-second electrocardiographic strip in lead II showing a background sinus rhythm

with occasional ventricular premature complexes (VPCs) and a run of ventricular tachycardia (VT) at
approximately 250 bpm for almost 10 seconds. [25 mm/s, 10 mm/mV].
ECHOCARDIOGRAPHY
Two-dimensional and Doppler measurements were all within reference for
body weight. No systolic dysfunction or chamber dilation was present (Fig.
2).
FIGURE 2. Right parasternal echocardiographic views: long-axis four-chamber (a), short-axis at the
chordae tendineae (b), and short-axis optimised for left atrium-to-aortic root ratio (avoiding the
pulmonary vein) (c). No structural abnormalities can be seen in the left or right heart. Systolic
function appeared normal. Ao, aorta; LA, left atrium; LV, left ventricle; PV, pulmonary vein; RA,
right atrium; RV, right ventricle.
ABDOMINAL ULTRASONOGRAPHY
An abdominal ultrasound scan was performed and was normal. No evidence
of hepatic or splenic abnormality was identified.
ELECTROCARDIOGRAPHY
Twenty-four-hour Holter monitoring (Fig. 3) revealed the presence of a
background sinus rhythm, with common ventricular ectopy (10,410
ventricular ectopic beats) and complexity (ventricular bigeminy and
episodes of VT). During several periods of ventricular ectopy, the owners
noted heavy panting in the patient event diary (Fig. 4). Maximum
ventricular rate was recorded at 320 bpm, with R-on-T phenomenon.
Findings were consistent with VT as the cause of clinical signs. No
underlying cardiomyopathy could be appreciated. Acute myocarditis was
ruled out because the echocardiogram was normal and cTnI levels were not
severely increased.
FIGURE 3. Image of the patient fitted with a 24-hour Holter monitor to record heart rate and rhythm
outside of the hospital environment.
FIGURE 4. Selected electrocardiographic strips from the 24-hour Holter recording demonstrating
the start (a) and end (b) of an episode of ventricular tachycardia (VT) at a heart rate of approximately
300 bpm, evidenced by wide, bizarre QRS complexes in all leads. This episode lasted around 1
minute. [25 mm/s, 10 mm/mV].
TREATMENT
Holter monitoring results suggested that anti-arrhythmic medication was
indicated: although no syncope occurred during the recording period, heavy
panting was associated with almost 1 minute of VT. Oral anti-arrhythmic
drug choices are as follows:
■ Class I. Sodium channel blockers (e.g. mexiletine). Good for ventricular
arrhythmias caused by damaged cells (hypoxia, fibrosis, inflammation).
■ Class II. β-blockers (e.g. atenolol). Good for ventricular arrhythmias
which occur most often at times of high sympathetic tone (exertion,
stress).
■ Class III. Potassium channel blockers (e.g. sotalol—also class II action
—or amiodarone—also class I, II, and IV actions). Good for ventricular
arrhythmias caused by after-depolarisations. Mixed-action drugs provide
cover for different causes of arrhythmia.
■ Class IV. Calcium channel blockers. Not suitable for ventricular
arrhythmias.
■ Cardiac glycosides. May worsen ventricular arrhythmias.
Sotalol was selected in this case. Its mix of class II and III actions provides
a balance of anti-arrhythmic activity, and the β-blockade may have other
cardioprotective effects. Sotalol is initiated at 1 mg/kg PO every 12 h for 1
week, and then increased to a target dose of 2–3 mg/kg PO every 12 h in
order to minimise any adverse effects upon initiation. In this case, 40 mg
every 12 h was up-titrated to 80 mg every 12 h. A Holter performed 3
weeks into treatment showed a reduction in the frequency of ventricular
ectopy overall (1,129 ectopics over 24 h) and no significant complexity.
Now that the arrhythmia was stabilised, further diagnostics were performed.
■ Thoracic and abdominal CT scan. No abnormalities were detected.
■ Cardiac MRI scan. No evidence of fibrosis or occult tissue damage was
present (Fig. 5).
No further syncope had occurred, and the patient was no longer

experiencing episodes of heavy panting. Treatment with sotalol was
maintained at 80 mg every 12 h, and a repeat Holter was recommended 6
months later for monitoring arrhythmia recurrence.
Holter electrocardiography should be used as a monitoring tool to assess

treatment safety as well as efficacy. A baseline Holter recording prior to
starting treatment is preferable to identify potential proarrhythmic effects
of drugs, but it is not always possible in unstable cases.
FIGURE 5. Cardiac MRI scan showing normal heart structure and no evidence of fibrosis. This
image is a four-chamber view, similar to the echocardiographic view but in a different orientation.
LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
DISCUSSION
Ventricular arrhythmias are common in dogs with heart disease (e.g. dilated
cardiomyopathy) but may be diagnosed in dogs without an identifiable
cardiac cause. In such cases, significant intra-abdominal disease should be
excluded using a combination of screening blood work and abdominal
imaging. The link between splenic or hepatic masses and ventricular
arrhythmias is well known, but the mechanism of the association is not
understood. Similarly, splenic torsion or gastric dilation/volvulus can cause
ventricular arrhythmias. Although rarely complex or life-threatening, these
secondary arrhythmias may present with risk factors for sudden cardiac
death, such as a high instantaneous rate and the presence of R-on-T
phenomenon.
Other possible causes of ventricular arrhythmias in the absence of
echocardiographic changes are electrolyte abnormalities, myocarditis, or
paraneoplastic disorders. In this case, electrolyte abnormalities and acute
myocarditis were excluded (normal blood test results, including cTnI), and
thoracic and abdominal CT scan did not detect evidence of primary or
metastatic neoplasia. In dogs like this, the most likely cause of ventricular
arrhythmias is an unknown insult to the myocardium, such as a small
infarction or area of fibrosis which is undetectable using echocardiography.
To exclude this, the highly motivated owners pursued MRI of the heart; the
results did not show any structural or functional abnormalities, suggesting
that no macroscopic lesion was present.
Although ventricular tachycardia is a common feature of dilated

cardiomyopathy in certain breeds, noncardiac causes (e.g. intra-
abdominal disease, electrolyte abnormalities, toxicity, sepsis, neoplasia)
are possible. In some cases, no primary cause can be identified, and
arrhythmias should simply be treated to control clinical signs.
The decision to treat with anti-arrhythmic drugs should be taken based on

the results of Holter monitoring and echocardiography. If a patient presents
with haemodynamically significant VT and requires drug stabilisation,
treatment should be prioritised over diagnostics to ensure survival and
improved quality of life. If possible, a baseline Holter recording is
recommended, as any anti-arrhythmic medication can also have a
proarrhythmic effect. In this case, the dog appeared stable enough to obtain
a Holter recording before prescribing medication, and results indicated that
treatment was required; the follow-up Holter recording showed reduction in
arrhythmia frequency and complexity.
The decision to treat ventricular arrhythmias should be taken based on
risk factors for sudden death, including frequent ventricular tachycardia,
high instantaneous rates, and the presence of R-on-T phenomenon.
Up to 90 % day-to-day variability in the frequency of ventricular

arrhythmia in dogs has been reported. This means that in this case, where
initial Holter electrocardiography detected around 10,000 VPCs, a
reduction to 1,000 may be on the boundary of normal variation and not
represent a genuine treatment response. However, complexity (namely,
presence of VT, episodes of ventricular bigeminy, couplets and triplets, and
instantaneous rates >250 bpm) was also significantly reduced, and the
clinical signs had resolved. These are better markers of treatment efficacy
than simply the VPC number. Once this patient had stabilised, anaesthesia
for advanced diagnostics was performed. In many cases, diagnostics may be
limited at the point of Holter assessment owing to cost of cross-sectional
imaging or accessibility of a centre that performs cardiac MRI.
Sotalol is generally a safe anti-arrhythmic drug and works well for
controlling ventricular arrhythmias. Care should be taken because of its β-
blocking effects in patients with systolic dysfunction, left atrial dilation, or
a history of heart failure. These patients may be reliant on low numbers of
β-receptors (which are downregulated in the failing heart), so β-blockers
will have a profound effect. Gradual introduction of the dose may
circumvent this, but owners should be advised to return for reassessment if
respiratory rate or effort increases, and echocardiography should be
performed early in this protocol to detect dogs that are not tolerating the
drug well.
Periodic Holter monitoring and echocardiography are recommended for
dogs receiving anti-arrhythmic treatment in order to identify early signs of
cardiomyopathy and ensure appropriate control of ventricular arrhythmias.
In some cases, discontinuing drug therapy may be possible if the primary
cause (e.g. splenic mass) has been removed, or simply to test whether
lifelong treatment is genuinely required. However, a candid discussion with
owners about the risk of clinical deterioration, or even death, should be
undertaken before reducing the dose of medication.
CASE 9.
SUPRAVENTRICULAR
TACHYCARDIA
SIGNALMENT
Breed: Labrador Retriever
Age: 1 year, 11 months old
Sex: Male, neutered
Presenting complaint: Syncope associated with low-level exercise or
excitement. Recent onset abdominal distension and reduced appetite
Auscultation revealed severe tachycardia at a rate too high to accurately
count (300 bpm or more). No heart murmur was audible at this rate. The
mucous membranes were pale pink, with a prolonged capillary refill time (4
seconds). The patient’s pulse rate was lower than his heart rate, at 50 bpm,
and pulse quality was weak. Abdominal dissension was present, with a fluid
thrill on ballottement and jugular venous distension. He weighed 32 kg and
had a body condition score of 6/9.
ELECTROCARDIOGRAPHY
A narrow complex tachycardia was present (heart rate of 375 bpm). A
single bolus of diltiazem was administered intravenously at 0.2 mg/kg over
60 seconds, and the rhythm converted to sinus arrhythmia (Fig. 1). At the
point of conversion, S–T segment morphology during tachycardia differed
from that during sinus rhythm. This was highly suggestive of a hidden,
abnormal P wave (called a P’ wave), which confirmed the diagnosis of
supraventricular tachycardia (SVT). The distance between R and P’ waves
was shorter than that between P’ and R waves, and there was a negative P’
wave in leads II, III, and aVF and a positive P’ wave in leads I and aVL
(Fig. 2). These findings supported the presence of an accessory pathway
causing the SVT.
A narrow complex tachycardia (QRS duration <0.07 seconds) with an

upright morphology in leads II and aVF is likely to be supraventricular in
origin.
FIGURE 1. Electrocardiogram obtained at the time of conversion from supraventricular tachycardia

(SVT) to sinus rhythm after administration of diltiazem (0.2 mg/kg IV). The first QRS complex after
SVT termination differs in morphology to subsequent sinus beats and has no clear P wave associated
with it (circle). This may relate to the time taken for normal pacemaker currents to recover after
overdrive suppression during SVT or may be caused by an interaction of the arrhythmia with anti-
arrhythmic drugs. The 16th and subsequent beats have normal complex morphology. [50 mm/s, 10
mm/mV].
FIGURE 2. Detail from Figure 1 showing supraventricular tachycardia (SVT) and sinus rhythm,
particularly the differences in S–T segment morphology. P’ waves are most obvious in leads I and
aVL (arrows), and the timing of the P’ wave (dashed line) shows a R–P’ interval that is shorter than
the P’–R interval (marked in lead II). This timing is typical of an accessory pathway-mediated
supraventricular tachycardia, as is the negative P’ wave in leads II, III, and aVF and the positive P’
wave in leads I and aVL.
ECHOCARDIOGRAPHY
The left ventricle was dilated compared to weight-based reference intervals,
and mild left atrial dilation was also present (Fig. 3). Systolic dysfunction
was observed (fractional shortening 12 %, ejection fraction 30 %). No
pleural or pericardial fluid was identified, but a small volume of ascites was
confirmed.
FIGURE 3. Echocardiographic images obtained during sinus tachycardia. Right parasternal long-
axis view (a) showing that the left ventricle (LV) is enlarged compared to weight-specific reference
intervals (left ventricular internal dimensions in diastole and systole normalised for body weight,
respectively, LVIDd-N 1.79, reference <1.55; LVIDs-N 1.40, reference <1.09). The left atrium (LA)
is mildly dilated (left atrium-to-aortic root ratio 1.7, normal <1.5) (b). M-mode demonstrating poor
systolic function (c). A central jet of mitral regurgitation appears on colour Doppler scan, best seen in
the left apical four-chamber view (d). Ao, aorta; RA, right atrium; RV, right ventricle.
ELECTROCARDIOGRAPHY
Episodes of SVT were recorded 282 times (>60 % of all heartbeats), with
the longest run having >17,000 beats at a maximum rate of 390 bpm (Fig.
4). Aberrant beats were detected at the termination of SVT episodes, and
occasional ventricular premature complexes were identified. All SVT
episodes were of sudden onset and offset, and no nonconducted P’ waves
were identified. These features suggested an atrioventricular node-
dependent SVT, supporting an accessory pathway as the leading differential
diagnosis.
FIGURE 4. Holter electrocardiography detected frequent supraventricular tachycardia (SVT) for
prolonged periods of the day. The tachogram (a), a graph of minute-average heart rate plotted over
time, shows lengthy periods of heart rate over 200 bpm, with only a sleep period corresponding to
more normal heart rates overnight. The SVT was common and often prolonged. The onset of a
representative episode (b) shows sudden switch from sinus rhythm to SVT, without a gradual
increase in heart rate. The offset is similarly sudden (c), and difference in S–T segment morphology
was evident between the SVT (arrow) and sinus rhythm (arrowhead). [25 mm/s, 10 mm/mV].
TREATMENT
Diltiazem was prescribed orally at 90 mg twice daily (medium-release
formulation), approximately 2.8 mg/kg every 12 h. In addition, pimobendan
(7.5 mg every 12 h) was prescribed to assist systolic function, and
spironolactone (60 mg every 24 h) and benazepril (7.5 mg every 24 h) were
prescribed to reduce renin–angiotensin–aldosterone system (RAAS)
activation and control mild heart failure signs.
After 2 weeks, Holter monitoring was repeated to assess arrhythmia
control. Very few episodes of SVT were present (Fig. 5), ascites had
resolved, and the owner reported that clinical signs of lethargy and syncope
were no longer a problem. Echocardiography at 4 weeks into treatment
showed reduced heart chamber size and improved systolic function. RAAS
blockade drugs were discontinued at that time, and pimobendan was
discontinued 2 weeks later.
Now that the patient was stabilised, he was referred for
electrophysiological mapping and radiofrequency ablation of a suspected
accessory pathway. A right-sided accessory pathway was confirmed on
intracardiac electrocardiography (ECG) and ablated, which prevented SVT
from being induced (Fig. 6). Postoperatively, diltiazem was weaned, and the
follow-up Holter monitoring performed without anti-arrhythmic treatment
was normal at 4 weeks after ablation.
FIGURE 5. Tachogram from the Holter recording performed 2 weeks into treatment with diltiazem.
No significant breakthrough of supraventricular tachycardia can be seen, and the heart rate response
to stimuli is normal.
FIGURE 6. Fluoroscopic intraoperative image showing intracardiac catheter position during

radiofrequency ablation. Three catheters are inserted cranially via the jugular vein (top), and each of
their tips is located in the coronary sinus (1), in the right ventricle (2), and at the bundle of His (3).
The fourth catheter, inserted caudally via the femoral vein (bottom), has the tip located in the right
atrium (4). Black marks on each catheter show the point of intracardiac electrocardiogram electrodes.
Image courtesy of Dr Pedro Oliveira.
DISCUSSION
A common arrhythmia in dogs, SVT can be caused by a number of separate
electrophysiological processes. Under the category of SVT are:
■ Atrioventricular reciprocating tachycardia (AVRT). Mediated by an
accessory pathway.
■ Focal atrial tachycardia (FAT). Caused by a single focus of abnormal
activity in the atrium.
■ Atrial flutter. Caused by a macroreentrant atrial circuit around right
atrial structures.
■ Atrial fibrillation (AF). Chaotic wavelets passing through the atrial
myocardium in a disorganised manner.
Diagnosis of AF is typically straightforward on surface ECG owing to its

characteristic irregularity. Differentiating AVRT, FAT, and atrial flutter
rhythms is challenging without electrophysiological mapping (intracardiac
ECG) and relies upon identifying the waveform of atrial depolarisation,
usually present in the S–T segment of the preceding complex. This P’ wave
(or F wave in atrial flutter) has a characteristic timing and electrical axis
according to the underlying arrhythmia. Identifying the P’ wave is easiest if
a recording captures the onset and/or offset of SVT, so that sinus beats can
be compared to those during the tachycardia, and a 12-lead ECG may be
required to gather sufficient data to make a decision. In the case presented
here, ECG was most revealing when drug therapy was used to terminate the
SVT.
In the case of accessory pathway-mediated SVT (e.g. AVRT), congenital
bundles of tissue connect the atria and ventricles in sites other than the
atrioventricular node. These pathways are often right-sided, lateral to the
tricuspid annulus, but can be left-sided or even within the atrioventricular
node itself. Circuits form when impulses pass through the atrioventricular
node as normal and then back up the accessory pathway into the atria,
generating another impulse through the node and leading to a “short circuit”
which causes SVT. If located away from the atrioventricular node,
radiofrequency ablation can be used to very focally heat the tissue and
induce a conduction block, preventing the arrhythmia from being generated.
This has a high rate of cure when performed by an experienced operator,
and anti-arrhythmic drugs can be discontinued in most cases. The
prevalence of congenital accessory pathways in dogs is unknown, but the
Labrador Retriever seems to be a predisposed breed. In humans, an
estimated one in three people has an accessory pathway, but most remain
clinically silent.
Young Labrador Retriever dogs with supraventricular tachycardia and a
dilated cardiomyopathy phenotype are likely to be affected by an
accessory pathway that causes a reentrant circuit between atria and
ventricles.
Dogs with frequent and persistent tachycardia, as commonly occurs in

SVT, may develop a tachycardia-induced cardiomyopathy.
Echocardiographic images often mimic dilated cardiomyopathy (DCM),
known as a DCM phenotype, and affected dogs can present with right-sided
or bilateral signs of congestive heart failure, as in this case. At the point of
presentation, it is impossible to determine whether an individual dog has
DCM causing SVT or an SVT-associated DCM phenotype. The diagnosis
of tachycardia-induced cardiomyopathy is therefore retrospective, once the
arrhythmia is controlled and reverse remodelling is observed on the
echocardiogram. In the case presented here, reverse remodelling occurred
and SVT was definitively controlled using radiofrequency catheter ablation;
therefore, all medical treatment could be stopped, and the patient was likely
to have a good prognosis.
Radiofrequency catheter ablation is potentially a definitive treatment

option for different causes of supraventricular tachycardia and may
prevent the need for lifelong medical therapy and repeated
electrocardiographic monitoring.
CASE 10. THIRD-DEGREE
ATRIOVENTRICULAR BLOCK
SIGNALMENT
Breed: English Springer Spaniel
Presenting complaint: Single episode of syncope, followed by persistent
lethargy and episodes of heavy panting
On presentation, the dog was quiet and panting excessively. The mucous
membrane colour was normal, but the capillary refill time was prolonged (3
seconds). The patient’s body condition score was normal (6/9). Auscultation
detected a severe bradycardia (40 bpm) with a quiet, regular sound in the
background at 160 bpm. No heart murmur was present and pulmonary
auscultation was normal. Femoral pulse quality was hyperkinetic and
synchronous with the low heart rate. Abdominal palpation was
unremarkable.
The complete blood cell count and biochemical profile were unremarkable,
as was the urinalysis.
ELECTROCARDIOGRAPHY
QRS complexes were slow and regular (40 bpm), with an abnormal
morphology, characteristic of a ventricular escape rhythm. An independent
rhythm of P waves was identified at 170 bpm. These findings were typical
of third-degree atrioventricular (AV) block (Fig. 1).
FIGURE 1. Electrocardiogram showing findings typical of a third-degree atrioventricular block. [25

mm/s, 10 mm/mV].
ECHOCARDIOGRAPHY
No evidence of significant cardiac remodelling was present, but rhythm was
persistently abnormal on simultaneous ECG. Colour flow Doppler
echocardiography showed diastolic mitral regurgitation after nonconducted
P waves (Video 1), typical for dogs with third-degree AV block, and M-
mode imaging of the left ventricle at the level of the mitral valve
demonstrated atrioventricular mechanical dissociation (Fig. 2). Systolic
function was subjectively normal.
The diagnosis was third-degree AV block, presumably idiopathic.
Since escape foci in third-degree atrioventricular block in dogs may fail,
referral to a centre for pacemaker implantation should occur on the day
of diagnosis, if possible
Video 1
Right parasternal short-axis echocardiographic view at the level of the papillary muscles, prior
to pacemaker implantation. The arrhythmia can be seen on simultaneous ECG.
FIGURE 2. Preoperative echocardiographic images showing no significant cardiac remodelling (a,

b). In the colour flow Doppler scan, diastolic mitral regurgitation can be detected after atrial
contraction (c). M-mode imaging of the mitral valve demonstrates mitral opening with each atrial
contraction (d).
TREATMENT
Medical treatment is rarely useful in dogs with third-degree AV block.
Sympathomimetic drugs, such as theophylline or terbutaline, tend to only
increase the rate of the ventricular escape focus to a minor degree. In dogs
with clinical signs, pacemaker implantation is the only treatment expected
to assist in controlling clinical signs and restoring quality of life.
Dogs with third-degree atrioventricular block rarely respond to medical

treatment, but they may have a good prognosis and quality of life after
pacemaker implantation
The dog was anaesthetised after placement of temporary transthoracic

pacing pads and connection to a defibrillator with pacing function. Surgical
access to the right jugular vein was achieved, and an active fixation
pacemaker lead was advanced under fluoroscopic guidance from the jugular
vein into the right ventricular apex. After deploying the active fixation tool
at the tip of the lead (a small corkscrew that tethers the tip into the
endocardial layers of ventricular muscle) and confirming its function and
thresholds, the jugular vein was triple ligated onto the lead’s silicone
sewing sleeve to secure it in place. In addition, the jugular vein was
permanently ligated cranial to the incision site for haemostasis. The heart
was then paced via this lead, instead of transthoracically.
Next, an incision was made cranial to the spine of the right scapula, and a
pocket in the fascia below the omotransversarius muscle was created by
blunt dissection. Using a long pair of artery forceps, a tunnel was made
from the pocket to the previous surgical incision site. After slowly reducing
the heart rate by 30 bpm on a temporary pacing device, the pacemaker lead
was disconnected from it, pulled through the tunnel, and connected to the
permanent pacemaker pulse generator. After screwing the lead in place and
confirming function, the pulse generator was inserted into the pocket of
tissue along with a coil of spare lead length. Before closing both surgical
sites, a postoperative radiograph was taken using fluoroscopy to obtain a
baseline lead position for future monitoring (Fig. 3). The heart rate was set
at 80 bpm, with no variation. This assists in monitoring for lead
dislodgement; pacemaker function can be checked by simply taking a pulse,
as the heart rate should never be below 80 bpm.
The patient was strictly cage rested in hospital for 2 days to minimise the
risk of postoperative lead dislodgement, with appropriate analgesia and a
light pressure bandage on the neck to reduce the risk of seroma formation
over implant sites. After discharge from the hospital, a regime of strict lead
walks in the owners’ garden to toilet was observed. At a revisit appointment
4 weeks after surgery, the pacemaker was checked by echocardiography
(Fig. 4, Video 2) and pacemaker interrogation to ensure appropriate position
and function. The patient was using the pacemaker 100 % of the time at 80
bpm. Base rate was reduced to 60 bpm to maximise battery life. The
functionality of the device was altered to rate responsive mode: sensors in
the pulse generator detect movement and allow heart rate to increase
accordingly to meet the needs of the patient at exercise. ECG showed
ongoing third-degree AV block, with a distinctive, regular heart rate with a
ventricular morphology and pacing spikes immediately preceding the QRS
complexes (Fig. 5).
FIGURE 3. Composite image created from two intraoperative fluoroscopic still images taken after
pacemaker placement. The pacemaker lead tip (arrow) can be seen inserted into the right ventricular
apex. From the right jugular vein entry point (arrowhead), the lead passes through a connective tissue
tunnel that permits the connection to the pacemaker pulse generator (PG), itself secured in a pocket
of tissue on the right side of the neck, cranial to the scapular spine.
FIGURE 4. Long-axis (a) and short-axis (b) echocardiographic views of the heart 4 weeks
postoperatively, showing the pacemaker lead as a hyperechoic structure (delineated with arrows) in
the right ventricle. No lead thrombus was present, and lead position appeared appropriate.
Video 2
Left apical four-chamber echocardiographic view (slightly oblique) showing the position of the
pacemaker lead after the procedure. It is seen as a hyperechoic artefact passing from the right
atrium through the tricuspid valve
FIGURE 5. Electrocardiogram 4 weeks after pacemaker implantation showing ongoing third-degree
atrioventricular block and a regular, paced rhythm at 60 bpm. Pacing spikes are visible in all leads,
but most obvious in lead III, as a small, negative deflection immediately prior to the wide QRS
complex. [50 mm/s, 5 mm/mV].
DISCUSSION
Third-degree AV block is believed to be idiopathic in most cases, caused by
AV node fibrosis of unknown origin; however, case reports of neoplasia or
inflammatory disease as primary inciting causes exist. With pacemakers set
to rate responsive mode, physiology at exercise is mimicked by adaptations
in heart rate, which can be tailored to the dog’s requirements at subsequent
visits. Dual-chamber pacing, where an additional lead is placed in the right
atrium, has an even better physiological outcome. However, since the most
common complication of pacing is lead dislodgement, complication rates
may be higher with two-lead systems, and no improved longevity for dual-
chamber pacing has been reported versus single-chamber pacing.
Unlike most minimally invasive cardiac procedures, patients’ activity
levels should be significantly restrained for 1 month after pacemaker
implantation. Dislodgement rates are highest in the first 48 hours
postoperatively, so patients must be hospitalised for this period, with careful
handling observed by an experienced nursing team. Seroma formation may
occur at either implant site, and should be treated by improving physical
rest and using nonsteroidal anti-inflammatory drugs. Light pressure
bandages may be used if required. Seromas should not be drained, as this
may increase the risk of infection around the device, which would
necessitate revision of the whole pacemaker procedure. Development of a
pacemaker lead thrombus in the right heart may occur, and can be treated
with clopidogrel. Patients must never wear a neck lead or collar again in
order to reduce the risk of pacemaker lead damage and should only be
walked on a harness which does not put pressure on the device system.
Rough play with other dogs around the neck or shoulder should be avoided,
as should jugular venepuncture, to prevent damage to the pacemaker lead.
MRI scans or any contact with strong magnetic fields will reset the
pacemaker to factory settings. After death, the patient’s remains should only
be cremated or buried after removal of the battery unit and appropriate
disposal via the manufacturer or a human hospital.
Lifelong precautions for dogs with a pacemaker include avoiding neck
leads, jugular venepuncture, and strong magnetic fields where possible.
Most dogs with third-degree AV block will have a good prognosis after
pacemaker implantation. Rare cases may even cease using their pacemaker
after a return of sinus rhythm; presumably the result of a transient
myocarditis or ischaemic AV node damage. Complications 1 month after
surgery are rare; however, trauma to the lead, resulting in fracture, or an
insulation break to the lead silicone coating can trigger pacemaker
malfunction, which requires revision of the procedure.
CASE 11. SICK SINUS
SYNDROME
SIGNALMENT
Breed: West Highland White Terrier
Age: 13 years, 1 month old
Presenting complaint: Sudden onset signs of frequent collapse 24 hours
ago. No prior relevant history aside from occasional stopping on walks for
unexplained reasons over the last 3 months and sleeping more at home
On cardiac auscultation, long pauses of up to 12–15 seconds in duration
were identified. Longer pauses were associated with weakness and sitting
down. Short runs of tachycardia were also identified, with a heart rate over
200 bpm. The mucous membranes were pink and moist, but the capillary
refill time was prolonged (3 seconds). Pulse quality varied with heart rate.
Pulmonary auscultation and abdominal palpation were unremarkable.
ELECTROCARDIOGRAPHY
Sinus rhythm was present for the majority of the trace recorded, but an
extremely long pause of 21 seconds was detected (Fig. 1), followed by a
ventricular escape rhythm at a rate of 16 bpm for six beats. After this, sinus
rhythm rapidly returned at 100 bpm.
FIGURE 1. Electrocardiogram showing an extreme episode of sinus arrest, lasting 21 seconds,
followed by a slow ventricular escape rhythm and an eventual return to sinus rhythm (not shown).
[25 mm/s, 10 mm/mV].
ECHOCARDIOGRAPHY
No significant abnormalities were identified on echocardiography. Only
mild mitral valve prolapse was detected (Fig. 2).
FIGURE 2. Right parasternal echocardiographic views showing normal cardiac structure. No
significant chamber dilation is present in the long-axis four-chamber view (a) or in the short-axis
view at the level of the papillary muscles (arrows) (b). Left atrium-to-aortic root ratio is normal (c).
Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
ELECTROCARDIOGRAPHY
Ambulatory electrocardiography showed episodes of supraventricular
tachycardia and frequent, unexplained pauses, some of which were
followed by a ventricular escape complex. Occasional episodes of
atrioventricular block were present, as were ectopic atrial depolarisations
(Fig. 3). The patient was strictly rested, and no collapse episodes were
detected during the recording.
Findings were consistent with a diagnosis of sick sinus syndrome (SSS).
Clinical signs of sick sinus syndrome may include syncope or presyncope

(i.e. the patient stops and may appear weak or vacant).
FIGURE 3. Selected electrocardiographic strips from the 24-hour Holter monitoring. No full
collapse episodes were reported during the recording period. Episodes of supraventricular
tachycardia (SVT) are present (a). Unpredictable pauses can be seen (b, d). Some pauses are followed
by a ventricular escape beat (VEB). Occasional nonconducted P waves are present (arrows) (c, d),
and ectopic atrial activity can also be observed, evidenced by a P wave with abnormal electrical axis
(arrowhead). These findings are consistent with sick sinus syndrome. [25 mm/s, 10 mm/mV].
TREATMENT
Transvenous pacemaker implantation was performed (Fig. 4) in order to
prevent pauses in the rhythm from causing syncope. The patient recovered
well from the procedure, and clinical signs were abolished. Four weeks
after pacemaker implantation, the dog was asymptomatic and
echocardiography confirmed that the pacemaker lead remained in an
appropriate position in the right heart (Fig. 5).
FIGURE 4. Left lateral radiograph of the thorax taken after transvenous pacemaker implantation.
The lead tip (arrow) is visible in the apical region of the right ventricle. The pacemaker pulse
generator (PG) is located in a pocket beneath the omotransversarius muscle, cranial to the scapula.
FIGURE 5. Right parasternal long-axis echocardiographic images showing the position of the
pacemaker lead (delineated with arrows) 4 weeks after placement. In the long-axis view (a), the lead
can be identified as a hyperechoic linear object extending from the right atrium (RA) to the right
ventricle (RV). In the short-axis view (b), the lead appears as a bright, hyperechoic dot within the RV.
LV, left ventricle.
DISCUSSION
SSS is an idiopathic disorder of the conduction system, which leads to
episodes of tachycardia, bradycardia, long pauses (called sinus arrest), and
associated ventricular escape beats on electrocardiography. Second-degree
atrioventricular block and ectopic atrial pacemaker activity may also be
detected. All of these, which were present in the case described here,
suggest that this disease is not isolated to the sinoatrial node. In addition,
hearts with SSS fail to respond to normal stimuli which should increase
heart rate. The disease is almost entirely diagnosed in old age, and an
overwhelming majority of dogs affected are one of two breeds: West
Highland White Terrier or Miniature Schnauzer. The cause of SSS in dogs
is unknown. In humans, it is often idiopathic but can be associated with
particular polymorphisms in genes encoding ion channels as well as with
drug use and physical trauma.
Dogs with SSS may present incidentally or with only mild clinical signs
that have been mistaken for aging, such as reduced exercise tolerance and
play, increased sleep time, or lethargy. In addition, SSS may be present for
some months or even years prior to becoming so problematic that it causes
clinical signs of syncope or episodic weakness. Ideally, treatment should be
instigated only in cases where the arrhythmia affects quality of life.
However, this can be difficult to identify in the absence of severe clinical
signs. Pacemaker implantation is not risk free, and complications can occur,
such as lead dislodgement, infection, or thrombus formation. For these
reasons, implantation should not be performed in dogs with SSS that are
truly free of clinical signs (sometimes referred to as “sinus node
dysfunction” when no overt symptoms are present). If in doubt, medical
treatment can be trialled using a β-receptor agonist (e.g. terbutaline) or a
methylxanthine derivative (e.g. theophylline). These drugs may reduce the
pause length and increase overall heart rate in dogs with earlier disease or
when high vagal tone is a contributing factor, but they are generally found
to be ineffective in dogs with a history of syncope. In such cases,
transvenous pacemaker implantation is the standard of care.
Sick sinus syndrome may be diagnosed with only mild clinical signs,
which can be mistaken for changes associated with aging such as reduced
exercise tolerance and sleeping more
Even without pacemaker implantation, sudden cardiac death is rare in

dogs with SSS. The reason to treat is to improve quality of life by
controlling clinical signs of low cardiac output. Dogs with SSS that do not
undergo pacemaker implantation have a similar survival time to those that
receive a pacemaker, but their quality of life is likely to be much lower,
with frequent episodes of feeling faint and a poor exercise capability.
Pacemaker implantation is the only successful treatment for dogs with

sick sinus syndrome that present with syncope, but medical treatment
may increase heart rate in the earlier stages of disease.
CONGENITAL HEART
DISEASE
Congenital heart disease (CHD) affects approximately 0.13 % of mixed-

breed dogs and 0.14 % of mixed-breed cats. In certain pedigree breeds, and
especially within particular family lines, prevalence may exceed this level.
The most common CHD in dogs is pulmonic stenosis (32 %), followed by
subaortic stenosis (21 %) and patent ductus arteriosus (PDA, 21 %). In cats,
the most common CHD is a ventricular septal defect (VSD, 18 %),
followed by PDA (11 %). Although relatively rare compared with acquired
heart disease, CHD is important for clinicians to identify, as various modern
treatment options exist to help improve quality of life in affected animals or
even provide a haemodynamic cure (e.g. PDA occlusion).
Considering basic embryologic events can help the clinician to better
understand the congenital diseases they may see. For example, a PDA is
caused by a congenital lack of smooth muscle around the ductus arteriosus.
This smooth muscle normally responds to a reduction in prostaglandin
concentration and increased oxygen tension in the blood around the time of
birth, causing vasoconstriction. The lack of muscle leaves the ductus open
and blood flows through the PDA from systemic to pulmonary vascular
beds because of a persistent pressure difference. Another example is a VSD:
the lack of the normal formation of the ventricular septum leaves a window
between the left and right ventricles, through which blood flows from the
left ventricle to the right ventricle and pulmonary artery during systole.
Pulmonic stenosis is caused by a lack of normal valve leaflet separation
(primary valve dysplasia), causing fusion and thus narrowing of the valve
orifice during ejection of blood. In contrast, subaortic stenosis does not
have an obvious embryologic trigger; in most dogs, stenosis worsens over
the first year of life, and dogs with a steeper angle between the ventricular
septum and the ascending aorta are known to be more likely to develop
severe stenosis. The hypothesis that best explains this is that dogs that
develop subaortic stenosis do so because they have remnants of
embryologic tissue in their left ventricular outflow tract, which respond to
shear stress of blood flow by proliferating. This would explain why
turbulence associated with a steeper aortoseptal angle could drive
worsening proliferation and thereby a more severe stenosis.
In humans, malformations such as tricuspid atresia, hypoplastic left heart
syndrome, and truncus artriosus are much more frequently reported than in
dogs and cats. Case reports exist from horses and production animals of
many congenital defects that would be considered extremely rare in pets.
This probably reflects the nature of the diseases that allow survival to the
age of first vaccination (or later); that is, dogs and cats have to have a
disease that allows them to live long enough to be seen by a veterinary
surgeon (2–3 months). In humans, foetal echocardiographic screening
allows detection and early intervention in babies with complex congenital
disease. In horses and production animals, veterinary checks are usually
performed earlier than in companion animals. It seems likely that puppies
and kittens with severe CHD do not survive, and their demise is attributed
to pneumonia or fading puppy syndrome.
Most CHDs are believed to be genetic in origin and therefore heritable.
Pedigree analysis suggests that a familial link is present for a number of
diseases, including PDA in Poodles, Cocker Spaniels, and Chihuahuas;
aortic stenosis in Newfoundlands; tricuspid dysplasia in Labrador
Retrievers, and conotruncal malformations in Norwegian Keeshonds. A
spectrum of CHD severity exists in almost all conditions reported. To take
the example of a PDA, the mildest form is a ductus arteriosus which does
not constrict along its entire length (as is normal postpartum), but which
constricts only at the pulmonic end. This is not a patent vessel, but merely a
blind-ending aortic branch (forme fruste PDA). The next level of severity is
a tapering vessel which restricts flow somewhat at the pulmonic ostium and
causes left-sided cardiomegaly and potentially congestive heart failure in
time; this is the most common form of PDA identified in clinical practice.
The most severe form of a PDA is a nontapering vessel which leads to
severe pulmonary volume overload and either severe congestive signs in
early life or the development of pulmonary hypertension and a right-to-left
(reverse) shunt flow. Even though forme fruste PDAs are not clinically
detectable, affected dogs may pass on the genes, thereby enabling a truly
patent PDA in their offspring.
More common than CHD in primary care practice are animals with
physiologic “flow” murmurs (also known as innocent or nonpathological
murmurs). Flow murmurs are common in juvenile animals because of
changes in blood viscosity during development; a period of lower viscosity
is anecdotally associated with transient development of a heart murmur.
However, this occurs around the same time as general health screening and
possibly neutering, leading to a potential conundrum for veterinary
surgeons who detect these murmurs: to investigate or not? If a murmur is
left too long and CHD is the cause, a valuable opportunity for early
treatment may be missed. In addition, particular breeds, such as Boxers and
Sighthounds, seem to have a higher prevalence of flow murmurs because of
the conformation of their left ventricular outflow tract, or heart size relative
to aortic diameter.
Based on physical examination, veterinary surgeons can stratify the risk
of a heart murmur being associated with CHD or not, and therefore decide
upon how far to pursue investigation by echocardiography.
In dogs, nonpathological flow murmurs tend to be:

■ focal (mostly localised to the left heart base, not radiating widely)
■ low grade (up to grade II, or rarely III, out of VI)
■ short (limited duration)
■ systolic (diastolic or continuous murmurs are always an indication for
investigation)
■ dynamic (may vary in intensity, becoming louder at higher heart rates)
■ isolated (not associated with other auscultatory or clinical abnormalities).
In cats, owing to a much higher prevalence of flow murmurs at all ages,

challenges can be even greater. Epidemiological data from a shelter
population of mostly mixed-breed cats reported that heart murmurs in
young cats were more likely to be associated with a normal heart on
echocardiography than with an abnormal one. In fact, fewer than one in five
juvenile cats with heart murmurs had any abnormalities on
echocardiography. Factors that suggest that a heart murmur is pathological
in a cat are similar to those in dogs: intensity of grade III or louder,
association of the murmur with clinical signs or other auscultatory
abnormalities (e.g. gallop sound, arrhythmia), or a point of maximal
intensity on the right side.
The diagnosis of CHD can be challenging, especially as congenital
diseases do not always travel alone. Multiple defects are common, and
echocardiography by an experienced cardiologist is recommended for an
accurate assessment of haemodynamic significance. Closure of a PDA is
almost always beneficial, whilst treatment of other diseases may or may not
be required. Especially when anaesthetic or procedural risks are involved,
the decision to treat needs to be made based upon complex
echocardiographic measurements of flow and remodelling.
Over the last 30 years, the surgical treatment of CHD in veterinary
patients has become commonplace in Europe and the USA. Minimally
invasive transvascular procedures, carried out by experienced interventional
cardiologists, are associated with a low morbidity and mortality and a high
success rate. For diseases that are not amenable to minimally invasive
treatment, surgical repair under cardiopulmonary bypass or using inflow
occlusion techniques is available in a handful of centres worldwide;
however, increasing expertise in these techniques means that they are likely
to become more available over the coming decade.
CASE 12. PULMONIC
STENOSIS
SIGNALMENT
Breed: Crossbred dog (Cocker Spaniel and Poodle)
Age: 12 weeks old
Sex: Male, intact
Presenting complaint: Loud heart murmur detected incidentally by a
veterinary surgeon at vaccination
The dog was bright and had no apparent signs of disease, aside from a grade
V/VI systolic heart murmur at the left base, radiating dorsally. His mucous
membranes were pink and moist, with a prolonged capillary refill time (>2
seconds). Pulmonary auscultation and abdominal palpation were normal, as
was femoral pulse quality.
ECHOCARDIOGRAPHY
Echocardiography was performed to evaluate the cause of the murmur.
Severe hypertrophy and dilation of the right ventricle were present (Fig. 1).
The tricuspid valve was normal and the left heart appeared normal in
structure and function.
Evaluation of the pulmonary artery showed fused valve leaflets, typical
of a type A pulmonic stenosis (PS) (Fig. 2). The colour flow Doppler scan
showed a turbulent systolic flow through the pulmonic valve, as well as
diastolic insufficiency. Continuous wave Doppler interrogation of the flow
across the pulmonic valve showed a peak velocity of 5.8 m/s, which
inferred that the pressure gradient across the stenotic valve was 134.6
mmHg (normal <30 mmHg, severe stenosis >80 mmHg). There was no
evidence of any concurrent congenital heart disease.
The diagnosis was severe type A PS: valve leaflet fusion with no
evidence of annular hypoplasia.
FIGURE 1. Right parasternal echocardiographic views showing myocardial remodelling. A dilated

and hypertrophic right heart can be seen in the near field, above a normal-appearing left heart. In the
long-axis view (a), the enlargement of the right ventricle (RV) is so severe that the heart has a
“double-apex” appearance. Note that the right atrium (RA) is larger than the left atrium (LA). The
short-axis view shows subjective right ventricular dilation and hypertrophy (b). LV, left ventricle.
FIGURE 2. Echocardiographic images from the right parasternal cranial oblique view of the
pulmonic valve. In diastole (a), the valve can be seen in a closed position (arrowheads indicate the
valve annulus). In systole (b), the valve has the typical domed appearance due to the fused leaflets,
indicating a type A pulmonic stenosis. A small orifice is visible between the fused leaflets (arrow).
PA, pulmonary artery; RV, right ventricle.
TREATMENT
The patient was treated with atenolol, up-titrated to 2 mg/kg over 2 weeks,
to reduce right ventricular myocardial oxygen demand and protect against
the detrimental effects of catecholamines. Definitive treatment by pulmonic
balloon valvuloplasty was recommended, and the dog returned after 4
weeks on atenolol for this minimally invasive procedure.
The treatment of choice for pulmonic stenosis is balloon valvuloplasty,

which is an image-guided minimally invasive technique performed via a
transvascular route.
After positioning the anaesthetised dog in left lateral recumbency,

percutaneous access to the right jugular vein was performed using a
modified Seldinger technique. Under fluoroscopic guidance, a right
ventriculogram was performed to assess the position and size of the stenotic
pulmonic valve (Fig. 3). The annulus diameter measured 15 mm (compared
to a diameter of 13 mm on echocardiography). Therefore, for effective
balloon dilation, a working balloon diameter of 18–22 mm would be
required (1.2–1.5× measured annulus size). However, when using a balloon
dilation catheter at working diameters over 18 mm, the burst pressure of the
balloon can be low enough to lead to balloon rupture during the procedure,
risking damage to the right ventricular outflow tract and tricuspid valve. To
reduce the risk of balloon rupture whilst still providing an effective orifice,
two smaller balloons can be inflated alongside one another.
To perform this, two Rosen guidewires were advanced into the right
ventricle and then through the stenotic valve, using a 6 F balloon-tipped
pressure measurement catheter to guide them. Two balloon dilation
catheters were advanced, one over each guidewire, and simultaneous
inflation of both 12 and 14 mm balloons was performed (effective diameter
of 21.3 mm). A loss of the balloon waist was identified on fluoroscopy,
which suggested an adequate stretching of the fused pulmonary valve
leaflets (Video 1). The balloons, guidewires, and vascular introducers were
removed, and pressure was applied to the site of vascular access for 30
minutes for haemostasis. The patient was discharged 24 hours later.
Four weeks after the procedure, the dog returned for a repeat
echocardiogram. At this time, the Doppler-derived pressure gradient had
reduced by approximately 70 % (Fig. 4). The pulmonic valve had a wider
orifice in systole and no doming of the valve leaflets was seen (Fig. 5).
Improved exercise tolerance and a shorter recovery time after exercise were
reported. Consequently, atenolol treatment was progressively discontinued
over the following weeks, and no clinical signs were observed.
Reduction of the transvalvular pressure gradient by 50 % or more is

associated with a favourable long-term prognosis.
FIGURE 3. Angiocardiographic image demonstrating the typical lesions associated with valvular
pulmonic stenosis. The right ventricle was accessed advancing a balloon-tipped angiographic
(Berman) catheter through the right jugular vein and cranial vena cava. Contrast passes from the right
ventricle, which has a normal trabecular appearance, into the pulmonary artery (PA) via a stenotic
pulmonic valve (arrowheads). Note the profound poststenotic dilation of the main pulmonary artery,
before bifurcating into the left (dorsal) and right (sternal) branches. The right ventricular outflow
tract (RVOT) is severely narrowed by concentric hypertrophy in this systolic frame.
Video 1
Fluoroscopic video of a double-balloon valvuloplasty. Two balloon dilation catheters are
simultaneously inflated when positioned across the stenotic pulmonic valve. This procedure has
an advantage over using a single large balloon in dogs with a pulmonic annulus measuring 14 mm
or greater: two smaller balloons are less likely to burst than one large one, so a higher pressure
can obtain effective valve dilation.
FIGURE 4. Continuous wave Doppler interrogation of blood flow across the stenotic pulmonic
valve. At diagnosis (a), the maximum velocity implied a pressure gradient of 135 mmHg across the
pulmonic valve (>80 mmHg is severe). Four weeks after balloon valvuloplasty (b), a maximum
pressure gradient of 34 mmHg was measured, which suggested a very successful procedure.
FIGURE 5. Two-dimensional echocardiographic images acquired at peak valve opening, comparing

valve morphology before (a) and after (b) pulmonic balloon valvuloplasty. Note the significantly
greater valve opening and orifice diameter (solid lines) after the procedure. PA, pulmonic artery;
RVOT, right ventricular outflow tract.
DISCUSSION
Although no clinical signs were initially noticed, the owners reported
improved exercise capacity after pulmonic balloon dilation. This is
common in puppies treated using this method and probably reflects the
congenital nature of PS in dogs, as owners may not be aware of their dog’s
true exercise tolerance because the limitation is present from birth. This
patient presented like most cases of PS, with a loud heart murmur found
incidentally.
PS is best diagnosed by echocardiography since the dysplastic pulmonary
valve can be directly visualised and the effects of high right ventricular
pressure assessed. Right ventricular hypertrophy is present in most cases of
severe PS, and it can become so severe in the subvalvular region that the
hypertrophy itself may contribute to a dynamic subvalvular stenosis. This
can complicate catheterisation of the pulmonary artery and may increase
procedural risks during a balloon valvuloplasty. In some cases,
echocardiography may detect a concurrent congenital heart disease, most
often tricuspid dysplasia or patent ductus arteriosus. Radiographic findings
may hint at the presence of PS; specifically, right ventricular enlargement, a
bump in the region of the pulmonary artery (Fig. 6), and hypovascular
appearing lung fields. However, radiography is rarely used by cardiologists
owing to the ease of diagnosis by echocardiography.
Echocardiographic findings of right-sided cardiomegaly, right ventricular

hypertrophy, and a fused pulmonic valve are typical of type A pulmonic
stenosis.
FIGURE 6. Dorsoventral radiograph of the chest of a different dog with severe pulmonic stenosis.
Right-sided cardiomegaly with a rounded appearance of the right ventricle is seen. There is also a
bulge in the position of the main pulmonary artery (1- to 2-o'clock, arrows). A diffuse mild
bronchointerstitial pattern is also present.
Classification of PS into types A and B has been described. Whereas type

A is suggested to be pure valve leaflet fusion, hypoplasia of the pulmonic
valve annulus is present in type B. Patients often have a mixed form evident
on echocardiography. Dogs with valve leaflet fusion are best treated with
pulmonic balloon valvuloplasty, as the success rate appears to be higher
than when pure annular hypoplasia is present. Many cardiologists
recommend performing a minimally invasive pulmonic balloon
valvuloplasty in all patients in order to relieve any valve fusion which may
be present and optimise cardiac output. If a patient with type B PS fails to
respond adequately to balloon valvuloplasty, a minimally invasive stent
placement may help to reduce pressure gradient. Current experience of this
technique is limited to a handful of centres worldwide, but it is likely to
expand in the future.
CASE 13. SUBAORTIC
STENOSIS
SIGNALMENT
Breed: French Bulldog
Age: 1 year, 1 month old
Sex: Male, intact
Presenting complaint: Incidentally detected heart murmur, poor body
condition, and possible exercise intolerance
On presentation, the dog was bright and responsive. The mucous membrane
colour was normal, but the capillary refill time was prolonged (3–4
seconds). The femoral pulse was impalpable. His body condition score was
poor (3/9). Auscultation revealed a loud, grade IV/VI systolic heart murmur
at the left base and a heart rate of 120 bpm. Abdominal palpation was
unremarkable, as was the respiratory rate (20 breaths per minute).
The complete blood cell count and biochemistry profile were unremarkable.
FIGURE 1. Thoracic radiographs (dorsoventral [a] and left lateral [b] projections) of a different dog
with subaortic stenosis. A prominent aortic arch in both projections is present, more visible in the
dorsoventral view, in the area of the aortic arch (12- to 1-o'clock; arrows). The lung parenchyma is
normal. Although, generally, thoracic radiography in dogs with subaortic stenosis is of limited value,
it does serve to screen for left atrial dilation, pulmonary infiltrates, or evidence of pulmonary
hypertension, all of which may occur secondary to fixed obstruction to forward flow.
ECHOCARDIOGRAPHY
Left ventricular hypertrophy was present, with a bright appearance of the
subendocardial myocardium in places which may suggest ischaemia. A
thick ridge of fibrous tissue was present in the left ventricular outflow tract,
just below the aortic valve, suggestive of subaortic stenosis (SAS). Doppler
interrogation measured a blood flow velocity across the outflow tract lesion
of over 6.2 m/s, consistent with an outflow tract pressure gradient over 153
mmHg (Fig. 2).
The diagnosis was severe SAS.
The echocardiographic findings of subaortic stenosis reflect left

ventricular pressure overload, such as myocardial hypertrophy and signs
of subendocardial ischaemia.
FIGURE 2. Echocardiographic images demonstrating subaortic stenosis. The patient did not permit
simultaneous ECG. Right parasternal long-axis view (a) showing subjective hypertrophy of the left
ventricle (LV) and a left atrium (LA) of relatively normal size. The anterior mitral leaflet appears
subjectively thickened (arrow). Right parasternal view of the left ventricular outflow tract (b)
showing the fibrous band (arrows) immediately below the aortic valve. Right parasternal short-axis
view at the level of the papillary muscles (c) illustrating hyperechoic regions of endocardium
consistent with ischaemia or fibrosis (arrows). Right parasternal short-axis view at the level of the
aortic root (d) showing a LA of normal size and a ridge on the free wall of the atrium, consistent with
a normal variant morphology (Coumadin ridge, arrow). The left coronary cusp of the aortic valve
appears thickened, possibly associated with extension of the fibrotic lesion or with a jet lesion on the
valve caused by the impact of turbulent blood flow. Colour flow Doppler image from the right
parasternal outflow tract view (e) showing turbulent blood flow starting at the subaortic ridge.
Continuous wave Doppler interrogation of aortic flow from the subcostal window (f) showing a
maximum flow velocity exceeding 6.2 m/s, consistent with severe aortic stenosis. Ao, aorta; LVOT,
left ventricular outflow tract; RA, right atrium.
TREATMENT
Atenolol was prescribed at 2 mg/kg every 12 h to reduce myocardial
oxygen demand and therefore the risk of arrhythmias and ischaemic events.
Given the evidence of severely poor perfusion on physical examination,
interventional treatment using an aortic balloon procedure was elected.
Medical treatment with atenolol may be useful, but interventional

procedures to dilate the fibrous ring may improve quality of life more
notably in dogs with marked clinical signs.
The dog was anaesthetised and placed in left lateral recumbency, and
right carotid artery access was achieved via a surgical cutdown. A pigtail
catheter was advanced into the left ventricle and contrast was injected using
a pressure injector. The resultant ventriculo-aortogram showed the position
of the fibrous lesion in the subaortic region and a poststenotic dilation of the
aortic arch (Fig. 3a, Video 1). Next, a small guidewire was used to advance
an 8 mm cutting balloon into the left ventricular outflow tract and across the
stenotic ring (Fig. 3b, Video 2). Inflation of this balloon was aimed at
scoring the fibrous tissue prior to forceful dilation by using microtomes
(small blades on the balloon surface that are ensheathed in folds when the
balloon is deflated). The cutting balloon was then replaced with a 10 mm
high-pressure balloon, which was used to tear open the fibrous ring of
subaortic tissue upon inflation (Fig. 3c, Video 3). After the procedure,
catheters were removed and the right carotid artery was ligated. The patient
recovered well and was discharged the following day.
At re-examination 4 weeks after surgery, the dog was brighter and his
body condition had improved. He was keen to exercise and appeared more
able to exert himself without becoming fatigued. Echocardiography showed
greater mobility of the fibrous subaortic ring, and Doppler-derived pressure
gradient had reduced from 153 to 92 mmHg. The stenosis was still severe,
but had reduced approximately 40 %. Atenolol treatment was continued at
the previous dose, and annual re-examination was recommended.
FIGURE 3. Fluoroscopic images showing the cutting balloon procedure. Ventriculo-aortogram
outlining the subaortic stenosis lesion (arrowheads) and poststenotic dilation (arrows) (a). An 8 mm
cutting balloon was inflated across the subaortic lesion (b), followed by the inflation of a 10 mm
high-pressure balloon across the stenosis (c). Ao, aorta; LV, left ventricle.
Video 1
Angiogram performed using a pigtail catheter located in the left ventricle. A ridge of subaortic
tissue is clearly visible below the valve, and the aortic arch appears dilated.
Video 2
Fluoroscopic video showing inflation of an 8 mm cutting balloon across the stenotic lesion.
Video 3
Fluoroscopic video showing inflation of a 10 mm high-pressure balloon dilation catheter
across the stenosis.
DISCUSSION
SAS is the second most common heart disease in dogs in Europe, after
pulmonic stenosis. Some breeds are overrepresented for this disease, such
as the Boxer, English Bulldog, French Bulldog, American Bulldog,
Bullmastiff, Dogue de Bordeaux, and Golden Retriever. Although classified
as a congenital disease, most dogs with aortic stenosis develop the fibrotic
outflow tract lesion over the first year of life, and stenosis appears to
worsen in dogs with more acute angles between the interventricular septum
and the ascending aorta. The disease might represent persistence of
embryonic tissue in the left ventricular outflow tract. The growth of this
tissue, which forms a stenotic lesion, is promoted by increased shear stress
in the outflow tract where a steeper aortoseptal angle is present. Dogs with
an outflow tract gradient greater than or equal to 80 mmHg are classified as
having severe SAS. In the case presented here, the patient had a gradient
over 150 mmHg and evidence of subendocardial ischaemia, which lead to a
higher level of concern.
Subaortic stenosis is common in certain Molossian-type breeds (such as
Boxer- and Bulldog-like breeds), and the clinical signs associated may
worsen over the first year of life.
Medical treatment of dogs with SAS can be attempted using a β-blocker,

such as atenolol (which is cardioselective). This reduces the transvalvular
pressure gradient in many cases, but probably by reducing systolic function
rather than by acting on the lesion in any way. In dogs with severe SAS,
atenolol may reduce myocardial oxygen demand and promote preferable
metabolic pathways within the myocardium, thereby reducing the degree of
myocardial ischaemia and therefore the risk of ventricular arrhythmias. In
the presence of clinical signs that limited this patient’s quality of life, an
interventional procedure was carried out to relieve some of the pressure
load on the left ventricular myocardium. There is currently no published
data on the lifetime outcome of dogs after an aortic cutting balloon
angioplasty, but dogs with marked clinical signs have been anecdotally
reported to improve after the procedure. Restenosis seems to occur in some
cases, possibly those with steeper aortoseptal angles; in others, aortic
regurgitation some months after the procedure can lead to left heart volume
overload and clinical signs of congestive heart failure.
CASE 14. PATENT DUCTUS
ARTERIOSUS
SIGNALMENT
Breed: Jack Russell Terrier
Age: 4 months old
Sex: Female, intact
Presenting complaint: Loud heart murmur, with a palpable precordial
thrill, detected incidentally by a veterinary surgeon at vaccination. A heart
murmur had been reported when she was 10 weeks old, but no diagnostic
investigation had been performed
The dog was bright and alert, but her body condition score was slightly low
(4/9). A grade V/VI continuous heart murmur was detectable high at the left
heart base, behind the triceps muscle. It radiated widely, but at the left apex
only a systolic component was audible. Her mucous membranes were pink
and moist, with a capillary refill time of <1 second. Pulmonary auscultation
and abdominal palpation were normal. The femoral pulse was hyperkinetic.
Clinical findings of a loud, continuous left-sided heart murmur behind

the triceps muscle and a hyperkinetic femoral pulse are highly suggestive
of a patent ductus arteriosus.
ECHOCARDIOGRAPHY
Echocardiography was performed to evaluate the murmur. Volume loading
of the left heart was evident, and the main pulmonary artery was dilated. A
vessel was seen entering the pulmonary artery, in the region of its
bifurcation (Fig. 1). On the colour flow Doppler scan, a continuous
turbulent flow was detected in the pulmonary artery. Continuous wave
Doppler ultrasonography showed a continuous flow from the vessel into the
main pulmonary artery and directed retrograde towards the pulmonic valve
(Video 1). Aortic outflow velocity was elevated, which is consistent with a
clinically significant systemic-to-pulmonary shunt. Findings were
diagnostic of a patent ductus arteriosus (PDA) (Fig. 2). No evidence of any
other heart disease was detected.
The diagnosis was PDA, with a left-to-right flow.
FIGURE 1. Echocardiographic images. Right parasternal long-axis view of the left atrium (LA) and
left ventricle (LV) (a), showing a subjectively volume-loaded appearance. Right parasternal short-
axis view (b) showing an enlarged left atrium-to-aortic root ratio of 2.10. Right parasternal short-axis
oblique view (c) showing a vessel (arrow) inserting above the bifurcation of the main pulmonary
artery (PA); the pulmonary ostium is shown between arrowheads. Ao, aorta.
Video 1
Simultaneous 2D and colour flow Doppler echocardiography showing the typical tapering
morphology of a patent ductus arteriosus, with the narrow ostium inserting at the bifurcation of
the pulmonary artery. Continuous flow can be seen throughout the cardiac cycle, with laminar
(red) flow within the ductus itself, becoming turbulent (green mosaic) at the ostium and into the
pulmonary artery.
FIGURE 2. Continuous wave Doppler interrogation of the presumed patent ductus arteriosus (PDA),
showing a continuous flow from the PDA into the pulmonary artery, caused by a persistently high
pressure difference between the aorta (source of the PDA) and the pulmonary artery (approximately
120 to 20 mmHg in systole; 80 to 10 mmHg in diastole).
TREATMENT
In the absence of clinical signs of heart failure, no medication was
prescribed. Primary closure of the PDA is indicated, either surgically or
using a minimally invasive approach. Interventional occlusion was elected
in this case, as it has the lowest risk and a higher rate of complete closure
than surgery.
The treatment of choice for patent ductus arteriosus is a transarterial

Amplatz Canine Duct Occluder owing to a very low complication rate
and a good long-term outcome in most patients.
The anaesthetised dog was positioned in right lateral recumbency. The

right femoral artery was surgically exposed and isolated, and access was
achieved using a modified Seldinger technique. Under fluoroscopic
guidance, angiography was performed with a pigtail catheter to locate the
position of the PDA and measure the size of the pulmonary ostium (Fig. 3).
A diameter of 3.4 mm was measured.
An angle-tipped guidewire was used to cross the PDA from the
descending aorta. Over this wire, a delivery sheath for a 6 mm Amplatz
Canine Duct Occluder (ACDO) was advanced into the pulmonary artery.
After withdrawal of the guidewire, the ACDO was loaded into the delivery
sheath and advanced into its tip. The distal disc of the ACDO was deployed
into the main pulmonary artery and the delivery sheath and disc retracted as
a whole to engage the disc with the ostium. The delivery sheath was then
retracted as the ACDO delivery cable was gently eased forwards,
facilitating deployment of the proximal cup of the ACDO within the PDA
(Fig. 4, Video 2). After checking that the device was secured, the delivery
cable was unscrewed from the device and the sheath was retracted into the
descending aorta, leaving the ACDO securely deployed and occluding the
PDA. This procedure can be visualised in some detail using
transoesophageal echocardiography (Fig. 5). After removal of the vascular
sheath, the femoral artery was ligated and the surgical incision closed.
Radiographs were taken after the procedure as a baseline to record device
position (Fig. 6).
At discharge 24-hours later, no heart murmur was present and the pulse
was no longer hyperkinetic. Echocardiography 4 weeks later revealed
reverse cardiac remodelling and confirmed that the ACDO remained in an
appropriate position (Fig. 7). The aortic outflow tract velocity had
normalised (Fig. 8). The dog’s exercise tolerance and activity levels were
reported to have significantly increased and her body condition had
normalised.
Echocardiographic evidence of reverse cardiac remodelling can be

observed as early as 4 weeks after occluding the patent ductus arteriosus,
and reduction in left heart dimensions can be seen at 24 hours.
FIGURE 3. Aortic angiogram showing the patent ductus arteriosus (PDA), which originates on the
descending aorta (Ao) and inserts on the main pulmonary artery (PA). The simultaneous
opacification of the aorta and pulmonary artery after injection in this location is proof of an
extracardiac shunt. Note the PDA ostium (arrow).
FIGURE 4. Sequential fluoroscopic images illlustrating the stages of the Amplatz Canine Duct
Occluder (ACDO) deployment. The distal disc (asterisk) is deployed in the main pulmonary artery
and withdrawn together with the delivery sheath to engage the patent ductus arteriosus (PDA) ostium
(arrowheads) (a). Whilst maintaining tension on the delivery system, the sheath is withdrawn to
deploy the proximal cup (double asterisk) within the PDA ampulla (b). The ACDO can be seen in its
intended position, still attached to the delivery system but entirely withdrawn from the delivery
catheter (c).
Video 2
Fluoroscopic video of the transarterial deployment of an Amplatz Canine Duct Occluder to
occlude a patent ductus arteriosus (PDA). The distal disc is deployed in the main pulmonary
artery, then the device and delivery sheath are retracted to bring the disc into contact with the
PDA ostium. The proximal cup is then unsheathed in the PDA ampulla. Once an angiogram
through the delivery sheath confirms position, the device is deployed by unscrewing the
attachment cable.
FIGURE 5. Transoesophageal echocardiographic images illustrating the stages of the Amplatz
Canine Duct Occluder (ACDO) deployment. The patent ductus arteriosus (PDA) can be seen
inserting on the main pulmonary artery (PA) (a). Colour flow Doppler scan showing a turbulent flow
into the PA (b). The delivery system is passed across the PDA (c). The distal disc (asterisk) is
deployed and engaged with the PDA ostium (d). The proximal cup (double asterisk) is deployed
within the PDA (e). The ACDO has been completely deployed within the PDA (f).
FIGURE 6. Postoperative radiograph showing an appropriate position and conformation of the

Amplatz Canine Duct Occluder after its deployment.
FIGURE 7. Echocardiographic images 4 weeks after the procedure. Left atrial size had reduced
compared to preoperatively: left atrium-to-aortic root ratio of 1.46 (a). The Amplatz Canine Duct
Occluder (arrow) is seen as a hyperechoic structure at the point of bifurcation of the main pulmonary
artery (b).
FIGURE 8. Continuous wave Doppler echocardiographic images from a subcostal window, before
(a) and after (b) occlusion of the patent ductus arteriosus (PDA). A reduction in the aortic outflow
velocity can be observed, which illustrates that the large shunt flow through the PDA caused a
“relative aortic stenosis”.
DISCUSSION
A palpable heart murmur present in systole and diastole in a dog is usually
indicative of a PDA, and very few differential diagnoses exist. Though very
rare, an aorticopulmonary window may lead to similar clinical findings.
Aorticopulmonary collateral vessels, often referred to as “aberrant broncho-
oesophageal vessels”, may cause a continuous heart murmur that is often
quiet (grade II murmur, compared to a grade V murmur found in a PDA).
Sometimes, patients with aortic stenosis have a loud systolic murmur (due
to stenosis) followed by a diastolic murmur with a decrescendo profile
(associated with aortic insufficiency). This is referred to as a “to-and-fro”
murmur, rather than a continuous murmur, as it is caused by two different
flows, and sounds different from a single-flow PDA murmur. A
hyperkinetic pulse is supportive of a PDA: blood running off through the
PDA lowers diastolic arterial pressure, thereby increasing the gap between
systolic and diastolic pressures, which translates into a palpable pulse. This
can also be detected in patients with severe aortic insufficiency, but murmur
characteristics should aid in differentiating these diseases.
Echocardiography should confirm the diagnosis of PDA and allow the
assessment of cardiac volume loading and the degree of remodelling. As
pulmonary overcirculation leads to increased pulmonary venous return, left
atrial dilation is often present, and the left ventricular diameter in diastole is
larger than body weight reference values. Echocardiography is a reasonably
accurate method of measuring the size of the PDA ostium, provided it is
performed by a cardiologist with particular experience in congenital heart
disease. Angiography can be used to characterise the shape of the PDA and
to confirm the echocardiographic measurements of the ostium size; when
measurements are not in agreement, angiographic sizing should be used.
Transoesophageal echocardiography can reduce fluoroscopy time during
interventional procedures and provides additional confidence in measuring
ductal dimensions and assessing device security prior to deployment.
Occlusion of a PDA using an ACDO has been reported to completely
stop flow through the PDA by 24 hours postoperatively in 98 % of dogs and
yield good long-term survival rates. Other methods of occlusion are less
successful. Coil occlusion provides complete flow attenuation in
approximately 75 % of dogs, similar to the results obtained by surgical
ligation. Ligating a PDA by a thoracotomy is associated with a significant
risk of mortality, even in the hands of an experienced surgeon, compared to
the very rare cases that do not survive an interventional procedure.
CASE 15. VENTRICULAR
SEPTAL DEFECT
SIGNALMENT
Age: 1 year old
Sex: Male, intact
Presenting complaint: Incidentally detected heart murmur
On presentation, the dog was bright and alert. The mucous membrane
colour and capillary refill time were normal, as was the femoral pulse. He
weighed 24.3 kg and had an ideal body condition score (5/9). Upon
auscultation, a loud, grade IV/VI systolic heart murmur was detected at the
left base, with a grade III/VI holosystolic murmur at the right apex.
Abdominal palpation was unremarkable and the respiratory rate was
normal.
ECHOCARDIOGRAPHY
The left heart appeared moderately volume loaded (normalised left
ventricular internal dimension in diastole [LVIDd-N] was 1.8, reference
<1.7) and the left atrium was dilated (left atrium-to-aortic root [LA:Ao]
ratio was 1.8, reference <1.5), despite normal function. Right ventricular
dilation and moderate hypertrophy were present, with evidence of pulmonic
stenosis (PS)—which was the cause of the left basilar murmur and right
ventricular remodelling. In addition, a large defect in the muscular portion
of the ventricular septum was detected, measuring 19 mm in diastole and 11
mm in systole. In systole, the ventricular septal defect (VSD) diameter was
almost the same as the aortic diameter (Figs. 1a–c). Colour flow Doppler
examination of the VSD showed left-to-right systolic flow with a maximum
velocity of 2.1 m/s, which suggested an elevated systolic pressure in the
right heart—if pressure in the right heart remained normal, the gradient
between the left and right ventricles would generate a velocity of
approximately 5 m/s (Fig. 1d, Video 1). Real-time 3D imaging suggested
that the VSD orifice was very dynamic and changed in size significantly
during the cardiac cycle (Fig. 2, Video 2).
The diagnosis was VSD with concurrent PS.
FIGURE 1. Echocardiographic images of the muscular ventricular septal defect (VSD). The 2D
images from the right parasternal short-axis view show the VSD (a) and moderate left atrial dilation
(b). The right parasternal long-axis view determines the position of the defect in the interventricular
septum (arrowheads) (c). Colour flow Doppler interrogation demonstrates flow through the VSD
from the left to the right ventricle (d).
Video 1
Right parasternal long-axis echocardiographic view showing a large muscular ventricular septal
defect in the inferior interventricular septum, with colour Doppler flow through the defect.
FIGURE 2. Two-dimensional echocardiographic images from orthogonal views through the

ventricular septal defect (VSD) (left). Resulting real-time 3D image of the elliptical VSD orifice
viewed from the right ventricle (right).
Video 2
Four-dimensional echocardiographic assessment of the muscular ventricular septal defect from
the body of the right ventricle. The defect in the interventricular septum is clearly seen, as is its
dynamic size during the different phases of the cardiac cycle.
TREATMENT
Deciding upon treatment plans for complex congenital cases can be
challenging. In this case, two defects are present: a large VSD that could
cause significant volume overload of the left heart and clinical signs of
pulmonary oedema, and a stenotic pulmonary valve which is increasing the
pressure on the right heart. For either defect alone, it may be suitable to
perform interventional closure of the VSD using a septal occlusion device,
or balloon dilation of the PS lesion. However, in this particular patient, the
limitation to right heart output caused by the PS was also helping to limit
VSD flow and thereby reducing the risk of pulmonary oedema.
Consequently, this dog was considered to be “balanced” and, in the absence
of clinical signs, no treatment was performed. Monitoring every 6–12
months was recommended.
At the 6-month re-examination, the dog remained free of clinical signs
and exercising well.
DISCUSSION
Pathologically, VSDs are classified according to their anatomical location
in the right ventricle (Fig. 3). Perimembranous VSDs, the most common
type, communicate the subaortic and subtricuspid regions (Fig. 4). They are
mostly small and likely to be clinically insignificant, unless the distortion of
the normal support structure of the aorta leads to a significant aortic valve
regurgitation. Inlet VSDs often occur as part of complex congenital
diseases, such as the tetralogy of Fallot. In the case presented here, a large
muscular VSD is described despite being uncommon in dogs.
Most ventricular septal defects are located in the perimembranous

septum, from a subaortic to a subtricuspid position.
FIGURE 3. Diagrams showing the classification of ventricular septal defects according to their
location on the surface of the right ventricle. LV, left ventricle; PM, perimembranous; RA, right
atrium; RV, right ventricle.
FIGURE 4. Postmortem image of the heart of a horse with a perimembranous ventricular septal
defect (arrow). PA, pulmonary artery; TV, tricuspid valve.
Heart murmurs associated with a VSD are located on the right

hemithorax, generally apical and radiating cranial and towards the sternum.
In an uncomplicated case, where the normal pressure difference between
the left and right ventricles is maintained, VSD murmurs are often very
loud (grade IV/VI or louder); animals with louder murmurs tend to have
smaller defects with a better prognosis. In the case presented here, the
loudest murmur (on the left) was associated with the concurrent PS lesion.
On the other hand, the VSD murmur (on the right) was quieter than
expected, which related to the presence of PS altering right ventricular
pressure and therefore flow dynamics.
Ventricular septal defects are almost always associated with a loud, right-
sided heart murmur.
Animals with a large VSD are at risk of left-sided congestive heart failure
signs. Flow through a VSD, under normal circumstances, proceeds in
systole from the high-pressure left ventricle to the low-pressure right
ventricle. In diastole, there is little or no pressure difference across the
interventricular septum. Since the pulmonic valve is open during systole,
flow from the left ventricle enters the right ventricle and then the
pulmonary vascular bed. This blood returns to the left atrium, so the right
heart is not significantly affected but the left heart may struggle to cope.
Echocardiographic estimation of flow through both the pulmonic valve and
the aortic valve can be used to calculate a “shunt ratio”, a method to assess
the risk of developing clinical signs in patients with a VSD.
Animals with a large ventricular septal defect are at risk of clinical signs
of left-sided heart failure owing to volume overload of the lungs and left
atrium.
In this case, the large VSD was rendered clinically insignificant by the
concurrent PS. This combination of congenital diseases is not uncommon.
When stenosis is severe and systolic pressure in the right heart is increased,
affected dogs may not experience complications associated with the VSD
because the pressure difference that normally exists across the
interventricular septum is balanced out. In addition, the VSD may not be
associated with an obvious heart murmur on physical examination. In such
cases, treatment of the PS using interventional or surgical techniques may
be contraindicated unless an attempt to repair the VSD is also made. Since
this patient showed no clinical signs, the cardiologists elected not to treat
for fear of causing destabilisation. Monitoring was the key
recommendation.
CASE 16. TRICUSPID VALVE
DYSPLASIA
SIGNALMENT
Sex: Male, intact
Presenting complaint: Incidental heart murmur detected at routine
consultation. There are no apparent clinical signs, but the patient does not
exercise well compared to another dog in the household
On auscultation, a grade IV/VI systolic heart murmur was detected at the
right apex. It radiated widely, so it was audible to a lesser degree on the left
side. The patient’s heart rate was 80 bpm, and a respiratory sinus
arrhythmia was present. His respiratory rate was 20 breaths per minute, and
lung auscultation was normal. Pulse quality and mucous membranes were
also normal. He weighed 32 kg and had a body condition score of 7/9.
ECHOCARDIOGRAPHY
The right heart was severely dilated, especially the right atrium. The
tricuspid valve appeared to have long leaflets that were thick and distorted,
with a 15-mm portion of the septal valve leaflet tethered to the proximal
interventricular septum (Fig. 1). The 2D images clearly showed that the
valve leaflets did not close or open completely (Fig. 2). The right
ventricular papillary muscles were overlong and no chordae tendineae were
present—the papillary muscles attached directly to the valve leaflets after
appearing to fuse in the mid-ventricle (Fig. 3). A large jet of tricuspid
regurgitation was present. Real-time 3D imaging showed poorly mobile
leaflets and confirmed the absence of chordae tendineae (Fig. 4).
FIGURE 1. Right parasternal long-axis four-chamber echocardiographic view showing severe right
heart enlargement (should be approximately one third the size of the left) and long, distorted tricuspid
valve leaflets (arrowheads). The image is timed to show maximal valve closure (peak systole), when,
however, a large orifice in the valve remains visible. The septal tricuspid leaflet is tethered to the
interventricular septum for 15 mm along its length, which is diagnostic of Ebstein’s anomaly. The
white arrows show the tethered portion of the septal tricuspid leaflet; the red arrow indicates the
location of the true tricuspid valve annulus. LA, left atrium; LV, left ventricle; RA, right atrium; RV,
right ventricle.
FIGURE 2. Right parasternal short-axis echocardiographic view taken at the level of the tricuspid
valve at peak systole showing incompletely closed valve leaflets and a large regurgitant orifice
(arrowheads). LV, left ventricle; RV, right ventricle.
FIGURE 3. Left apical four-chamber echocardiographic views optimised to show the right heart.
The papillary muscles (arrows) in the right ventricle (RV) are excessively long and fused (at X) prior
to attaching directly to the edges of the tricuspid valve leaflets (arrowheads). No normal chordae
tendineae are visible (a). Colour flow Doppler shows a large jet of tricuspid regurgitation (b). RA,
right atrium.
FIGURE 4. Real-time 3D left apical four-chamber echocardiographic views optimised for the right
heart at end-diastole. The 3D volumetric image (a) is shown from a top-down view (also called
surgeon’s view): from the atria, looking through the valve orifices and into the ventricles. The right
atrium (RA) appears significantly larger than the left atrium (LA). The tricuspid valve appears as a
wide shelf between the atrium and ventricle, whilst the mitral valve is difficult to see in this diastolic
image—the mitral valve opened normally, but the tricuspid valve did not open well (stenosis) in
addition to its incomplete closure. Echocardiographic views of complex congenital disease can assist
in surgical planning. The 3D multiplane image (b) shows the selected 3D volume in a series of 2D
image slices, which from left to right and top to bottom show progressively more basilar views
through the tricuspid valve apparatus. In the central row, note the fusion point of the papillary
muscles (PM) (left), the fibrous-appearing direct attachment of the papillary muscle to the valve
leaflets (centre), and the edges of the tricuspid valve leaflets (arrowheads) which open incompletely
in diastole (right). LV, left ventricle; RV, right ventricle.
ELECTROCARDIOGRAPHY
Respiratory sinus arrhythmia was present at a heart rate of 100 bpm. P
waves were top normal in amplitude (0.4 mV) and had prolonged duration
(0.05 seconds), supporting the right atrial dilation seen on
echocardiography. QRS complexes were splintered and had a negative axis
in lead II, a common finding in dogs with tricuspid dysplasia, presumably
because of disrupted interventricular conduction tissue associated with the
septal tricuspid apparatus (Fig. 5).
FIGURE 5. Electrocardiogram showing sinus arrhythmia and splintered QRS complexes in all leads.
This finding is associated with Ebstein’s anomaly and is due to disruption of the intraventricular
conduction tissue of the septum which is close to the tricuspid apparatus. [50 mm/s, 10 mm/mV].
ELECTROCARDIOGRAPHY
Sinus rhythm with normal conduction was present throughout, with no
periods of unexplained tachycardia.
Findings were consistent with congenital tricuspid valve dysplasia
(TVD), particularly a form of the disorder known as Ebstein’s anomaly.
Ebstein’s anomaly is a form of tricuspid valve dysplasia in which the

septal leaflet is adhered to the septum. Since this can be associated with
life-limiting arrhythmias, Holter monitoring is recommended.
TREATMENT
In the absence of life-limiting clinical signs, no treatment was prescribed.
Although mild hepatomegaly was present, no signs of right-sided
congestive heart failure (e.g. ascites or pleural fluid) were detectable.
Repeat echocardiography and Holter monitoring in 6 months were
recommended to assess for significant progression of chamber dilation or
the development of arrhythmias, particularly supraventricular tachycardia
or atrial fibrillation.
DISCUSSION
The diagnosis of atrioventricular valve dysplasia is somewhat challenging,
with little or no consensus amongst veterinary cardiologists as to what
exactly constitutes a dysplastic valve. Generally agreed-upon features of
dysplasia include abnormal or fused papillary muscles, short or absent
chordae tendineae, and elongated valve leaflets. In the case described here,
all of these features were present. In addition, the septal tricuspid valve
leaflet was adhered to the wall of the basilar interventricular septum for 15
mm beyond the normal hinge point. This is a particular type of TVD known
as Ebstein’s anomaly, in which the septal tricuspid leaflet fails to
delaminate from the basilar interventricular septum during development.
The Labrador Retriever and Border Collie breeds are overrepresented in

studies of tricuspid valve dysplasia.
Diagnosis of Ebstein’s anomaly relies upon high-quality

echocardiographic images where the septal tricuspid anatomy can be clearly
seen. Displacement of the origin of the tricuspid hinge point from its normal
location should be identified, and this value should be indexed to body
surface area. In humans, a displacement index above 8 mm/m2 is diagnostic
for Ebstein’s anomaly; in this patient, the displacement index measured
14.8 mm/m2. In humans, around 50 % of affected people also suffer from an
accessory atrioventricular pathway, which predisposes to supraventricular
tachycardia and ventricular preexcitation. In this case, Holter
electrocardiography did not show any evidence of either of these
conditions, and there was no history of clinical signs induced by
tachyarrhythmias (e.g. syncope or episodic weakness).
Mild to moderate valve abnormalities may be detected incidentally and
have a good prognosis, but severe cases can present with heart failure
prior to adulthood and open-heart surgery is the best hope for long-term
survival.
The most common consequence of severe TVD is severe valve

regurgitation. This can increase mean right atrial pressure and lead to right-
sided congestive heart failure signs. In a small proportion of dogs with
TVD, stenosis of the valve is present. In this patient, stenosis was detected
but was relatively mild compared to the severity of regurgitation. If
tricuspid stenosis is the predominant feature of TVD, a conservative balloon
valvuloplasty can be performed to partially dilate the valve and relieve
stenosis. Given the likelihood of worsening tricuspid regurgitation during
this procedure, it should be reserved for dogs in which regurgitation is a
minor feature at initial diagnosis.
Tricuspid valve repair is a relatively novel surgical procedure, performed
under cardiopulmonary bypass, in which abnormal or absent chordae
tendineae are replaced by artificial chordae, using polytetrafluoroethylene
(PTFE) suture, and redundant valve leaflets are resected. Successful cases
have been reported, but access to centres currently performing this
advanced technique is limited. Valve replacement has also been reported in
dogs, but almost all cases are associated with thrombosis on the prosthetic
valve material, resulting in patient death. At this time, management of most
cases of TVD in dogs is limited to careful monitoring, early intervention to
treat heart failure or arrhythmias as they occur, and advice to limit breeding
from affected lines.
CASE 17. MITRAL VALVE
DYSPLASIA
SIGNALMENT
Breed: (English) Bull Terrier
Sex: Male, intact
Presenting complaint: Reduced exercise capability with episodes of
stopping and panting heavily during exertion. One episode of syncope the
previous week
On auscultation, the heartbeat was irregular: periods of what sounded like
sinus rhythm (at 100–120 bpm) were interspersed with episodes of
tachycardia (up to 200 bpm). A grade IV/VI left apical systolic murmur was
present, which extended through systole and partially over the second heart
sound (S2). In addition, an early diastolic murmur was also present at lower
heart rates. The mucous membranes were pale pink, with a prolonged
capillary refill time (2.5 seconds). The remainder of the physical
examination was normal. The patient weighed 34.7 kg and had a body
condition score of 7/9.
ELECTROCARDIOGRAPHY
Electrocardiographic findings were typical of atrial fibrillation (AF) (Fig.
1).
FIGURE 1. Six-lead electrocardiogram showing atrial fibrillation (AF) and notched QRS complexes
(arrows). The typical features of AF can be identified: irregular R–R interval, supraventricular
complex morphology, absence of P waves, and irregular baseline. The baseline in this case is
suggestive of coarse AF, which is common in recent onset, rather than the finer undulations often
present in more chronic cases. [50 mm/s, 20 mm/mV].
ECHOCARDIOGRAPHY
Left-sided cardiomegaly was present, evidenced by the increased
dimensions of the left ventricle (compared to weight-referenced intervals)
and the dilation of the left atrium (left atrium-to-aortic root ratio of 1.9).
The mitral valve had an abnormal J-tip morphology, a common feature of
mitral valve dysplasia (Fig. 2, Video 1). Mitral valve motion was abnormal:
the diastasis phase of closure was absent and the posterior leaflet had
limited movement (Fig. 3). Although a large jet of mitral regurgitation was
present, no valve prolapse could be identified (Fig. 4, Video 2). Mitral valve
stenosis was evident on colour Doppler M-mode and spectral Doppler (Fig.
5). Simultaneous electrocardiography showed that AF was briefly
interrupted by a period of normal sinus tachycardia.
FIGURE 2. Right parasternal long-axis echocardiographic views of the mitral valve in diastole (a)
and systole (b). The valve opens incompletely and has a J-tip morphology during peak diastolic flow
(arrows). The valve leaflet tips appear slightly thickened. There is no evidence of valve prolapse
during peak systole, which excludes degenerative valve disease as a differential diagnosis. LA, left
atrium; LV, left ventricle.
Video 1
Right parasternal long-axis echocardiographic view optimised for the mitral valve. The mitral
valve appears tethered at the tips, especially visible on the anterior (septal) leaflet, where opening
is incomplete. Left atrial dilation is visible, as is subjectively reduced left ventricular wall motion
and atrial fibrillation on simultaneous electrocardiography.
FIGURE 3. Right parasternal short-axis M-mode echocardiographic view at the level of the mitral
valve leaflets. The mitral valve is open throughout diastole; therefore, the normal E point and E–F
slope are absent because flow continued through the valve during diastole and the anterior leaflet
does not close in mid-diastole as normal (the diastasis period). The motion of the posterior leaflet is
poor.
FIGURE 4. Left apical four-chamber echocardiographic views in diastole (a) and systole (b). The J-
tip or hockey stick appearance of the mitral valve (arrows) and the absence of valve prolapse support
the diagnosis of mitral valve dysplasia. Note that the electrocardiogram appears different to the trace
seen in Figure 2: sinus rhythm was present at this point during the study, having previously been in
AF. LA, left atrium; LV, left ventricle.
Video 2
Left apical four-chamber echocardiographic view showing the typical J-tip appearance of the
mitral valve in diastole, a common feature of mitral dysplasia in dogs. No mitral valve prolapse is
visible, which differentiates this disorder from acquired degenerative atrioventricular valve
disease.
FIGURE 5. Left apical four-chamber echocardiographic views demonstrating transmitral flow
abnormalities. Two-dimensional colour Doppler (a) shows a large jet of mitral regurgitation in
systole. M-mode across the mitral colour flow (b) shows turbulence (green mosaic) in both systole
(below the mitral annulus; arrows) and diastole (above the mitral annulus), thus demonstrating a
degree of mitral valve stenosis in addition to regurgitation. Note that the electrocardiogram once
again shows atrial fibrillation. Transmitral spectral Doppler (c) shows flow through the mitral valve
throughout systole, with a long deceleration time (arrowheads) indicating stenosis, and high left atrial
pressure evidenced by increased transmitral flow velocity (2.7 m/s, normal <1 m/s). LA, left atrium;
LV, left ventricle.
ELECTROCARDIOGRAPHY
Holter monitoring was performed to evaluate the significance of AF.
Initially, the recording showed sinus rhythm and occasional ventricular
ectopy. Towards the end of the recording, during exercise, the dog
developed AF (Fig. 6), which was still present on a repeat Holter
monitoring performed 1 week later.
Findings were consistent with mitral dysplasia and AF, which became
permanent during the course of this investigation.
FIGURE 6. Three selected electrocardiographic strips from the 24-hour Holter recording. Sinus
rhythm with occasional ventricular premature complexes (VPCs) was present for the first 21 hours of
recording (a). At around 1:15 pm, during exercise (b), the dog experienced a change in rhythm from
sinus tachycardia to probable atrial fibrillation (AF). The owner reported an episode of weakness at
this time. As the heart rate reduced, during recovery from exercise (c), the rhythm was clearly AF,
and the typical features of absent P waves with irregular rhythm and baseline undulations
(arrowheads) are seen. The dog remained in AF for the remainder of the recording. [25 mm/s, 10
mm/mV].
TREATMENT
Pimobendan was prescribed to reduce the severity of mitral regurgitation,
by promoting systemic arteriodilation and increasing forward flow. On the
repeat Holter monitoring, mean 24-hour heart rate was 172 bpm (treatment
is indicated if >140 bpm). Digoxin was prescribed at 125 µg every 12 h.
Blood tests after 5 days of treatment showed an appropriate serum level of
digoxin (1.2 ng/ml 5–8 h after pill administration; target is around 1 ng/ml,
not exceeding 1.5 ng/ml because toxicity is more likely). Holter
electrocardiography was repeated in a further 3 weeks and showed
persistent AF with a mean heart rate of 119 bpm; this is an appropriate level
of control.
DISCUSSION
Mitral dysplasia is an uncommon congenital heart disease in dogs,
represented by <2 % of dogs presented to a cardiology referral centre and
only 0.004 % of a nonselected shelter population. Although this defect has
been reported in many breeds, it appears to be most prevalent in the
(English) Bull Terrier. In this breed, the disease is often diagnosed in
adulthood. This may relate to challenges in auscultation posed by thoracic
conformation which reduce the chance of early heart murmur detection.
(English) Bull Terrier dogs are overrepresented in breeds with mitral

dysplasia, but the German Shepherd Dog and the Springer Spaniel are
also potentially predisposed.
As in tricuspid dysplasia, affected valves may have variable degrees of

stenosis and regurgitation. Diagnosis of mitral dysplasia is commonly made
when valve leaflets appear to have tethered tips, giving a J-tip or hockey
stick appearance to the mitral valve in peak diastole. Other features of
dysplasia are direct attachment of papillary muscles to valve leaflets, short
or absent chordae tendineae, fenestrated mitral leaflets, or abnormally
positioned papillary muscles. Left atrial dilation and left-sided heart failure
are common at diagnosis.
In dogs with mitral stenosis, episodes of rapid onset, severe pulmonary
oedema are common (called flash pulmonary oedema). Since these episodes
may resolve with cage rest, oxygen therapy and sedation alone, they can
mimic respiratory disease; a thorough clinical examination allows
differentiation of these diseases, but it can be difficult to perform in a dog
with respiratory distress. In addition, pulmonary hypertension is prevalent
because of the fixed obstruction to forward transmitral flow. Pulmonary
hypertension can cause syncope, as can arrhythmias or even episodes of
high atrial pressure (owing to activation of atrial pressure receptors and
subsequent vagal outflow causing bradycardia and vasodilation). As a result
of this combination of factors, syncope is a common presenting sign of
mitral dysplasia.
Mitral dysplasia commonly causes syncope because of pulmonary

hypertension, arrhythmias, or increased atrial pressure leading to a
vagally induced bradycardia and vasodilation.
In the case presented here, the episodes of short-lived AF were suspected

to be responsible for the reported clinical signs, although vagal episodes
could not be excluded. It is rare to detect transient AF in dogs and, indeed,
in this case AF became persistent very soon after diagnosis. In large-breed
dogs with atrial dilation, AF is always a risk and, therefore, screening using
Holter monitoring should be considered. In this case, mean heart rate
exceeded 140 bpm, which is associated with a poor outcome. Heart rate
control was instigated using digoxin, and good control was achieved with
this drug alone. Dosing should be cautious and patients monitored for signs
of toxicity. Additional therapy with diltiazem may help to control heart rate
with fewer adverse effects than higher digoxin doses.
Dogs with mitral dysplasia may benefit from mitral valve repair surgery,
or balloon valvuloplasty if stenosis is the predominant problem. In most
cases, treatment of heart failure, pulmonary hypertension, and arrhythmias
is the primary goal to improve quality of life.
Atrial fibrillation is a common sequel to atrial dilation. The decision to

treat should be based on the mean 24-hour heart rate value obtained by
Holter monitoring.
CASE 18. TETRALOGY OF
FALLOT
SIGNALMENT
Breed: French Bulldog
Age: 8 months old
Sex: Male, intact
Presenting complaint: Exercise intolerance, cyanosis, heavy breathing
episodes, and loud heart murmur
On presentation, the patient could not walk more than a few steps without
severe dyspnoea. His respiratory rate was variable but increased to 60
breaths per minute with exertion. The mucous membranes were dull pink,
with a prolonged capillary refill time (3 seconds). The patient weighed 10.1
kg and had a subnormal body condition score (4/9). Auscultation revealed a
loud grade IV/VI systolic heart murmur at the left base and a heart rate of
132 bpm. Abdominal palpation was unremarkable.
A limited biochemical profile was performed and revealed no significant
abnormalities. The total protein concentration was 68 g/l. A packed cell
volume (PCV) of 84 % was measured (reference 35–55 %), which indicated
severe polycythaemia.
ELECTROCARDIOGRAPHY
Sinus rhythm was present, with a right axis deviation (deep S waves in lead
II and positive QRS complexes in aVR), suggestive of right ventricular
enlargement (Fig. 1).
FIGURE 1. Electrocardiogram showing sinus rhythm with a marked right axis deviation. [50 mm/s,
10 mm/mV].
ECHOCARDIOGRAPHY
Severe right ventricular hypertrophy and right atrial dilation were detected
(Fig. 2, Videos 1 and 2). A large subaortic ventricular septal defect (VSD)
was present, with malposition of the aorta to the right side of the septum.
Flow through the VSD was present from the right to the left side, which
explained the polycythaemia. The pulmonary artery was hypoplastic.
Doppler imaging defined a severe pulmonic stenosis and a narrowing of the
pulmonary trunk at the valvular and supravalvular levels (Fig. 3, Video 3).
The diagnosis was tetralogy of Fallot (TOF), based on the presence of a
VSD, a dextropositioned aorta, pulmonary hypoplasia, and right ventricular
hypertrophy.
FIGURE 2. Echocardiographic images showing major abnormalities in the heart. Severe right
ventricular hypertrophy and dilation can be seen in the right parasternal long-axis view (a) and short-
axis view (c) and in the left apical four-chamber view (e). A large ventricular septal defect (VSD) can
be identified in the long-axis view (b)—the VSD is indicated by arrowheads below a
dextropositioned aortic root—and in the short-axis colour flow Doppler scan (d). In image f, note the
hypoplastic region in the pulmonary artery (delineated by arrows). Ao, aortic root; LA, left atrium;
LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle.
Video 1
Right parasternal long-axis echocardiographic view showing severe right ventricular
hypertrophy in this case of tetralogy of Fallot.
Video 2
Colour flow Doppler echocardiogram showing a large inlet ventricular septal defect below
the aortic annulus with bidirectional flow.
FIGURE 3. Doppler assessment of the hypoplastic, stenotic pulmonary artery. Colour flow Doppler
mapping over the pulmonary valve (a) shows a tortuous, narrow route for blood flow and two
apparent regions of stenosis (arrowheads). Continuous wave Doppler interrogation of flow across the
hypoplastic region (b) identifies a maximum velocity of over 6 m/s, which is consistent with a very
severe stenosis and a systolic right ventricular pressure of at least 169 mmHg (normal 25 mmHg).
Video 3
Right parasternal short-axis echocardiographic view showing a hypoplastic pulmonary annulus
with components of annular and artery hypoplasia. Pulmonic stenosis and insufficiency can be
identified on colour flow Doppler.
TREATMENT
Phlebotomy was performed to lower the PCV (target approximately 65 %)
and thereby reduce the risk of complications associated with hyperviscosity
syndrome such as tissue ischaemia. According to the formula below, a
volume of 183 ml of blood was drawn from the left jugular vein with a
butterfly needle and an extension set. A replacement volume of crystalloids
was administered over a similar time frame, and then 4 ml/kg/h intravenous
crystalloids followed for 12 hours.
Propranolol was prescribed (0.5 mg/kg every 8 h, up-titrated to reduce
the heart rate) as a mixed-efficacy β-blocker to reduce right-to-left shunt
flow and myocardial work at exertion. Given the risk associated with a
primary repair surgery under cardiopulmonary bypass, a minimally invasive
stenting procedure was elected for this patient.
Minimally invasive pulmonary artery stenting or primary surgical

solutions are a more definitive treatment for tetralogy of Fallot than
medical therapy.
Under general anaesthesia, the right femoral vein was surgically exposed
and isolated. After securing vascular access, a pigtail angiographic catheter
was passed through the caudal vena cava and into the right ventricle. The
angiogram identified the position of the hypoplastic pulmonary trunk and
showed concurrent opacification of the aorta, which confirmed the right-to-
left shunt (Fig. 4a, Video 4). The angiographic catheter was then removed,
and a rigid guidewire was positioned across the pulmonic stenosis, in a
branch pulmonary artery. A delivery sheath was advanced over the
guidewire, and a balloon-expandable metallic vascular stent was positioned
to cover the stenotic region. After withdrawing the delivery sheath, the
balloon was inflated to expand the stent in position (Fig. 4b, Video 5).
Inflation at 8 atm of pressure was held for 3 seconds, and then the balloon
was deflated and withdrawn. A repeat right ventricular contrast injection
revealed that flow through the pulmonary trunk had improved and that the
right-to-left shunt had resolved (Fig. 4c, Video 6). Following catheter
removal, the femoral vein was ligated.
The patient recovered well and was discharged 24 hours later with
instructions for 10 days of lead rest. Clopidogrel was prescribed (18.75 mg
every 24 h) to reduce the risk of stent thrombosis and subsequent occlusion.
At 4 and 6 months after the procedure, the dog was clinically much
improved. Exercise tolerance had greatly improved and polycythaemia had
resolved (PCV 44 %).
FIGURE 4. Fluoroscopic images illustrating the deployment of the transvalvular pulmonic stent. A
transoesophageal echocardiography probe is visible dorsal to the heart in all images. Contrast
injection in the right ventricle (RV) (a) showed simultaneous opacification of the pulmonary artery
(PA) and aorta (Ao), a characteristic sign of a right-to-left intracardiac shunt; the pulmonary artery is
very small in comparison to the aorta and a marked stenosis is visible just beyond the pulmonic valve
(arrows). The balloon was inflated to deploy the metallic stent (b). An angiogram performed after the
procedure (c) showed resolution of the stenosis and no further evidence of shunt flow.
Video 4
Angiogram performed from a femoral vein approach with a pigtail catheter located in the right
ventricle. Contrast can be seen opacifying the pulmonary artery first (hypoplastic) followed by
simultaneous opacification of the aorta, confirming a right-to-left shunting ventricular septal
defect.
Video 5
Fluoroscopic video showing inflation of a high-pressure balloon to deploy a transvalvular
pulmonic stent across the stenotic lesion.
Video 6
Repeated injection of contrast in the right ventricle after stenting, showing good flow across the
transvalvular pulmonic stent with no visible right-to-left shunt flow across the ventricular septal
defect.
DISCUSSION
TOF is a complex conotruncal malformation that occurs due to a failure in
the process of spiral septation of the embryonic structures of the cardiac
conus and truncus arteriosus, which fail to develop normally into the basilar
interventricular septum, aorta, and pulmonary artery. Dogs with TOF
experience high right ventricular systolic pressure because of pulmonary
artery hypoplasia and exposure of the ventricle to systemic pressures by
malpositioning of the aorta over a large VSD. This leads to a right-to-left
intracardiac shunt. A range of patient presentations exist for TOF, but
exertional dyspnoea and cyanosis are the most common. The key findings
which should raise concern of TOF are a loud left basilar murmur (from the
pulmonic stenosis), a prominent right-sided apical impulse (from the right
ventricular hypertrophy), and polycythaemia.
Dogs with tetralogy of Fallot commonly present with exertional
dyspnoea, cyanosis, and polycythaemia.
Polycythaemia secondary to the release of erythropoietin is an

appropriate physiological response of the body to systemic hypoxaemia
associated with TOF. Hyperviscosity syndrome, caused by an excessively
high PCV (typically >75 %), can cause exercise intolerance owing to poor
muscle perfusion, tachypnoea owing to poor pulmonary perfusion, and
neurological signs caused by poor brain perfusion. When this syndrome is
present, treatment is urgent. In the case presented here, the PCV of 84 %
was considered an emergency. Phlebotomy, followed by appropriate fluid
therapy, is the fastest way to relieve the clinical signs.
In the longer term, the signs may be controlled using a mixed β-blocker
such as propranolol: β1-receptor blockade reduces myocardial oxygen
demand and has a cardioprotective effect, and β2-receptor blockade reduces
the degree of systemic vasodilation that occurs at exertion and thereby
limits the right-to-left shunt at exercise. However, such β-blocker therapy to
control the shunt direction is unlikely to be effective alone in the medium-
to long-term. A more definitive solution may be to reduce right ventricular
afterload and thereby promote more balanced or even left-to-right flow.
In the case described here, pulmonary artery stenting was performed to
abolish the right-to-left shunt. The PCV normalised within weeks, and the
owners reported a great improvement in the dog’s quality of life. If stenting
fails or is not an option, pulmonary flow may be surgically increased either
by using a modified Blalock–Taussig–Thomas shunt or by operating
directly on the right ventricular outflow tract to overcome the pulmonary
artery hypoplasia. Other techniques, such as using a conduit or a patch
graft, have also been reported. As a last resort and when surgery is not
possible, hydroxyurea may be administered to control the clinical signs.
This drug is a bone marrow suppressant which reduces erythropoiesis and
therefore PCV. Titration to effect is necessary (target PCV of 50–60 %).
Adverse effects are possible, including gastrointestinal signs, skin and hair
coat changes, and damage or loss of the claws. Despite these
considerations, hydroxyurea can be an effective drug that maximises the
quality of life in dogs with TOF.
Medical treatment of tetralogy of Fallot includes propranolol to reduce
vasodilation associated with exertion and phlebotomy or bone marrow
suppressants, such as hydroxyurea, to control the packed cell volume.
CASE 19.
ATRIOVENTRICULAR SEPTAL
DEFECT
SIGNALMENT
Breed: Chihuahua
Age: 5 months old
Sex: Female, intact
Presenting complaint: Almost complete absence of exercise tolerance.
Heavy breathing on exertion or excitement, occasionally noticed to be
associated with grey or blue-tinged mucous membranes
Cyanosis was evident on presentation, as was heavy breathing with a
seemingly expiratory effort and increased expiratory noise. Upon cardiac
auscultation, a loud, grade IV/VI systolic heart murmur was detected
bilaterally and had a musical quality to it. An apical impulse was easily
palpable on the right hemithorax. Pulmonary auscultation revealed loud
adventitious sounds but no pulmonary crackles or wheeze. The patient was
small for her age: she weighed 1.8 kg and had a body condition score of 4/9
(thin).
A routine complete blood cell count and biochemistry profile revealed
erythrocytosis (packed cell volume [PCV] of 68 %, reference 35–55 %) and
a total serum protein level of 62 g/l (reference 55–75 g/l).
ECHOCARDIOGRAPHY
Right heart dilation was obvious, and a large atrial septal defect (ASD) was
present in the primum region (Fig. 1, Video 1). A ventricular septal defect
(VSD) in the inlet portion of the muscular septum was also evident (Fig. 2).
Flow was bidirectional through both holes, and bilateral atrioventricular
valve regurgitation was also present. The atrioventricular valve apparatus
was abnormal. First, the tricuspid valve hinge points were not in a normal
position (i.e. slightly displaced compared to the mitral apparatus), they were
level with the hinge points of the mitral valve. Second, in short-axis
echocardiographic images, the anterior mitral leaflet had a cleft (Fig. 3,
Video 2). From the left apical view, the atrioventricular valve apparatus of
the septum appeared to be “floating” between the ASD and the VSD (Fig.
4).
Findings were consistent with a complete atrioventricular septal defect
(AVSD).
Dogs with atrioventricular septal defect tend to develop erythrocytosis

because of a large right-to-left intracardiac shunt.
FIGURE 1. Right parasternal long-axis echocardiographic views of the atrial septal defect (ASD).
The right heart is dilated (similar in size to the left heart), and a large primum-type ASD (indicated
by arrowheads) can be seen (a). The mitral and tricuspid annuluses are level with one another and
appear continuous, rather than the tricuspid valve annulus being apically displaced by a few
millimetres. This latter finding is typical of an atrioventricular septal defect. Arrows indicate the
septal leaflets of the atrioventricular valve. Colour flow Doppler (b) shows large jets of both tricuspid
and mitral regurgitation, and flow through the ASD could be seen in systole and diastole. LA, left
atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Video 1
Right parasternal long-axis four-chamber echocardiographic view showing a huge defect in the
low interatrial septum (septum primum region). The mitral and tricuspid valves are positioned
level with each other. Severe right heart dilation is present, and the left atrium is also enlarged.
FIGURE 2. Right parasternal short-axis echocardiographic view at the level of the chordae tendineae
showing a large ventricular septal defect (indicated by arrowheads) in the inlet region of the muscular
septum. LV, left ventricle; RV, right ventricle.
FIGURE 3. Right parasternal short-axis echocardiographic view at the level of the atrioventricular
(AV) valves. The mitral valve appears tricuspid or to have a cleft anterior leaflet, but this, in fact,
represents the complex anatomy of a common AV valve bridging an AV septal defect (see schematic
diagram on the right). Two bridging leaflets cross the common AV canal, whilst one posterior leaflet
is present in the left AV valve region and two anterior leaflets are present in the right AV valve
region. These leaflets are named according to the anatomic position in humans: left mural (LM),
inferior bridging (IB), superior bridging (SB), right inferior (RI), and right anterosuperior (RAS). LV,
left ventricle; RV, right ventricle.
Video 2
Right parasternal short-axis echocardiographic view optimised for the mitral valve. The anterior
mitral leaflet appears cleft, which indicates the presence of a common atrioventricular valve
(typical of a complete atrioventricular septal defect). The ventricular septal defect is intermittently
visible during the cardiac cycle.
FIGURE 4. Left apical four-chamber echocardiographic view showing the anatomy of the
atrioventricular septal defect. The large atrial septal defect (ASD) is clearly visible, in addition to the
ventricular septal defect (VSD) located apical to one of the bridging leaflets (arrows) which crosses
the atrioventricular valve orifice from right to left. LA, left atrium; LV, left ventricle; RA, right
atrium; RV, right ventricle.
TREATMENT
Although primary surgical repair is widely performed in humans, it is
currently not an option in small animal medicine owing to the very limited
access in veterinary practices and the lack of experience of veterinary
surgeons. The patient was treated with propranolol, a mixed β1- and β2-
blocker, in order to reduce the vasodilation in skeletal muscle associated
with exercise and excitement (mediated by β2-receptors; aims to promote
pulmonary blood flow by preventing large or sudden decreases in systemic
vascular resistance) and to potentially induce antiremodelling effects on the
myocardium (β1-blocking effects). Although erythrocytosis was present, no
treatment was prescribed at this time and PCV was monitored monthly, as
clinical signs of erythrocytosis tend to occur when PCV is over 75 %, and
target PCV for dogs with a right-to-left shunt is around 65 %. A repeat
echocardiogram for reassessment was recommended at the time of skeletal
maturity (around 1 year old).
DISCUSSION
Although the currently accepted nomenclature is AVSD, this disorder has
historically been referred to by terms such as endocardial cushion defect or
atrioventricular canal defect. There are three main types of AVSD: the
complete defect (ASD and VSD, bridging leaflets to a common AV valve)
and the partial defect, which can have an atrial dominance (no VSD) or a
ventricular dominance (no ASD). The case described here is an example of
a complete AVSD.
Diagnosis of atrioventricular septal defect is challenging but relies upon

identification of either an atrial septal defect, a ventricular septal defect,
or both, with associated abnormalities of the atrioventricular valves.
This defect has been reported in dogs and cats, in addition to horses,
cattle, and other production species (e.g. camelids, in which complex
congenital heart disease is relatively common). Confirmation of an AVSD
relies upon high-quality echocardiography, but it should be suspected if
severe cardiomegaly and large septal defects are detected on a more focused
echocardiogram. Affected individuals often have very poor exercise
tolerance and episodes of heavy breathing with cyanosis. These particular
clinical signs may be referred to as “tet spells” by human cardiologists, as
they are identical to the signs seen in young patients with a right-to-left
shunt caused by tetralogy of Fallot.
Treatment of dogs with AVSD is generally palliative, aimed at
controlling clinical signs. Erythrocytosis is likely to occur, and once the
PCV rises above 75 %, there is a risk of neurological or prothrombotic
signs. With a PCV below 70 %, clinical signs are unlikely, aside from
cyanosis, which may occur more easily in patients with erythrocytosis. This
is because the blue-tinged colour to mucous membranes is identified when
the absolute level of deoxyhaemoglobin present in the blood is >5 g/dl;
therefore, when a higher number of erythrocytes (and thus more
haemoglobin) are present, cyanosis may occur at a more normal level of
blood oxygenation. In other words, a dog with erythrocytosis may become
cyanotic at a relatively normal arterial oxygen level, whereas a dog with
normal haemoglobin concentrations would need worryingly low arterial
oxygen levels to develop cyanosis. Controlling erythrocytosis in AVSD
requires either periodic phlebotomy and intravenous fluids or the use of
drugs specifically toxic to the erythroid line in the bone marrow (e.g.
hydroxyurea). The use of a mixed β-blocker, such as propranolol, may help
reduce the severity of erythrocytosis by reducing the severity of the right-
to-left shunt. The effect will be more pronounced if the shunt is only present
at the ventricular level (if balanced or right-to-left shunts occur through a
VSD, the balance of shunt flow is dependent upon the differences in
pulmonary and systemic arterial resistance; with a bidirectional or right-to-
left ASD, shunt flow is more dependent on the differences in compliance of
the two ventricles). In the case described here, right ventricular remodelling
was quite marked and the right ventricle was exposed to systemic pressure;
therefore, the compliance of the right ventricle was likely to be low,
promoting right-to-left shunt flow. Despite this, the β2-receptor blocking
effects of propranolol were expected to help to some degree.
Most dogs with AVSD develop severe clinical signs in youth, and almost
all have a shortened life span because of the disease. Ultimately, patients
develop refractory erythrocytosis or signs of congestive heart failure or
pulmonary hypertension.
Treatment is limited to controlling clinical signs related to either
systemic hypoxaemia, high packed cell volume, or congestive heart
failure.
CASE 20. COR TRIATRIATUM
DEXTER
SIGNALMENT
Presenting complaint: Exercise intolerance and abdominal distension
The dog was bright and alert on presentation. Physical examination
demonstrated distension of the abdomen, with a fluid thrill on abdominal
ballottement. However, no jugular venous distension or pulsation was
present, and the hepatojugular reflux test was normal (abdominal pressure
did not yield distension of the jugular vein). No pain or masses were
detected. The patient’s body condition score was low (4/9). No heart
murmur was present, and the heart rate was 100 bpm. Her mucous
membranes were pale pink, with a prolonged capillary refill time (>2
seconds). Pulse quality was subnormal. Pulmonary auscultation was
unremarkable.
The complete blood cell count and serum biochemical profile were normal,
aside from slightly low albumin and sodium concentrations, suggestive of a
dilutional effect.
ULTRASONOGRAPHY
Abdominal and thoracic focused ultrasonography confirmed the presence of
abdominal fluid and excluded a pericardial effusion. However, an
echocardiogram was performed, as the right heart appeared somewhat
dilated.
Echocardiography confirmed that the right heart was slightly large
relative to the left heart, and revealed a striking atrial abnormality. The right
atrium was divided into two chambers by a fibrous membrane, giving the
appearance of a “heart with three atria” (Fig. 1). Blood from the caudal
vena cava entered the caudal right atrial chamber (RA-1), which
communicated with the true right atrium (RA-2, where the tricuspid valve
could be found) by a small, centrally located orifice. Doppler interrogation
of this orifice showed a flow velocity of up to 2 m/s from RA-1 to RA-2,
suggestive of a clinically significant pressure gradient between the two. The
caudal right atrial chamber was dilated and subjected to high pressure. The
coronary sinus entered RA-1 and was also dilated (Fig. 2). No evidence of
any other heart disease was detected.
FIGURE 1. Echocardiographic images from the right parasternal long-axis view showing cor
triatriatum dexter. Three chambers can be visualised at the level of the atria: the normal left atrium
(LA), the caudal right atrial chamber (RA-1), and the true right atrium (RA-2), where the tricuspid
valve annulus can be seen (arrowheads). LV, left ventricle; RA, right atrium; RV, right ventricle.
FIGURE 2. Echocardiographic images from an oblique, modified right parasternal long-axis view
(top), optimised for the caudal right atrium, showing the orifice in the dividing membrane of the right
atrium (arrowheads) and a dilated coronary sinus (CS) connected to the caudal right atrial chamber
(RA-1). Note the low velocity (up to 2 m/s) flow from RA-1 to the true right atrium (RA-2) on the
colour flow Doppler scan (middle), measured by continuous wave Doppler echocardiography
(bottom).
THORACIC RADIOGRAPHY
Thoracic radiographs were taken to screen for complicating factors. They
confirmed a dilated caudal right atrium and showed a distended caudal vena
cava and a lack of abdominal serosal detail consistent with ascites (Fig. 3).
The diagnosis was cor triatriatum dexter. Literally translated from Latin
as “heart with three atria on the right”, in more modern terminology it is
referred to as “divided right atrium”.
Although rare, dogs with cor triatriatum dexter may be underdiagnosed;

however, cases like this are good candidates for treatment and often have
good long-term survival with a favourable quality of life.
FIGURE 3. Dorsoventral (a) and right lateral (b) radiographic projections of the thorax showing
cardiomegaly, particularly in the region of the right atrium and caudal vena cava. Note the markedly
distended caudal vena cava (arrowheads) and the loss of serosal detail in the lateral view, typical of
patients with cardiogenic ascites.
TREATMENT
Furosemide was administered at 1 mg/kg PO every 12 h in addition to an
ACE inhibitor (0.5 mg/kg PO every 24 h) and spironolactone (2 mg/kg
every 24 h), as the patient was congested and the renin–angiotensin–
aldosterone system (RAAS) was activated.
The definitive treatment of a divided right atrium is to remove or reduce
the obstruction caused by the membranous division. Although surgical
excision is possible using inflow occlusion techniques, interventional
treatment via balloon dilation of the orifice is widely performed, and was
elected in this case.
A CT angiogram was performed under general anaesthesia to evaluate
collateral blood flow and gain a better understanding about the position of
the orifice within the 3D structure of the transatrial membrane between RA-
1 and RA-2. Contrast injected into a lateral saphenous vein was diverted
away from the caudal vena cava into a dilated azygous vein because of the
high pressure at the level of RA-1. It then entered the cranial vena cava
immediately cranial to RA-2, where it flowed into the heart and pulmonary
vasculature as normal. Contrast failed to opacify RA-1, and the orifice (2
mm in diameter) could be visualised by the presence of a jet of negative
contrast (non-contrast-enhanced blood) entering from RA-1 into the
opacified RA-2 (Fig. 4).
FIGURE 4. CT angiographic images (sagittal [a] and transverse [b] reconstructions of the thorax)
showing contrast opacification of the cranial vena cava (CrVC) and true right atrium (RA-2) before
significant opacification of the caudal right atrial chamber (RA-1) could occur. Note the orifice in the
dividing membrane (arrowheads) highlighted by the flow from RA-1 to RA-2, which is visible as
“negative contrast”. CVC, caudal vena cava; RV, right ventricle.
The patient was then transferred to the operating theatre for

interventional balloon dilation. Femoral venous access was obtained via a
surgical cutdown to expose the vessel and using a modified Seldinger
technique. A vascular introducer sheath was inserted and a nonselective
angiogram was performed. Fluoroscopy was used to track the path of
collateral flow back to the heart, which was evident through not only the
azygous vein but also multiple vertebral veins. No flow was seen entering
RA-1 (Fig. 5a). A 120 cm 0.035″ angle-tipped hydrophilic guidewire, in
combination with a 5 F multipurpose angiocatheter, was advanced from the
femoral vein to the caudal vena cava, and then into RA-1. After passing
through the orifice into RA-2, the guidewire–catheter combination was
advanced out through the cranial vena cava. To provide support for the
balloon, the guidewire was exchanged for a more rigid Rosen wire. The
multipurpose catheter was then removed and replaced with an 8 mm
balloon dilation catheter. After being positioned through the orifice in the
transatrial membrane, the balloon was inflated several times for 30 seconds
each. Once loss of the balloon waist associated with successful dilation was
observed, this balloon was exchanged over the guidewire for a 12 mm
balloon, and the procedure was repeated.
After removing both the balloon and the guidewire, a nonselective
angiogram was repeated and showed a significant improvement in venous
return to the heart, with the heart now filling predominantly from the caudal
vena cava through RA-1 and into RA-2. Collateral circulation remained
present but was reduced (Fig. 5b). The femoral vein was ligated after
removing the introducer sheath, and the dog recovered from anaesthesia
smoothly.
The patient was discharged from the hospital the following day, and
abdominal distension resolved within 5 days. Medical treatment was
discontinued in the following weeks. One year after the procedure, she was
clinically well and showed no signs of heart failure. The owner perceived
that the dog’s exercise tolerance had returned to normal.
FIGURE 5. Nonselective angiographic images before (a) and after (b) balloon dilation of the orifice
in the right atrial dividing membrane. Before dilation, no flow (circle) can be seen entering the heart
through the caudal right atrial chamber (RA-1). Contrast goes through collateral circulation via
vertebral veins and a dilated azygous vein into the cranial vena cava, true right atrium (RA-2), and
right ventricle. After dilation, contrast passes more readily into the heart through the now dilated
orifice in the membrane between RA-1 and RA-2; note that collateral flow is diminished (dashed
arrows).
DISCUSSION
Cor triatriatum dexter is a rare congenital heart disease: the estimated
prevalence is only 0.3 % among dogs with congenital heart diseases
presenting to cardiology referral centres. The cause of a divided right
atrium is thought to be incomplete regression of the right valve of the sinus
venosus. This embryonic valve normally diminishes to form part of three
right atrial structures: the crista terminalis, between the cranial and caudal
venae cavae; the eustachian valve, at the entrance of the caudal vena cava;
and the thebesian valve, at the coronary sinus.
This disease may well be underreported, as clinical findings are not
typical of primary heart disease. Most patients with cor triatriatum dexter
do not have a pathological heart murmur, as in the case described here,
because the pressure gradient between the chambers of the divided right
atrium is relatively low, so blood flow turbulence and the resultant
reverberation of cardiac structures are minimal. Although ascites might
suggest right-sided heart failure, the absence of jugular distension may lead
some clinicians to initially exclude heart disease from their differential
diagnoses. In dogs with primary right-sided myocardial failure, tricuspid
dysplasia, cardiac tamponade, or ascites due to most other cardiogenic
causes, pressure in the right atrium is high, and therefore the pressure in
both the cranial and caudal venae cavae is increased. In patients with a
divided right atrium, although pressure caudal to the heart is high, pressure
in the cranial vena cava is near normal, which leads to a lack of abnormal
jugular findings. This is often referred to as “Budd–Chiari-like syndrome”
(ascites secondary to hepatic vein obstruction).
Clinical findings in cases of cor triatriatum dexter are often atypical for
cardiac disease.
Echocardiography in dogs with a divided right atrium often demonstrates

the characteristic “three atrium” appearance, with a grossly dilated caudal
right atrium and often a distended coronary sinus, as in this case. In most
dogs with cor triatriatum dexter, the right atrial division occludes the caudal
vena cava and the coronary sinus together, but in some cases the caudal
vena cava is alone obstructed. An ostium in the septating membrane should
be visible on 2D and colour flow Doppler scans. In this case, CT
angiography helped to localise the orifice within the dividing membrane, to
evaluate the proximity to nearby cardiac structures and to plan the
interventional approach. Despite not being necessary in all cases, use of this
imaging technique before a procedure may help to anticipate complications
before they occur.
Echocardiography can be combined with other imaging methods, such as

computed tomography or fluoroscopic angiography, to understand the
complex anatomy and collateral circulation in dogs with a divided right
atrium.
Balloon dilation of a right atrial membrane is widely reported by

cardiologists as being a successful procedure to relieve the pressure in the
caudal vena cava and thereby controlling ascites and improving cardiac
output. Most dogs seem to have a good long-term outcome, but occasional
reports of restenosis requiring a repeat procedure have been published.
CASE 21. DIVIDED LEFT
ATRIUM
SIGNALMENT
Age: 3 years old
Sex: Male, neutered
Presenting complaint: Heavy breathing at exercise and systolic heart
murmur
The cat presented with respiratory distress after transport, and only a
limited examination could initially be performed. He responded well to
furosemide (2 mg/kg IM), butorphanol (0.3 mg/kg IM), oxygen therapy,
and cage rest. A patient-side ultrasound examination showed no pleural
fluid, but cardiomegaly was present. A grade I–II/VI heart murmur was
audible on the left, as were occasional premature beats. No ascites or
jugular distension was evident, and femoral pulse quality was normal.
The complete blood cell count and serum biochemical profile were normal
(PCV 34 %, total protein 63 g/l, and electrolytes within reference ranges).
ELECTROCARDIOGRAM
Sinus rhythm was present at 182 bpm, with frequent atrial premature
complexes (Fig. 1).
FIGURE 1. Electrocardiogram (leads I, II, and III) demonstrating background sinus rhythm with
frequent atrial premature complexes (circled on the first two occurrences). Premature complex
morphology is different owing to conduction aberrancy, which sometimes occurs when the
ventricular electrical system is not fully repolarised in time for the early stimulus. Note that the P
waves of the premature beats (arrows) are taller than those of sinus complexes, suggesting a point of
origin higher in the atria than the sinoatrial node. [50 mm/s, 20 mm/mV].
ECHOCARDIOGRAPHY
The left atrium was divided into two chambers: the true left atrium,
containing the mitral valve, and a proximal left atrial chamber, connected to
the pulmonary veins and left auricular appendage (Fig. 2, Video 1). A
fibromuscular band of tissue with a small orifice divided the two chambers.
Doppler interrogation revealed flow back and forth through this orifice (Fig.
3, Video 2), reversing in atrial systole. Spontaneous echocontrast was
present in the severely dilated auricle (Video 3). The pulmonary artery also
appeared larger in diameter than the aorta.
FIGURE 2. Right parasternal short-axis echocardiographic view showing the relatively small true
left atrium (LA) and the larger proximal left atrium (P-LA) which contains the left auricular
appendage. Ao, aorta.
Video 1
Right parasternal short-axis echocardiographic view showing a small left atrial chamber below
the aortic root, with an enlarged auricle to the right of the image.
FIGURE 3. Colour flow Doppler image identifying the small orifice (arrowheads) across the
dividing fibromuscular membrane. This orifice allows blood flow from the dilated proximal left
atrium to the true left atrium, the latter connected to the mitral valve.
Video 2
Right parasternal short-axis echocardiographic view with colour flow Doppler mapping, showing
flow between the auricle and the true left atrium. The ostium seen in the video is narrow because
of a fibrous ring of tissue around the “neck” of the auricle where it connects to the true atrium.
Video 3
Oblique left cranial echocardiographic view optimised to show the body of the severely dilated
auricle. The trabecular wall of the auricle is visible in the near field, and the true left atrium is
located to the left of the image. No thrombus can be seen in the video, but it is a common site for
thrombus formation in affected cats owing to a low flow environment.
Cardiomegaly was present, as was pulmonary venous distension and a
generalised, patchy alveolar lung pattern, suggestive of cardiogenic
pulmonary oedema (Fig. 4).
The diagnosis was supravalvular mitral stenosis (SVMS), causing
congestive heart failure.
FIGURE 4. Right lateral (a) and dorsoventral (b) thoracic radiographs showing cardiomegaly and a
patchy alveolar lung pattern. Cardiomegaly is obvious in the dorsoventral view (double arrow) with a
bulge in the position of the left atrium (arrowheads). Pulmonary venous distension is evident
(arrows) in both projections.
TREATMENT
Managing heart failure signs was the first priority; therefore, furosemide
and oxygen therapy were continued to effect over the following few hours.
By 6 hours after presentation, the patient was no longer oxygen dependent
and oral furosemide was prescribed at 2 mg/kg every 12 h thereafter.
Clopidogrel (18.75 mg/cat every 24 h) was also prescribed to reduce the
risk of arterial thromboembolism.
The cat was discharged at 24 hours after presentation; he was eating,
normotensive, and with a respiratory rate of 28 breaths per minute out of
oxygen therapy. He continued to do well at home, receiving medication as
before for 3 years. During this time, the cat presented four times to
emergency clinics with episodes of presumed heart failure, which resolved
after cage rest, mild sedation, and oxygen therapy. Intensification of oral
furosemide was recommended each time, then the dose was tapered
according to the sleeping respiratory rate at home.
Eventually, diuretic resistance was suspected, as the cat had a persistently
high respiratory rate, and euthanasia was elected after signs became
refractory. Necropsy examination was performed and lesions associated
with SVMS were identified (Fig. 5).
FIGURE 5. Postmortem images of the patient’s heart illustrating supravalvular mitral stenosis. A
hugely distended left auricular appendage is visible from the caudal aspect of the heart (arrowheads)
with a much smaller true left atrium (LA) present alongside (a). Opening the distended chamber
above the membrane, the fibrous ring (arrow) above the mitral valve can be clearly seen (b).
DISCUSSION
SVMS is one of two forms of a congenital division of the left atrium, along
with cor triatriatum sinister (CTS). In veterinary medicine, they are reported
almost exclusively in cats. The difference between the two forms is the
position of the division: animals with SVMS have the division positioned
below the fossa ovalis and the left auricle, whereas cases with CTS have the
division positioned above the fossa ovalis and left auricle. The most striking
echocardiographic difference is that the auricle is grossly dilated in cases
with SVMS, owing to its inclusion in the proximal chamber, and therefore it
is subject to high pressures along with the pulmonary veins. In cats with
CTS, the auricle is often small as it communicates directly with the true left
atrium, which is not under high pressure, but the pulmonary veins are
severely dilated owing to their high-pressure state above the dividing
membrane (Fig. 6). The case presented here was a convincing case of
SVMS owing to the huge auricular dilation, visible on echocardiographic
and radiographic images. Nevertheless, the differentiation between these
two conditions is largely academic, as management options are similar.
Supravalvular mitral stenosis is caused by failure of the embryologic
common pulmonary vein to be incorporated into the developing left
atrium.
FIGURE 6. Diagram highlighting the different anatomy of cor triatriatum sinister and supravalvular
mitral stenosis.
Cats presenting with SVMS or CTS can pose a particular clinical

challenge as they often have no heart murmur—the flow between the
divided left atrial chambers is often at a relatively low velocity with
minimum reverberation of surrounding structures (unlike, for example,
mitral regurgitation), so the abnormality is usually inaudible. Signs of left-
sided congestive heart failure are typical of respiratory distress, and
occasionally patients present with supraventricular arrhythmias, ranging
from isolated atrial premature complexes, as in this case, to atrial
fibrillation. The stagnant flow in the dilated auricle or pulmonary veins may
predispose to thrombus formation, posing a high risk of arterial
thromboembolism. This is rare amongst congenital diseases; significant left
atrial dilation is rarely caused by congenital disease aside from patent
ductus arteriosus (PDA) and mitral dysplasia (MD), both of which are
uncommon in cats. Dogs are more commonly affected by PDA or MD, but
they are very rarely affected by the thromboembolic consequences to which
cats are predisposed.
Heart failure signs often relate to stressful events in cats with SVMS or
CTS, because increases in preload (associated with tachycardia and
venoconstriction caused by catecholamine surges) are not well tolerated
when a fixed stenosis exists at the premitral level. The stress of travel or a
cat fight can trigger heart failure signs, which then apparently respond
rapidly to cage rest and oxygen and furosemide therapy. Affected cats may
experience these episodes of flash pulmonary oedema periodically, as
occurred in this case, but in-between episodes they may be able to tolerate a
low-dose or even no furosemide therapy.
Affected cats may be predisposed to episodes of flash pulmonary oedema

caused by stressful events and well responsive to stabilisation.
Pulmonary hypertension is relatively common in cats with SVMS, again

because of a fixed stenosis at the premitral level. If diagnosed, cats with
pulmonary hypertension may benefit from treatment with sildenafil in
addition to standard feline heart failure therapy.
Surgical treatment, or hybrid procedures using a cutting balloon through
the atrial roof at thoracotomy, have been attempted in some centres, but
complications are common as atrial tissue in cats appears to be relatively
friable. Consequently, invasive options should be considered a last resort.
PULMONARY DISEASE
Case 27. Pneumocystic pneumonia. Pneumocystis carinii
Case 28. Parasitic pneumonia. Angiostrongylus vasorum
PLEURAL DISEASE
MEDIASTINAL DISEASE
Case 31. Thymoma
Case 32. Vascular ring anomalies. Persistent right aortic arch
PULMONARY DISEASE
The respiratory section of this book includes several of the most common
case studies that present to veterinary practices. In all cases, the patient’s
history, physical examination findings, laboratory test results, and imaging
studies are needed to achieve a definitive diagnosis.
AIRWAY DISEASE
■ Chronic bronchitis. Slow, chronic, progressive, inflammatory condition
of the airways, common in small-breed dogs and typically affecting
middle-aged to older patients. Clinical signs include dry cough, gagging,
and exercise intolerance. Physical examination reveals crackles and
wheezing. Thoracic imaging may show a bronchial/bronchointerstitial
pattern. In cats, hyperinflation of the lungs and atelectasis of the right
middle lung lobe is commonly seen. Bronchoscopy shows an
erythematous and thickened wall with mucus buildup. Cytology of the
bronchoalveolar lavage (BAL) fluid reveals neutrophils, eosinophils, and
macrophages. As it is a progressive, incurable disease, treatment is
symptomatic and includes bronchodilators, corticosteroids, and cough
suppressants, as well as antibiotics in cases of secondary infections.
■ Feline chronic lower airway disease/asthma. Eosinophilic
inflammation of the airways affecting cats of all ages. Clinical signs
include coughing, dyspnoea, sneezing, laboured breathing, and
wheezing. In severely affected cats, extreme respiratory distress,
cyanosis, and open-mouth breathing can be seen. Thoracic imaging,
bronchoscopy, and cytology of the BAL is needed for a definitive
diagnosis. Treatment depends on the severity of the clinical signs, but
long-term therapy should be expected.
■ Airway collapse. Dynamic reduction of the intraluminal diameter of the
airways, generally affecting small/toy-breed dogs. Clinical signs include
dry cough with retching, tachypnoea, and exercise intolerance. The
collapse can be localised or generalised associated or not with bronchial
collapse. The collapse can be congenital/familial or secondary. Diagnosis
can be challenging in some patients as radiography only identifies 60 %
of cases. Bronchoscopy and fluoroscopy are the techniques of choice and
allow grading. Treatment includes diet, client education, and drugs to
suppress the cough, dilate the airways, and reduce tracheal inflammation.
Surgical stent placement has been shown to decrease clinical signs and
improve the patient’s quality of life.
■ Tracheal foreign body. Uncommon disease that can result in acute or
chronic respiratory signs, ranging from partial to complete obstruction of
the airways. Plain radiographs can be normal or reveal the foreign body.
Most foreign bodies can be retrieved via bronchoscopy. The prognosis is
good if the material is removed without complications.
LUNG PATHOLOGIES
■ Lung mass. The most common masses affecting the pulmonary
parenchyma are neoplasms. Others include granulomas secondary to
mycosis, parasites, or foreign bodies; abscesses; cysts; and haematomas.
■ Gas-containing pulmonary lesions. These are mainly bullae and blebs,
although abscesses and cavitating neoplasms should also be considered.
They can rupture and cause spontaneous pneumothorax. Imaging
techniques are needed for diagnosis.
■ Lung emphysema. Congenital or acquired accumulation of air in the
alveoli. Congenital emphysema is a rare condition reported in young
dogs; predisposed breeds include Jack Russell Terrier, Old English
Sheepdog, Pekingese, Pomeranian, Shih Tzu, Pug, and West Highland
White Terrier. Obstruction of the developing airway will cause bronchial
collapse on expiration and progressive hyperinflation. Patients show
acute dyspnoea in the first 6 months of age. Diagnostic imaging
techniques (radiology, CT) are required for the diagnosis. The right
middle lung lobe is the most commonly affected, and treatment requires
lobectomy.
Any obstructive bronchial disease (e.g. asthma, foreign body) can lead to
dynamic airway collapse and air trapping, causing secondary lung
emphysema.
■ Lung lobe torsion. Rotation of a lung lobe along its longitudinal axis,
which collapses the pulmonary vein but not the artery. Blood
continuously enters the lobe, leading to congestion and pleural effusion
due to fluid accumulation. The most commonly affected lung lobes are
the left cranial lobe in small-breed dogs (chondrodystrophic) and the
right middle lobe in large, deep-chested dogs. Common clinical signs are
dyspnoea, tachypnoea, lethargy, and anorexia. Thoracic auscultation
demonstrates decreased ipsilateral lung sounds. Radiological,
ultrasonographic, and computed tomographic studies reveal a lobar sign
with a mixed alveolar/vesicular lung pattern. In some cases, obstruction
of the airway is seen on CT, providing a definitive diagnosis. Lobectomy
is the treatment of choice, and the prognosis after surgery is good.
■ Pneumonia. Inflammation/infection of the lungs and airways. Common
signs include cough, tachypnoea, fever, anorexia, weight loss, lethargy,
exercise intolerance, and nasal discharge; severity depends on the type of
pneumonia and on the amount of lung affected. The most frequent types
are:
■ Bacterial (most common type). Causes include Bordetella
bronchiseptica, Streptococcus zooepidemicus, Pasteurella multocida,
Escherichia coli, and Mycoplasma.
■ Aspiration pneumonia. Secondary to pulmonary intake of particles or
fluid. In case of aspiration of gastric contents, the damage is more
severe (chemical injury). Distribution is mostly ventral.
■ Secondary to inhaled foreign bodies.
■ Viral. Canine distemper, adenovirosis, and parainfluenza in dogs;
calicivirosis and infectious peritonitis in cats.
■ Fungal/mycotic (rare in Europe). The most common pathogens are
Aspergillus spp., Blastomyces dermatitidis, Candida spp.,
Coccidioides immitis, Cryptococcus neoformans, and Histoplasma
capsulatum.
■ Parasitic (depends on geographic location). Causes include
Toxoplasma gondii, Dirofilaria immitis, Angiostrongylus vasorum, and
Aelurostrongylus abstrusus.
■ Eosinophilic bronchopneumonia.
■ Interstitial pneumonia.
Diagnosis includes history, clinical examination findings, thoracic
imaging, bronchoscopy, and BAL fluid cytology. Treatment and
prognosis depend on the type of pneumonia.
■ Interstitial fibrosis. Chronic, progressive interstitial lung disease most
commonly reported in Terriers. Clinical signs include coughing, exercise
intolerance, and tachypnoea. The presumptive diagnosis is based on the
signalment and clinical and imaging findings.
■ Pulmonary haemorrhage. Blood accumulation in the lung and airways.
Causes include trauma, coagulopathies (e.g. rodenticide toxicity),
thrombocytopenia, neoplasia, parasites, leptospirosis, pulmonary
thromboembolism, and acute respiratory distress syndrome. Clinical
signs vary depending on the extent of the bleeding, but include
tachypnoea, dyspnoea, spontaneous coughing, haemoptysis, crackles,
cyanosis, and diminished lung sounds. Treatment involves supportive
and symptomatic therapy and addressing the underlying cause.
■ Pulmonary contusion. Lung damage secondary to blunt thoracic
trauma. The alveoli fill up with fluid and blood, causing secondary
inflammation. It occurs in 40–50 % of cases of chest injury, mainly
secondary to road traffic accidents, and it is usually associated to other
changes. Clinical signs vary depending on the severity of the injury.
■ Pulmonary oedema. Accumulation of fluid in the lung parenchyma and
airways. It is divided in:
■ Cardiogenic. Increased pulmonary capillary hydrostatic pressure
secondary to cardiac disease. There are multiple causes, the most
common being degenerative mitral valve disease and dilated
cardiomyopathy. Radiology and echocardiography are needed to
confirm the diagnosis.
■ Noncardiogenic. Low alveolar pressure and increased vascular
permeability and hydrostatic pressure. Multiple underlying diseases
have been associated with this oedema, including neurogenic, acute
respiratory distress syndrome, vasculitis, and trauma. The patient’s
history and physical examination is crucial for the diagnosis.
■ Neoplasia.
■ Primary. Epithelial neoplasms are the most common. They tend to be
solitary masses, cavitated/mineralised, localised in the periphery of the
caudal lung lobes. Metastases to the rest of the lung, regional lymph
nodes, pleura, abdominal organs, or bones can occur. Histiocytic
sarcomas are typical of the Bernese Mountain Dog and Rottweiler.
They are solitary masses, most commonly located on the ventral
aspect of the right middle lung lobe, with a high incidence of spread to
the regional lymph nodes; concurrent pleural effusion is common.
Lymphoma can infiltrate the lung (interstitial pattern) as a primary or
secondary tumour and is associated with lymph node enlargement.
■ Secondary/metastatic. Neoplastic lung infiltration secondary to any
neoplastic process. Imaging techniques are needed for the diagnosis. A
nodular/miliary pattern is usually present in dogs, while poorly
marginated nodules are more common in cats.
Staging and sampling from lesions are needed to achieve a definitive

diagnosis and identify the best treatment choice and prognosis.
CASE 22. FELINE ASTHMA
SIGNALMENT
Age: 6 years old
Presenting complaint: Two-month history of dyspnoea and laboured
breathing that has deteriorated over the last week. No improvement on
antibiotics was noted
The cat was bright, alert, and responsive on presentation at the veterinary
hospital. She showed an increased respiratory rate (40 breaths per minute)
and intermittent open mouth breathing. Thoracic auscultation revealed no
cardiac murmurs, but pulmonary wheezes were noted. Abdominal palpation
and body temperature were normal.
Thoracic radiographs were taken by the referring veterinary surgeon and
reviewed at the time of presentation. They showed a moderate to marked
diffuse thickening of the bronchial walls, with presence of tramlines and
doughnuts, and secondary flattening of the diaphragm suggesting
hyperinflation of the lungs (Figs. 1 and 2).
A diffuse bronchial pattern is the most common radiographic sign found
in cats with feline asthma.
FIGURE 1. Right lateral (a) and left lateral (b) projections of the chest showing flattening of the
diaphragm (arrows) and a marked diffuse bronchial pattern.
FIGURE 2. Closer image from Figure 1b, showing multiple tramlines and doughnuts (arrows).
COMPUTED TOMOGRAPHY
A CT scan was performed under general anaesthesia to try to identify
possible subtle lesions not seen on the radiographs (Fig. 3). It confirmed the
presence of diffuse thickening of the bronchial walls with a moderate
amount of hyperattenuating material in the lumen of some of the bronchi
(Fig. 4).
FIGURE 3. Image of the anaesthetised patient positioned in the CT scan.
FIGURE 4. Transverse CT image of the chest in lung window, showing moderate generalised
thickened bronchial walls (arrowheads).
BRONCHOSCOPY AND BRONCHOALVEOLAR

LAVAGE
Bronchoscopy and bronchoalveolar lavage (BAL) were performed under
the same anaesthesia. Cytological examination of the BAL fluid showed a
mixed degenerate cell population, with some epithelial cells and a mixed
inflammatory population including mainly eosinophils and some
neutrophils (Fig. 5).
PCR testing was negative for Mycoplasma but revealed growth of
Staphylococcus.
A diagnosis of feline asthma was done based on the clinical, imaging,
and cytological findings.
FIGURE 5. Cytological image of the material from the bronchial lumen (500×). There is a large
amount of eosinophils (arrows), some neutrophils, and macrophages. Image courtesy of Tim
Williams.
TREATMENT
A short course of prednisolone (5 mg every 24 h) was started for 10 days in
addition to inhalers (beclometasone 10 µg every 12 h, salbutamol 100 µg
every 12 h) and amoxicillin–clavulanic acid (50 mg every 12 h) for 6 days.
The dose of steroids was tapered over 2 months. The owners reported
marked improvement in the cat’s clinical signs a month after the start of the
treatment.
DISCUSSION
Inflammatory airway disease is common in cats and affects approximately
1–5 % of the feline population. This group of inflammatory diseases is
characterised by chronic inflammation of the lower airways (bronchi and
bronchioles) and is first observed both in young and middle-aged cats. This
group includes two conditions: feline asthma and feline chronic bronchitis.
These two entities are often very difficult to differentiate. Both diseases
can cause similar clinical signs, but asthma can also be associated with
substantial acute mortality if the condition goes undiagnosed and not treated
promptly.
Chronic bronchitis tends to cause a more persistent and daily cough,
whilst asthma signs are mainly derived from acute bronchoconstriction with
limitation of the airflow due to a combination of inflammation, mucus
accumulation, and contraction of the airway smooth muscle, although daily
cough can also happen.
Like human asthma, feline asthma is an allergic condition where
exposure to inhaled aeroallergens causes inflammation of the airways and
smooth muscle contraction with secondary narrowing of the airways.
Middle-aged to older cats are predisposed. However, many cats have
history of chronic signs before being diagnosed and therefore it is likely
that the onset of the clinical signs occurs much earlier in life than thought.
There is no sex predisposition for the disease and Siamese cats seem to be
at higher risk of developing the disease. There are two main clinical
presentations: it can be very dramatic and sometimes life-threatening in
cases of an asthmatic crisis, with open mouth breathing, tachypnoea, and
increased respiratory effort, or it can be more chronic with an insidious
history of cough and lethargy.
The diagnosis is usually a diagnosis of exclusion based on the
combination of clinical history, physical examination findings, diagnostic
tests, and response to treatment. Therefore, although it is a common and
important disease, its diagnosis is often challenging. The major differential
diagnoses are chronic bronchitis, bacterial or parasitic bronchopneumonia
(e.g. Aelurostrongylus abstrusus), inhaled foreign body, and neoplasia.
Treatment includes mainly a combination of corticosteroids and

bronchodilators.
Thoracic radiographs and CT scans usually demonstrate a diffuse

bronchial or bronchointerstitial lung pattern as described in this case, with
areas of increased density within the bronchial lumen due to mucus
accumulation. Areas of atelectasis, mainly in the right middle lobe, can
sometimes be seen as well as signs of lung hyperinflation such as caudal
displacement of the diaphragm, suggesting air trapping. In chronic cases,
bronchiectasis, or even pneumothorax due to airway rupture, can also be
observed (Fig. 6). However, thoracic radiographs can be normal in up to 23
% of the cases with feline asthma.
Normal thoracic radiographs do not rule out feline asthma.

FIGURE 6. Thoracic radiographs (lateral [a] and dorsoventral [b] projections) of a different cat with
feline asthma (diffuse marked bronchial pattern) and secondary moderate bilateral pneumothorax
(delineated with arrows) producing retraction of the lung parenchyma.
In general, performing inflated radiographs should be avoided in those

cases where feline asthma is a possible differential due to the increased risk
of pneumothorax. Thus, other imaging techniques, such as CT scan, can be
performed to further characterise lung changes, as the authors did in this
case.
Bronchoscopy is used to visualise the airway as well as to take samples.
Changes include mucus accumulation, hyperaemia, and airway collapse.
BAL fluid examination usually reveals eosinophilic inflammation (>17 %
eosinophils), contrary to cases of chronic bronchitis, which show
neutrophilic inflammation. It is highly recommended to always culture the
samples as Mycoplasma spp. is a common opportunistic pathogen in these
cases (25 %).
Treatment is usually multifactorial, including environmental changes and
drug therapy. In emergency cases, some anxious and stressed cats may
benefit from mild sedation with acepromazine as well as oxygen therapy.
Traditional medical management of chronic airway disease, including
asthma and chronic bronchitis, includes lifelong bronchodilators and
corticosteroids to treat mainly the underlying chronic inflammation that
causes the acute clinical signs. Corticosteroids can be given orally or
through inhalation. Bronchodilators (terbutaline, metilxantines, and
anticholinergics) are very important in the acute phases of the disease to
reduce bronchoconstriction. Effectiveness of the treatment is based on the
observation of reduction in clinical signs. Patients should be re-evaluated
every 3–6 months to monitor treatment effect, progression of the disease,
and possible side effects.
Unfortunately, some cats are refractory to treatment and side effects are
common. Therefore, several new experimental therapies such as allergen-
specific immunotherapy, omega-3 fatty acids/nutraceuticals, inhaled
lidocaine, or tyrosine kinase inhibitors (TKIs) have been tried over the past
years.
CASE 23. BRONCHIAL
FOREIGN BODY
SIGNALMENT
Age: 4 years old
Sex: Male, neutered
Presenting complaint: Acute onset retching cough following off-lead
exercise in a field
The dog was bright, alert, and responsive on presentation at a referral
hospital. No abnormalities were detected on clinical examination. He
showed normal thoracic auscultation and abdominal palpation as well as
normal rectal temperature (37.4 °C). Intermittent cough was noticed during
the consultation.
Bronchial foreign bodies are common causes of cough in working dogs.

Caudodorsal localisation is the most frequently seen.
The complete blood cell count and biochemical profile were within
reference intervals.
Dorsoventral and lateral projections of the thorax taken by the primary
referring veterinary surgeon under general anaesthesia revealed a
generalised bronchointerstitial pattern, with a focal area of increased
opacity in the left caudodorsal lung field (Fig. 1). The remainder of the
thoracic structures, including intra- and extrathoracic structures, were
considered normal.
The clinical history and radiographic changes were strongly suspicious of
a focal pneumonia, likely secondary to an aspirated foreign body. A CT
scan was performed to identify the exact location of the possible foreign
material, to localise further pathologies, and to assess the remainder of the
pulmonary parenchyma.
FIGURE 1. Right lateral (a) and dorsoventral (b) projections of the patient showing a focal increased
opacity (focal pneumonia) in the left caudodorsal lung field (circle).
COMPUTED TOMOGRAPHY
The CT scan was performed under general anaesthesia with the patient in
sternal recumbency. A generalised increase in attenuation of the left caudal
lung field was present, mainly owing to thickening of the bronchial walls.
The left caudal bronchus was markedly dilated, up to 17 mm in diameter. A
large intraluminal foreign body of heterogeneous attenuation was
confirmed, almost completely obliterating the lumen and measuring
approximately 4 cm in length (Fig. 2).
Thoracic radiographs in cases with bronchial foreign bodies can be
normal or reveal changes compatible with focal pneumonia. CT can
identify the intraluminal foreign body.
FIGURE 2. Transverse (a), dorsal (b), and sagittal (c) CT images of the chest in lung window
showing a marked dilation of the left caudal main bronchus with an intraluminal foreign body
(arrows). Note the generalised bronchial thickening and the patchy interstitial appearance of the left
caudal lobe.
BRONCHOSCOPY
Bronchoscopy was performed under the same anaesthetic procedure (Fig.
3). It showed moderate inflammation and erythema of the bronchial
mucosa. It also localised the intraluminal foreign body, surrounded by
mucus and suspected purulent exudate (Fig. 4). Forceps retrieval of the
organic material (an awn of wheat) was performed without complications
(Fig. 5) and a sample of the surrounding discharge was taken for
bacteriology, including culture and sensitivity testing.
FIGURE 3. Image of the anesthetised patient during the bronchoscopy.

FIGURE 4. Bronchoscopic image of the left caudal bronchus with the intraluminal foreign body
(plant) surrounded by white mucus/pus.
FIGURE 5. Image of the foreign body (awn of wheat) after removal.
TREATMENT
After the bronchoscopic removal of the foreign body, the patient recovered
well from the anaesthesia and was prescribed a broad-spectrum antibiotic
(amoxicillin–clavulanic acid at 12.5 mg/kg PO every 12 h). He was
discharged from the hospital 24 hours after the presentation.
Bacterial culture of the bronchial exudate revealed a mixed aerobic
growth of microorganisms Staphylococcus spp. and Streptococcus spp.,
which proved sensitive to the current antibiotic therapy. A two-week course
of medication was completed.
Complete resolution of the clinical signs was obtained 3 days after
removal of the foreign body and no relapse was identified following
cessation of antimicrobials.
DISCUSSION
Coughing is a clinical sign that localises disease to the large or small
airways. The most common causes can be grouped according to anatomic
location of the possible pathology as follows:
■ Upper respiratory tract diseases involving lesions of the nasopharynx,
pharynx, larynx, and trachea:
■ inflammation/infection (e.g. infectious tracheobronchitis)
■ pharyngeal or tracheal foreign bodies
■ neoplasia of the pharynx, larynx, or trachea (e.g. lymphoma,
carcinoma)
■ laryngeal paralysis
■ tracheal collapse
■ Lower respiratory tract diseases involving the bronchi beyond the carina:
■ bronchopneumonia (e.g. aspiration pneumonia, bacterial infection,
fungal diseases)
■ extraluminal compression (e.g. neoplasia of large dimensions
[pulmonary, oesophageal, lymph node], severe left atrial dilation)
■ intraluminal obstruction (e.g. bronchial foreign body)
■ dynamic airway disease (e.g. bronchial collapse, “bronchomalacia”)
■ immune-mediated diseases (e.g. eosinophilic bronchopneumopathy)
■ pulmonary haemorrhage (e.g. contusions after trauma, rodenticide
intoxication)
■ severe pulmonary oedema: cardiogenic (fulminant left-sided heart
failure) vs. noncardiogenic (e.g. traumatic brain injury, electrocution,
systemic inflammatory response syndrome)
■ Other: cases of cough associated with pericardial disease and some
pleural diseases are reported, but the pathophysiology in small animals is
unclear.
In this case, cough was likely to be caused by large bronchial obstruction,

inflammation, and exudation triggering cough receptors. Bronchial foreign
bodies are a very common finding in general practice, mainly seen in dogs
exercised in fields or woodland, or in working dogs. Nonorganic foreign
bodies are also reported but rare.
Inhalation usually occurs via the nares or mouth, and the path of least
resistance carries the object to the right caudal lung lobe, but other airways
can be affected, as in this case. Usually, clinical history is suggestive of the
diagnosis, but imaging is vital for confirmation and localisation. In most
cases, only the secondary reaction around the affected bronchus can be seen
on radiography. Changes detected are usually a focal region of interstitial or
alveolar infiltrates, consistent with focal pneumonia. Occasionally,
pneumothorax is detected because of penetration of the lung by the foreign
body. Migration of the foreign body into the pleural space causing
pyothorax is also possible. In such cases, or where minimally invasive
bronchoscopic extraction is not possible, a thoracotomy should be
performed to facilitate the removal of the foreign body and a possible lung
lobectomy.
CT is much more sensitive than radiography in visualisation of a
bronchial foreign body. It also allows for a better description of secondary
changes, including bronchiectasis, pneumonia, or pleural effusion in more
severe or chronic cases. CT is also highly recommended to evaluate the
whole thoracic cavity in cases with suspected perforating foreign body plus
pneumothorax and/or pyothorax. It can help identify any possible
intraluminal foreign body-related abscesses/granulomas, which are
generally located in the pleura, thoracic wall, insertion of the diaphragmatic
crura, or sublumbar musculature.
Most dogs with a bronchial foreign body are treated with broad-spectrum
antibiotics even after extraction because of a high likelihood of bacterial
infection; bacteria can be introduced at the time of inhalation or secondary
to mucus production and inflammation. Ideally, antibiotic therapy should be
based on the results of bacterial culture and sensitivity testing, although
often patients have been pretreated with antibiotics and a negative culture
may be obtained.
CASE 24. ASPIRATION
PNEUMONIA
SIGNALMENT
Breed: Crossbred dog
Age: 2 years old
Presenting complaint: Lethargy, dyspnoea, and fever. Previous history of
aspiration pneumonia
The dog was presented to the veterinary hospital with a history of lethargy
and unwillingness to move. She was bright, alert, and responsive. She
showed tachypnoea (65 breaths per minute) and a normal heart rate. The
mucous membranes were pale, with a prolonged capillary refill time (3
seconds). Thoracic auscultation revealed decreased lung sounds and
crackles on the ventral aspects of the thorax. Abdominal palpation was
unremarkable. Her body temperature was 39.8 °C.
A complete blood cell count and biochemistry profile revealed a mild
increase in alkaline phosphatase levels and a normal blood cell count. The
urinalysis was unremarkable.
The thoracic radiographs taken 2 days before referral were reviewed at the
time of presentation and revealed moderate bilateral changes localised on
the ventral aspects of the lung lobes, with presence of air bronchograms
consistent with an alveolar pattern (Fig. 1). These changes were consistent
with aspiration pneumonia.
The ventral aspects of the cranial lung lobes are the most commonly
affected in cases of aspiration pneumonia.
FIGURE 1. Right lateral (a) and dorsoventral (b) radiographs of the thorax showing an alveolar lung
pattern in the cranioventral lung fields, which appears bilateral in the dorsoventral projection.
COMPUTED TOMOGRAPHY
A CT scan of the thorax was performed under anaesthesia to try to identify
a possible aetiology for the recurrent pneumonia. It revealed marked
bilateral changes localised in the ventral aspects of the cranial lung lobes
with consolidation of the affected lobes and the presence of air
bronchograms (Fig. 2), similar to those found in the radiographs.
FIGURE 2. Transverse CT images of the chest in lung window showing a bilateral alveolar infiltrate
in the dependent (ventral) aspects of the lung lobes with the presence of air bronchograms (arrow).
BRONCHOALVEOLAR LAVAGE
A bronchoalveolar lavage was performed after the CT scan and the samples
were sent to the laboratory for culture. The results revealed a mixed
infection with E. coli and Streptococcus spp.
TREATMENT
The patient was hospitalised with intravenous fluid therapy, broad-spectrum
antibiotics (amoxicillin–clavulanic acid, 12.5 mg/kg every 12 h, and
enrofloxacin, 5 mg/kg every 24 h), nebulisation, and coupage. She
improved dramatically in the following 3 days and was then discharged
from the hospital.
At follow-up a week after discharge, the patient only showed a mild
residual cough. Radiographs were repeated and showed that the lung
infiltration had decreased. The antibiotic therapy was continued for 3 more
weeks, after which the patient was reported to be back to normal by the
referring veterinary surgeon. Radiographs at that moment revealed
complete resolution of the previously present lung changes.
DISCUSSION
Aspiration pneumonia is a pulmonary infection caused by the inhalation of
abnormal irritant material, usually gastric or oropharyngeal in origin.
Damage to the lungs may result from exposure to gastric fluid with a pH
below 2.5 or containing colloidal antacid compounds, to large particulate
matter, or if a volume greater than 0.3–0.4 ml/kg is aspirated.
Aspiration pneumonia is a common disease in dogs.
Generally, aspiration pneumonia occurs in three phases:

■ Immediately after aspiration, the accumulation of irritants in the
pulmonary tissue causes necrosis, bronchoconstriction, haemorrhage, and
ultimately oedema and atelectasis.
■ The second phase (inflammatory phase), which occurs 4–6 hours after
aspiration, is characterised by infiltration of neutrophils into the alveoli
and interstitium. These two first phases constitute aspiration
pneumonitis.
■ The third phase involves bacterial colonisation of the airways and
pulmonary parenchyma.
In most cases, a single underlying cause or concurrent disease is present.

These include oesophageal dysfunction (e.g. megaoesophagus, motility
disorders, hiatal hernia), vomiting, neurological diseases (e.g. seizures,
spinal cord disease), laryngeal dysfunction (e.g. paralysis, foreign body,
previous surgeries), recent sedation/anaesthesia (5–26 %), myasthenia
gravis, or iatrogenic causes. Many of these predisposing factors occur in
hospitalised animals (Fig. 3).
The diagnosis of aspiration pneumonia can be suspected when a previous
aspiration has been reported, when gastric contents are detected in the
airways, or when acute respiratory distress develops approximately a few
hours after vomiting, regurgitation, or anaesthesia. The clinical history is
therefore very important in these cases.
Clinical signs, generally respiratory, include tachypnoea, cough,
dyspnoea, anorexia, lethargy, vomiting, and regurgitation (Fig. 4). Physical
examination usually reveals an increased respiratory rate, hyperthermia,
some degree of hypoxia, and increased bronchovesicular sounds.
Thoracic imaging, including radiography and CT, is very useful to
confirm the diagnosis. An alveolar pattern, with presence of air
bronchograms, in the ventral aspects of the lung lobes is the most common
finding. The right middle and left and right cranial lobes are typically
affected. However, mixed lung patterns can also occur and, although rarely,
normal radiographs have also been reported in some cases of aspiration
pneumonia. In very ill patients or in those with a clinical suspicion of
megaoesophagus a horizontal beam radiograph can be performed (Fig. 5).
Differential diagnoses of consolidated lung lobes include aspiration or
bacterial pneumonia, haemorrhage, neoplasia, lung lobe torsion, and
granulomatous disease.
The identification and correction of the possible predisposing factors is

important to achieve a good resolution of the clinical signs.
FIGURE 3. Left lateral radiograph of a dog with generalised megaoesophagus (arrowheads),

showing an alveolar pattern and the presence of air bronchograms in the right middle lobe (circle).
These findings are consistent with aspiration pneumonia.
FIGURE 4. Image of a dog that has regurgitated under anaesthesia.
FIGURE 5. Horizontal beam radiographs of a patient with congenital megaoesophagus (arrowheads)
taken at different moments showing the development of aspiration pneumonia. No signs of
pneumonia can be seen in the first image (a). In the second image (b), there is an ill-defined
interstitial–alveolar pattern in the ventral aspects of the right middle lobe (circle). The third image (c)
shows moderate pneumothorax (cross), and a marked ventral alveolar lung pattern consistent with
severe aspiration pneumonia.
Definitive diagnosis of aspiration pneumonia is based on the culture of

exudate from the pulmonary airways. Therefore, it is strongly
recommended to perform a tracheal wash or a bronchoalveolar lavage and
culture the material obtained. Generally, dogs with aspiration pneumonia
are positive to E. coli, Pasteurella spp., Klebsiella spp., Staphylococcus
spp., Streptococcus spp., and Mycoplasma spp.
Early clinical recognition allows appropriate treatment of the airway
injury and of any underlying pathological process. Treatment depends on
the degree of aspiration, but generally includes oxygen therapy, intravenous
fluid therapy, long-term (4–6 weeks) antimicrobial combinations
(ampicillin, enrofloxacin, marbofloxacin, doxycycline, and clindamycin),
nebulisation of sterile saline (to improve mucociliary clearance) and
coupage (to promote airway clearance), and any specific medication of the
cause.
Long-term broad-spectrum antibiotic therapy is needed in most cases.
Aspiration pneumonia can be a serious and potentially life-threatening

inflammatory lung process if not diagnosed appropriately. The prognosis
depends on the cause and amount of lung lobes affected, but overall it is
good if no underlying pathology, such as megaoesophagus, is present. A
survival rate of 77 % has been reported in dogs with aspiration pneumonia.
A quick and effective medical management helps in the recovery. The
presence of more than one affected lung lobe has been identified as a poor
prognostic indicator.
CASE 25. EOSINOPHILIC
BRONCHOPNEUMOPATHY
SIGNALMENT
Breed: Staffordshire Bull Terrier
Presenting complaint: History of retching, productive cough, and ongoing
lethargy. Intermittent nasal discharge was also reported
The dog was lethargic but responsive on presentation (Fig. 1). Her general
condition was good. Cardiac auscultation was normal, but pulmonary
auscultation revealed increased lung sounds. The patient’s body temperature
was within normal limits.
FIGURE 1. Image of the patient on presentation.
A complete blood cell count revealed leucocytosis (25,000 cells/μl) with
neutrophilia (31,756 cells/μl). The other parameters and the biochemistry
profile were unremarkable.
Thoracic radiographs were taken under mild sedation (butorphanol 0.2
mg/kg IV) and revealed severe diffuse changes. A generalised mixed
bronchointerstitial lung pattern, with almost a nodular appearance in some
areas, was present. A focal alveolar pattern in the left caudal lung lobe with
the presence of air bronchograms and a pleural line were also noted (Fig. 2).
FIGURE 2. Dorsoventral (a) and right lateral (b) radiographs of the chest showing marked diffuse
lung changes with air bronchograms in the left caudal lobe.

LAVAGE
Bronchoscopy was performed under general anaesthesia and revealed a
moderate amount of mucopurulent material (yellow-green secretions),
hyperaemia of the mucosa, and thickening of the bronchial walls.
The cytological examination of the bronchoalveolar lavage (BAL) fluid
showed a predominance of eosinophils (89 %) and a lower number of
nondegenerative neutrophils (7 %), lymphocytes (3 %), and large
vacuolated macrophages (1 %). These findings were consistent with
moderate eosinophilic inflammation (Fig. 3).
Culture of the BAL fluid was negative for aerobic microorganisms
(Bordetella spp. and Mycobacterium spp.) after 48 hours. A faecal
Baermann test was performed and was negative; no Angiostrongylus
vasorum larvae were seen.
The final diagnosis was eosinophilic bronchopneumopathy (EBN).
FIGURE 3. Cytological image of the bronchoalveolar lavage fluid showing a large amount of
eosinophils.
TREATMENT
Medical management was started with oral prednisolone (1 mg/kg every 12
h) for the first week. The patient improved dramatically within the first 3
days and therefore the dose of corticosteroids was reduced during the
second week to an alternate-day regimen (1 mg/kg every 48 h). She
continued to improve and had only mild cough after the third week. The
medication was decreased to maintenance levels (0.5 mg/kg every 3 days).
At follow-up 2 months after the treatment was initiated, the patient showed
no clinical signs. Thoracic radiographs were repeated and revealed only a
mild bronchointerstitial lung pattern.
Corticosteroid therapy is the treatment of choice for eosinophilic
bronchopneumopathy.
DISCUSSION
Canine EBP, formerly known as pulmonary infiltrate with eosinophils or
pulmonary eosinophilia, is characterised by eosinophilic infiltration of the
pulmonary interstitium and bronchial mucosa. It is thought to be an
immunological hypersensitivity reaction due to persistent antigenic
exposure, which results in chronic irritation and inflammation of the
respiratory mucosa.
This disease is most commonly seen in young adults (4–6 years), and
females have a higher prevalence. Some dog breeds, such as the Alaskan
Malamute and Siberian Husky, seem to be predisposed to this disease,
although it has also been reported in other large- and small-breed dogs.
The severity of EBP can vary from mild to severe. The main clinical sign
is cough (95–100 % of affected dogs), which is generally harsh and
persistent and is normally followed by gagging and retching. Other signs
include dyspnoea, tachypnoea, anorexia, lethargy, exercise intolerance, and
nasal discharge. Peripheral blood eosinophilia is common in these patients.
Eosinophilic bronchopneumopathy is an important differential diagnosis

in young dogs with cough.
Thoracic imaging is needed to rule out other diseases that could explain
the clinical signs. Although radiographic changes in EBP are usually
nonspecific, a mixed diffuse bronchointerstitial lung pattern can frequently
be seen (Fig. 4). In more severe and chronic cases, these changes can
include an alveolar pattern (up to 40 % of cases), bronchiectasis, pulmonary
nodules, and intrathoracic lymphadenopathy. Computed tomography mainly
shows generalised or multifocal areas of ground-glass pattern or
consolidation, with bronchial wall thickening or bronchiectasis in advanced
cases. Although most of the times these imaging changes can be identified
in patients with EBP, normal radiographs or CT scans of the chest do not
rule out the diagnosis of the disease and therefore a clinical history and a
BAL are always needed. In fact, imaging changes have been shown to
correlate with total cell and eosinophil counts in the BAL fluid of affected
dogs, but not with eosinophil counts in the blood.
Changes in thoracic imaging are nonspecific but generally consist of a

diffuse bronchointerstitial pattern.
FIGURE 4. Thoracic radiographs (dorsoventral [a] and right lateral [b] projections) of a different
dog with eosinophilic bronchopneumopathy showing only a mild diffuse bronchointerstitial pattern.
Chronic allergic bronchitis, primary parasitic lung disease

(Angiostrongylus vasorum), bacterial or fungal bronchopneumonia, and
diffuse neoplastic infiltration (lymphoma) should be included in the
differential diagnoses of EBP. However, the main diseases that can cause an
eosinophilic infiltration in the lungs are eosinophilic pulmonary
granulomatosis and lungworm infection. Eosinophilic granulomatosis,
which is thought to be a progressive form of EBP, is very uncommon and
causes very severe clinical signs; most of the cases present with pulmonary
masses that can be detected by thoracic radiography.
The definitive diagnosis is based on the BAL, which can also rule out or
confirm concomitant diseases such as parasitosis (lungworms, heartworms),
bacterial infection, or even neoplasia. Cases of EBP are characterised by an
increase in the number of eosinophils and neutrophils in the BAL fluid.
The response to steroid treatment (methylprednisolone) is generally good
and quick, with marked improvement in the clinical signs within the first 3–
5 days. Thoracic radiographs are used to assess the progression of the
disease and the response to the treatment.
The prognosis is generally good, although complete resolution of the
clinical signs is rare and most patients have a mild residual cough after
exercise. Relapse of the signs occurs in 30–70 % of patients, weeks or
months after interruption of the treatment. In these cases, lifetime treatment
at a lower dose is needed to control the clinical signs, with a maintenance
prednisolone dose of 0.25–0.5 mg/kg every 48 h. Unfortunately, this can
cause clinical iatrogenic hyperadrenocorticism.
Complete resolution of the clinical signs is uncommon.

CASE 26. IDIOPATHIC
PULMONARY FIBROSIS
SIGNALMENT
Breed: West Highland White Terrier
Age: 9 years old
Sex: Male, neutered
Presenting complaint: Six-month history of cough and reduced exercise
tolerance
The dog was bright, alert, and responsive on presentation at the referral
hospital (Fig. 1). His body weight was 10 kg and his body condition score
was 4/5. The mucous membranes were pink and moist, with a normal
capillary refill time. The peripheral pulses were firm and synchronous with
his heartbeat. Thoracic auscultation revealed marked generalised lung
crackles and a grade II/VI right-sided apical systolic heart murmur. The
patient’s heart rate was 120 bpm, with a regular cardiac rhythm. Abdominal
palpation was unremarkable, and his body temperature was within normal
limits.
ECHOCARDIOGRAPHY
Doppler echocardiography showed marked concentric hypertrophy of the
right ventricle, with flattening of the interventricular septum in systole and
a severely dilated right atrium (Fig. 2). Marked tricuspid regurgitation at an
elevated velocity of 5.6 m/s, which corresponded with a pressure gradient
of 120 mmHg (reference <25 mmHg), was present and was consistent with
severe pulmonary hypertension (Fig. 3). The left ventricle appeared
subjectively underfilled. The left ventricular systolic and diastolic functions
were adequate, and the left atrium was not dilated (left atrium-to-aortic root
ratio of 1.4, reference <1.5).
FIGURE 2. Echocardiographic right parasternal short-axis view of the left ventricle (LV) and right
ventricle (RV), showing marked right ventricular dilation and hypertrophy of the RV wall. IVS,
interventricular septum.
FIGURE 3. Echocardiographic left parasternal view of the heart, showing marked tricuspid
regurgitation (5.6 m/s) filling the right atrium (RA). LV, left ventricle; RV, right ventricle.
Thoracic radiographs were taken under sedation and revealed a moderate
generalised bronchointerstitial lung pattern. The right heart was noticeably
enlarged, and cardiac sternal contact was increased. Moderate
hepatomegaly was also noted in the cranial aspect of the abdomen (Fig. 4).
FIGURE 4. Right lateral (a), left lateral (b), and dorsoventral (c) radiographs of the chest showing a
moderate bronchointerstitial lung pattern. Moderate hepatomegaly can also be seen.
COMPUTED TOMOGRAPHY
A CT scan was performed under general anaesthesia to identify any other
pulmonary changes not seen on the radiographs. It revealed diffuse ground-
glass infiltration due to an interstitial pathology, and pleural bands. Marked
dilation of the pulmonary arteries in comparison to the veins was also noted
(Fig. 5).
Although not a common disease, idiopathic pulmonary fibrosis should be

considered in all dogs with chronic dyspnoea and interstitial pulmonary
changes in thoracic imaging.
FIGURE 5. Transverse CT images of the chest in lung window (at the level of the carina [a] and
caudal vena cava [CVC] [b]), showing a moderate increase in pulmonary parenchyma attenuation
due to a bronchointerstitial infiltrate. Note the larger size of the pulmonary arteries (arrow) in
comparison to the pulmonary veins (arrowhead).

LAVAGE
The bronchoscopic examination showed white nodular thickening and
generalised pallor of the airways, consistent with generalised fibrosis. No
erythema due to inflammation was visualised or suspected. Bronchoalveolar
lavage (BAL) fluid was obtained and submitted for cytological examination
and culture. A mixed neutrophilic eosinophilic bronchitis was detected, but
there was no underlying bacterial or fungal growth.
Based on the results of the tests performed, the most likely diagnosis was
idiopathic pulmonary fibrosis (IPF).
TREATMENT
The patient recovered from the anaesthesia uneventfully and was
discharged with sildenafil (2 mg/kg every 8 h), beclometasone (1 puff every
12 h), and salbutamol (2 puffs every 6–24 h as needed) for bronchospasm
relief.
Follow-up of the patient 4 weeks after the start of the treatment revealed
an improvement in the clinical signs. Unfortunately, follow-up was lost 3
months after the initial presentation.
DISCUSSION
Canine IPF, also known as canine interstitial pulmonary fibrosis, Westie
lung disease, or chronic diffuse infiltrative lung disease, is characterised by
inflammation and fibrosis of the pulmonary interstitium and peripheral
airspaces, causing impairment of gas exchange. It forms part of a group of
rare interstitial lung diseases (ILDs), which are noninfectious, nonmalignant
respiratory disorders, including eosinophilic pneumonia, bronchiolitis,
interstitial pneumonitis, and alveolar proteinosis, among others.
Although the aetiology of IPF is unknown, several factors are thought to
be involved, such as underlying connective diseases or prior acute lung
injury. It is more prevalent in West Highland White Terrier dogs and other
Terrier breeds, but it has also been reported in other small-breed dogs and in
cats. Middle-aged to older animals are most frequently affected, and no sex
predisposition has been reported.
Idiopathic pulmonary fibrosis is common in West Highland White Terrier

dogs.
The initial clinical signs of IPF are so subtle that many owners may think
they are normal aging changes. As the disease progresses, affected dogs
show exercise intolerance, chronic cough, increased respiratory rate, and
respiratory distress. Later in the disease process, dyspnoea even at rest and
collapsing episodes might be reported. Physical examination reveals
tachypnoea, inspiratory crackles, and abdominal breathing.
In many cases, pulmonary hypertension develops as a consequence of
pulmonary fibrosis. A right-sided systolic heart murmur is usually (but not
always) present in these patients, and pulmonary hypertension can lead to
right-sided congestive heart failure in severe cases. Diagnosis of pulmonary
hypertension is best made using Doppler interrogation of tricuspid
regurgitation if present; a velocity greater than 3 m/s suggests pulmonary
hypertension so long as no pulmonic stenosis is present. In dogs with little
or no tricuspid regurgitation, changes to 2D echocardiography and the
presence of right ventricular dysfunction may raise the index of suspicion
for pulmonary hypertension.
Thoracic imaging helps in the diagnosis and rules out other possible
diseases. Radiographs usually reveal a diffuse, moderate to severe
bronchointerstitial lung pattern. In advanced cases, bronchiectasis can also
be identified. If secondary pulmonary hypertension is present, right-sided
cardiomegaly (reverse D-shaped heart), pulmonary arterial enlargement,
and hepatomegaly can be seen. CT is more sensitive to evaluate lung
changes compared to radiography. It generally shows ground-glass opacity,
subpleural lines, subpleural interstitial thickening, bronchiectasis, and
honeycombing, with a predilection for the dorsocaudal lung lobes. The CT
appearance has been shown to correlate with the clinical signs.
Diffuse, interstitial or bronchointerstitial lung changes can be seen in

thoracic imaging.
Bronchoscopic findings in cases of IPF are not specific and may include
tracheal collapse, irregular bronchial mucosa, bronchomalacia, and
bronchiectasis. The BAL fluid generally shows an increase in the cellular
count (macrophages, neutrophils, and mast cells).
A definitive antemortem diagnosis is difficult to make due to the absence
of highly sensitive and specific tests, and histopathological confirmation is
needed. Diagnosis is therefore one of exclusion and based on a thorough
clinical history and physical examination, imaging tests, and
bronchoalveolar lavage findings. The differential diagnoses should include
chronic bronchitis, left-sided heart failure, pulmonary neoplasia such as
lymphoma, and bacterial or parasitic infection.
Since no curative treatment is available, palliation is the primary goal.
Medical treatment using oral or inhaled corticosteroids may elicit a positive
response in some cases. In addition, bronchodilator drugs can help in dogs
with concurrent airway disorders. Sildenafil, a phosphodiesterase 5
inhibitor, provides pulmonary-specific vasodilation in dogs with pulmonary
hypertension, and this alone may greatly improve quality of life in affected
dogs. IPF is generally considered an absolute contraindication to diuretics,
as many affected dogs tend to be rather dehydrated and diuretics may
increase the occurrence of collapsing episodes and exacerbate lethargy and
exercise intolerance. Patients suffering from an acute crisis may, in some
cases, require hospitalisation for oxygen administration and stabilisation
after cage rest, and sometimes, cautious intravenous fluid administration.
The prognosis depends on the stage and speed of progression of the
disease, but the long-term outcome is generally considered to be poor. A
mean survival time of less than a year after diagnosis has been reported,
although some dogs with milder forms of IPF live for years.
CASE 27. PNEUMOCYSTIC
PNEUMONIA. PNEUMOCYSTIS
CARINII
SIGNALMENT
Breed: Cavalier King Charles Spaniel
Age: 3 years old
Sex: Male, neutered
Presenting complaint: Four-week history of panting, tachypnoea, and
intermittent dyspnoea; clinical signs improved temporarily with antibiotics
and furosemide. Chronic history of skin disease which had been treated
with corticosteroids
The dog was quiet, alert, and responsive on presentation at the veterinary
hospital (Fig. 1). The patient slept and snored loudly during the
examination. His pulse rate was 120 bpm and his respiratory rate was 44
breaths per minute. Thoracic auscultation revealed harsh lung sounds and
referred upper respiratory noises. His breathing pattern was characterised
by rapid breathing with an expiratory grunt. Abdominal palpation and the
patient’s body temperature were normal.
A complete blood cell count and biochemistry profile revealed mild
neutrophilia and a mild increase in alkaline phosphatase levels (130 U/l,
reference 0–50 U/l), which was thought to be due to chronic steroid
administration.
The urinalysis (urine specific gravity was 1.050) and the echocardiogram
were unremarkable. A point-of-care Angiostrongylus ELISA test was
performed and was negative.
Thoracic radiographs were taken under sedation and revealed a marked and
dense interstitial pattern with loss of the normal vascular outline, mainly in
the caudodorsal lung fields. The cardiac silhouette and the pulmonary
vasculature were radiographically normal (Fig. 2).
FIGURE 2. Dorsoventral (a) and right lateral (b) radiographs of the chest showing a marked
caudodorsal interstitial pattern.
COMPUTED TOMOGRAPHY
The patient was anaesthetised and a bilateral laryngeal paralysis was noted
at induction. A CT scan of the thorax was performed to further assess the
pulmonary parenchyma and identify any possible underlying pathology. It
revealed similar changes to those found in the radiographs: a marked
interstitial infiltrate with a generalised ground-glass appearance, which
involved mainly the caudal lobes of the lungs (Fig. 3).
After the CT examination, the major differential diagnoses included
interstitial pneumonia secondary to Pneumocystis carinii and bacterial or
parasitic pneumonia. Diffuse infiltrative neoplasia, such as lymphoma, was
considered less likely.
FIGURE 3. CT images (transverse at the level of the carina [a], transverse at the level of the
accessory lobe [b], and dorsal [c] reconstructions) of the chest in lung window, showing a marked
diffuse interstitial infiltrate in the lungs. Note the differences in attenuation with the transverse CT
image of a dog with normal lungs (d).
A bronchoalveolar lavage was performed under the same anaesthesia. The
culture of the sample was negative for aerobic bacterial infections
(Bordetella bronchiseptica and Mycoplasma spp., among others) and
mycotic infections. The cytological examination of the sample revealed the
presence of Pneumocystis carinii and a minor neutrophilic population, most
likely a secondary inflammation (Fig. 4).
Consequently, the presumptive diagnosis of pneumocystic pneumonia
was confirmed.
FIGURE 4. Cytological image of the samples obtained by bronchoalveolar lavage, showing multiple
Pneumocystis carinii cysts (arrowheads) and a macrophage with several cysts in the cytoplasm
(arrow). Image courtesy of Tim Williams.
TREATMENT
The patient was started with trimethoprim–sulfadiazine (80 mg and 400 mg,
respectively, every 12 h) for 6 weeks. The owners reported an improvement
in the clinical signs 2 weeks after the initial presentation.
Thoracic radiographs were repeated under sedation a month after the
treatment was initiated and revealed a marked improvement, with decreased
lung opacity, but persistence of a mild bronchointerstitial pattern (Fig. 5).
FIGURE 5. Dorsoventral (a) and right lateral (b) projections of the chest taken a month after
diagnosis. Marked improvement can be seen and only a mild bronchointerstitial pattern remains.
DISCUSSION
Pneumocystic pneumonia is caused by Pneumocystis carinii, an
extracellular opportunistic pathogen which is now classified as a yeast-like
fungus, despite being previously thought to be a protozoan. This type of
pneumonia has been described in humans and mammals. In dogs, the
Cavalier King Charles Spaniel and Miniature Dachshund are predisposed to
the disease. While there is no sex predilection, pneumocystic pneumonia is
more common in young dogs and is considered to be related to an
underlying immunodeficiency, including long-term administration of
steroids (as in this case).
The Cavalier King Charles Spaniel and Miniature Dachshund are

predisposed to pneumocystic pneumonia.
Although P. carinii infection is usually subclinical, this pathogen can

cause life-threatening pneumonia in immunocompromised individuals if not
adequately managed. Clinical signs, when present, are nonspecific and
include nonproductive cough, dyspnoea, tachypnoea, and dry lung sounds.
Haematologic and serum biochemical abnormalities are also nonspecific.
The clinical signs of pneumonia secondary to Pneumocystis carinii are

nonspecific.
Thoracic imaging, including radiography and CT, usually reveals a

bilateral and symmetrical increase in the radiodensity of the lungs, with a
mixed bronchointerstitial or miliary interstitial pattern that can sometimes
become alveolar. Cardiac changes due to right-sided cardiac enlargement
secondary to pulmonary hypertension may also be present in advanced
cases and can be detected by echocardiography.
Radiographic and CT findings in dogs with pneumocystic pneumonia

consist mainly of bilateral, symmetrical mixed bronchointerstitial or
miliary interstitial infiltration of the lungs.
The diagnosis can be challenging in veterinary medicine. The major

differential diagnoses include pulmonary interstitial fibrosis, canine
distemper, heartworm disease, eosinophilic bronchopneumopathy,
environmental pneumonitis, and diffuse pulmonary neoplasia such as
lymphoma, among other causes of pneumonia (e.g. mycoplasma).
The definite diagnosis is made by detecting P. carinii in the
bronchoalveolar lavage fluid or in transthoracic fine needle aspiration
samples of the lung. However, special stains, such as Grocott–Gomori
methenamine silver, or PCR and in situ hybridisation are sometimes
required for the detection of the pathogen. The clinical history and imaging
findings also help to reach the final diagnosis.
The medical treatment for pneumocystic pneumonia requires adequate
antibiotic therapy, including potentiated sulphonamides such as
trimethoprim–sulfadiazine; however, dosage is poorly documented.
Response to treatment is variable. In fact, some dogs can deteriorate after
initiating therapy, which is thought to be due to the inflammatory response
when pathogens die. Although, in some cases, steroids may be warranted to
counteract this initial response, they are not generally recommended as they
can lead to further immunocompromise.
The prognosis is good if the diagnosis is made promptly and the patient is
treated correctly, although it can be guarded in advanced cases and in those
where there are already signs of pulmonary hypertension.
CASE 28. PARASITIC
PNEUMONIA.
ANGIOSTRONGYLUS
VASORUM
SIGNALMENT
Breed: Crossbred dog
Age: 3 years old
Presenting complaint: Ten-day history of anaemia, lethargy, tachypnoea,
and dyspnoea
The dog was quiet, alert, and responsive. The mucous membranes were
pale, with a prolonged capillary refill time. The peripheral pulses were
weak. The heart rate was 90 bpm and the respiratory rate was 60 breaths per
minute. Thoracic auscultation revealed increased lung sounds. Abdominal
palpation and the patient’s body temperature were normal. There was
marked bilateral scleral haemorrhage, multiple petechiae in the mucosa, and
large, ill-defined bruising and haematomas under the skin surface (Figs. 1
and 2).
FIGURE 1. Image of the patient with marked scleral haemorrhage.
FIGURE 2. Image of the thorax and abdomen prior to the ultrasound examination showing extensive
skin haemorrhages.
A routine complete blood cell count and biochemistry profile revealed a
moderate regenerative anaemia (PCV 15 %), marked thrombocytopaenia (7
× 109/l) and mild leucocytosis (18.3 × 109/l, reference 6.0–15.0 × 109/l).
Blood coagulation tests revealed increased activated partial
thromboplastin time (APTT) and prothrombin time (PT) with a markedly
increased buccal mucosal bleeding time (BMBT), suggesting a consumptive
coagulopathy.
ABDOMINAL ULTRASONOGRAPHY
A conscious abdominal ultrasound was performed and showed a moderate
amount of echogenic retroperitoneal effusion. The fluid was sampled under
ultrasound guidance and was consistent with blood (Fig. 3).
FIGURE 3. Transverse ultrasound image of the left kidney (LK) surrounded by echogenic fluid
(arrow).
The thoracic radiographs taken by the referring veterinary surgeon were
reviewed at the time of presentation. They showed a moderate interstitial
pattern with a peripheral and mainly caudodorsal distribution and decreased
vascular outline. The cardiac silhouette and pulmonary vessels were normal
(Fig. 4).
FIGURE 4. Thoracic radiographs. Right lateral (a), left lateral (b), and dorsoventral (c) projections
showing patchy and mainly peripheral areas of increased opacity and a diffuse bronchointerstitial
pattern.
COMPUTED TOMOGRAPHY
A CT scan of the thorax was performed under general anaesthesia to further
assess the pulmonary parenchyma and identify any possible underlying
pathology. It revealed increased lung changes compared to those seen on the
previous radiographs, including marked, generalised interstitial infiltrate
with a ground-glass appearance, and patchy areas of alveolar consolidation
that mainly involved the peripheral aspects of the caudal lobes (Fig. 5).
FIGURE 5. Transverse CT reconstructions in lung window at the level of the carina (a) and caudal
vena cava (CVC) (b). Note the ill-defined, multifocal, peripheral and mainly ventral interstitial-
alveolar infiltrates.
A bronchoscope-guided bronchoalveolar lavage (BAL) was performed after
the CT scan under the same general anaesthesia. The cytological
examination of the sample revealed a background of clumped eosinophilic
material and dispersed fresh blood with mixed inflammatory cells including
macrophages, mature neutrophils, eosinophils, and reactive lymphocytes.
The presence of coiled parasitic larvae embedded within the mucoid clumps
was also detected (Fig. 6).
The final diagnosis was parasitic bronchopneumonia due to
Angiostrongylus vasorum.
Identification of first-stage larvae in the lungs or faeces is needed to
diagnose the infection.
FIGURE 6. Typical image of a curled first-stage larva of Angiostrongylus vasorum.
TREATMENT
The patient was hospitalised to receive intravenous fluid therapy.
Antimicrobial (amoxicillin–clavulanic acid at 15 mg/kg every 24 h for 7
days) and anthelmintic therapy (fenbendazole at 50 mg/kg every 24 h for 14
days) was also initiated in hospital and continued after discharge.
The dog showed marked improvement in both clinical and laboratory
parameters 3 days after starting the treatment. The BMBT was measured to
confirm adequate primary haemostasis and was normal, so the patient was
discharged.
Re-examination 3 weeks after the initial consultation revealed no clinical
signs and unremarkable blood work results. Lungworms were not observed
in three consecutive faecal analyses.
DISCUSSION
Angiostrongylus vasorum, also called lungworm or “French heartworm”, is
a metastrongyloid nematode that affects dogs and other species of Canidae,
including foxes, via an indirect cycle that involves slugs, snails, and frogs.
The adult worms accumulate in the pulmonary artery and its branches,
where they lay eggs. The eggs remain in the pulmonary capillaries, where
they hatch into first-stage larvae (L1). These larvae then penetrate into the
alveoli, causing interstitial pneumonia, or even pulmonary thrombosis and
an inflammatory reaction leading to pulmonary hypertension. From there,
aided by the animal’s cough, they migrate to the pharynx and are swallowed
and excreted in the faeces. Erratic locations of L1 in the brain and other
organs have also been described.
The free L1 in the soil are ingested by the intermediate host and reach
infective stage (L3). The life cycle is completed when the definitive host
(dog) swallows the infected intermediate host and the L3 moult into L4 and
L5, which migrate through the circulatory or lymphatic system to the heart
and pulmonary arteries, where they mature.
Geographically, A. vasorum has a worldwide distribution. However, this
parasite generally lives in wet and moderate climates in Europe, Africa, and
America.
Angiostrongylus vasorum infection is an uncommon disease that can

cause respiratory, neurological, or systemic signs.
There is no breed or sex predisposition, but young to middle-aged dogs

are predisposed, which is thought to be due to the scavenging and playful
behaviour typical of younger ages. Some articles report that working dogs
are more predisposed to this disease during their training.
The clinical signs and severity of the disease are very variable, from
subclinical patients to sudden death. Respiratory involvement is most
common, with signs due to interstitial pneumonia such as cough (productive
or unproductive), exercise intolerance, tachypnoea, dyspnoea, or cyanosis.
In a minority of dogs (estimated 5 % in general practice, but up to 33 % in
referral clinics), pulmonary hypertension develops secondary to A. vasorum
infection and may cause clinical signs of syncope or right-sided heart
failure.
It is also frequent for affected dogs to suffer from bleeding abnormalities,
which are manifested as ecchymoses, petechiae, haematomas, or
abdominal/thoracic bleeding. Neurological signs due to larvae and
haemorrhage in the brain or the spinal cord can cause seizures, paresis, and
other neurological signs. Other nonspecific signs such as uveitis,
depression, weight loss, anorexia, and vomiting and diarrhoea may also be
observed.
Imaging of the thorax shows a multifocal, mainly peripheral,
bronchointerstitial pattern with alveolar patches, due to granulomas and
bleeding caused by the migration of L1. In chronic cases, an interstitial
pattern occurs secondary to pulmonary consolidation and lung fibrosis.
Other changes include right-sided heart enlargement, dilation of the main
pulmonary artery, pleural or mediastinal haemorrhage, and rarely
pneumothorax. After resolution of the infection, a mild interstitial pattern
can remain visible.
Thoracic radiographs usually reveal a multifocal, mainly peripheral,

bronchointerstitial pattern with patchy areas of alveolar consolidation.
Doppler echocardiography is useful to estimate pulmonary arterial

pressure and assess effects on the right heart. Dogs with moderate to severe
pulmonary hypertension tend to have concentric hypertrophy and right
ventricular dilation, with a distended pulmonary artery and potentially right
atrial dilation. Detection of peak pulmonic insufficiency over 2.2 m/s (mean
pulmonary artery pressure >20 mmHg) or tricuspid regurgitation over 3 m/s
(systolic pulmonary artery pressure >36 mmHg) is consistent with
pulmonary hypertension.
Even though a neurological presentation is less frequent, neurological
signs can occur from bleeding in or around the central nervous system. In
these cases, advanced imaging techniques such as computed tomography
and magnetic resonance imaging are necessary for the diagnosis.
The clinical presentation, blood analyses, and imaging findings are
helpful in the diagnosis, but the detection of L1 in the respiratory tract or
faeces or of antigens in the blood is needed for a definitive diagnosis. A
BAL may be performed, but it should be done with caution as these patients
may present with severe respiratory distress and a bleeding tendency.
Submitting faeces for a Baermann test is recommended. This test can be
insensitive owing to intermittent shedding of L1 in faeces. As such, it may
need to be carried out on faecal samples from three consecutive days.
Performing one test only detects half of infected dogs. In urgent cases,
point-of-care microscopy of direct faecal smears can detect the larvae with
a sensitivity of 54–61 %.
Since the Baermann test can be insensitive, faecal samples from three
consecutive days may maximize the diagnostic capability.
Treatment is based on a combination of anthelmintic therapy

(fenbendazole [25–50 mg/kg for 5–21 days], milbemycin oxime–
praziquantel [weekly oral administration for 4 weeks], and imidacloprid–
moxidectin [monthly spot-on administration]) and supportive care, which
depends on the patient’s clinical signs. The bleeding tendency resolves
approximately 24 hours after starting the anthelmintic treatment in most
dogs.
The prognosis depends on the severity of the clinical signs, but it is
usually good if the diagnosis is made at an early stage of the disease.
Respiratory signs generally disappear within 1–2 weeks after treatment.
However, approximately 40 % of severe cases have residual signs such as
cough and exercise intolerance after resolution of the infection. If mortality
occurs, it is due to severe bleeding or respiratory failure.
Noncomplicated cases have an excellent prognosis with anthelmintic

therapy.
Prophylactic treatment with imidacloprid 10 % combined with

moxidectin 2.5 % is currently effective against A. vasorum.
PLEURAL DISEASE
The pleural space is a potential space that contains a small amount (2–3 ml)
of fluid that lubricates the surface of the lungs to facilitate their movement.
This space separates the membrane surrounding the lungs (visceral pleura)
and the membrane in contact with the thoracic wall and diaphragm (parietal
pleura). The mediastinum divides the pleural space into two pleural
cavities, but since it can be fenestrated, both cavities may be connected.
Pleural disorders can be unilateral or bilateral. The presence of masses or
excess fluid or gas in the pleural space can cause decreased ventilatory
volume and a compensatory increase in the respiratory rate. The presence of
pleural disease does not necessarily reflect a primary pleural disorder, as it
might be secondary to pulmonary or airway disease.
Commonly seen pleural diseases in veterinary practice are:

■ Pleural effusion. Abnormal fluid accumulation in the pleural space. It is
generally asymptomatic if only a small amount of fluid builds up, but if
that amount increases, clinical signs can be severe, including dyspnoea,
tachypnoea, orthopnoea, open-mouth breathing, cyanosis, lethargy,
exercise intolerance, and cough.
In order to reach a diagnosis, it is crucial to classify the type of fluid
based on its aspect, protein concentration, cellularity, and specific
gravity. The different types of fluid and possible causes are summarised
in the table below.
Imaging techniques are essential in the diagnosis of this pathology. The
radiographic appearance depends on the amount of fluid present;
however, most of the times, there is increased opacity in the thoracic
cavity, with border effacement of the cardiac and diaphragmatic
silhouettes as well as pleural fissures and retraction of the lung lobes
from the thoracic wall. Repeat radiographs after thoracic drainage might
help to identify any underlying condition, such as mediastinal mass or
cardiac enlargement. Ultrasound is very useful to identify the presence,
volume, and echogenicity of pleural fluid. The presence of fluid in the
pleural space will allow to better evaluate intrathoracic structures,
including the heart, and determine the presence of mediastinal/pleural
disorders. Depending on the echogenicity of the fluid, its type can be
suspected: an anechogenic fluid is suggestive of a transudate, modified
transudate, or chylothorax; a more echogenic and cellular fluid is present
in cases of exudates, haemorrhage, and neoplastic effusion. Ultrasound
can also be used to guide thoracocentesis.
Thoracocentesis is necessary in cases of pleural effusion, as it provides
fluid samples for characterisation, and can also be therapeutic in
symptomatic patients.
■ Pneumothorax. Presence of air in the pleural space. Although
pneumothorax is bilateral in most of the cases, it can also be unilateral if
the mediastinum is not fenestrated. There are different types of
pneumothorax:
■ Traumatic. It can be closed if the thoracic wall is not compromised
(e.g. secondary to blunt trauma or road traffic accident), or open if
there is a lesion in the thoracic wall and communication with the
exterior.
■ Iatrogenic.
■ Spontaneous. Not associated with any traumatic event. It can be
primary when there is no underlying lung disease, or secondary to
lung disorders such as emphysema, bullae/blebs, abscess, migrating
foreign body, or asthma.
■ Tension. Rapid accumulation of air in the pleural space that occurs
when the pleural pressure exceeds the atmospheric pressure. Air enters
the pleural space during inspiration and accumulates, becoming a life-
threatening condition.
Clinical signs of pneumothorax include tachypnoea, dyspnoea,
orthopnoea, rapid abdominal breathing, tachycardia, and reduced lung
sounds.
Imaging is also necessary for the diagnosis; however, it should be
delayed until the patient is stable. Radiology shows presence of air in the
thoracic cavity, with absence of vascular outline. The accumulation of air
produces elevation of the cardiac silhouette from the sternum and
retraction of the lung lobes from the thoracic cavity. Depending on the
amount of air accumulated, there will be collapse and increased opacity
of the affected lung lobes. It is important to mention that, most of the
times, the cause of the pneumothorax will be obscured by the air, so it is
crucial to perform CT if the aetiology cannot be identified on plain
radiographs.
■ Pleuritis. Rare condition involving inflammation of the pleura. In cats,
the most common cause is feline infectious peritonitis. In cats and dogs,
possible causes include pyogranulomatous disease (tuberculosis,
actinomycosis, nocardiosis), trauma, perforating foreign bodies,
septicaemia, pleural effusion, and lung disease.
Fibrosing pleuritis is characterised by pleural thickening and formation
of fibrous bands between the pleural surfaces. It can occur in pyothorax,
chylothorax, haemothorax, and feline infectious peritonitis. This
inflammation causes adherences between the parietal and visceral pleura,
thereby decreasing the volume and movement of the lungs.
■ Pleural masses. Pleural neoplasms are uncommon in veterinary
medicine, and the pericardial sac can be involved as well. They can be
primary (e.g. mesotheliomas) or secondary to other types of tumours
(e.g. carcinoma). Diagnosis is very difficult to achieve, as often the only
clinical sign is the presence of pleural effusion. Cytology of the pleural
fluid and advanced imaging techniques, such a CT, can help to identify
irregular thickening of the pleura. However, most of the times,
histopathology is required for a definitive diagnosis.
CASE 29. SPONTANEOUS
PNEUMOTHORAX
SIGNALMENT
Age: 5 years old
Sex: Male, neutered
Presenting complaint: Acute onset of dyspnoea, tachypnoea, and
orthopnoea
The patient was lethargic but alert when presented to the referral hospital
(Fig. 1). He had mild tachycardia, tachypnoea, and moderate to marked
respiratory distress. The mucous membranes were pale, with a normal
capillary refill time. The respiratory rate was increased (80 breaths per
minute) and the heart rate was normal. Thoracic auscultation showed
bilaterally reduced lung sounds. There was no evidence of external trauma
and the owners did not report any history of trauma previous to the
beginning of the clinical signs. The patient had no history of travelling
abroad.
On arrival at the hospital, the patient was placed on oxygen
supplementation. Thoracic radiographs were taken under very mild sedation
to minimise stress to the patient and revealed moderate bilateral
pneumothorax, more marked on the left side. The left lung lobes were
collapsed and appeared radiopaque and with rounded borders, likely
secondary to the atelectasis (Fig. 2).
FIGURE 2. Left lateral (a) and dorsoventral (b) radiographs of the chest showing moderate bilateral
pneumothorax (crosses), more marked on the left side. The left lung lobes are collapsed and an
alveolar pattern can be seen (arrows).
TREATMENT
The pneumothorax was rapidly drained with a butterfly needle, and 700 ml
of air were removed from the left hemithorax. Once the patient was
stabilised, thoracic radiographs where repeated and revealed only a very
small residual pneumothorax. A round radiolucent lesion, with a thin
radiopaque wall, was then noticed in the right caudodorsal lung parenchyma
(Figs. 3 and 4).
Ruptured pulmonary blebs and bullae are the most common causes of
spontaneous pneumothorax in dogs. There are usually multiple lesions
located in the apices of the lungs.
FIGURE 3. Dorsoventral radiograph of the chest after pneumothorax drainage showing a round,
thin-walled, radiolucent lesion in the right caudodorsal lung field.
FIGURE 4. Right lateral radiograph of the chest showing an ovoid radiolucent lesion in the
caudodorsal lung field.
A diagnosis of spontaneous pneumothorax secondary to the rupture of a

bulla/bleb was then made.
Since the pneumothorax quickly recurred following air aspiration, and
after discussion with the owners, surgery was elected without further
imaging studies to remove the cause of the pneumothorax. A median
sternotomy was performed to obtain access to the thoracic cavity. The
thorax was filled with warmed, sterile saline and a leak was noted in the
right caudodorsal lung during ventilation. A partial lobectomy of the right
caudal lung lobe was then performed and a thoracostomy tube was left in
place for 24 hours to remove any residual air.
The patient recovered uneventfully and was discharged 5 days after the
procedure. There was no recurrence of pneumothorax in the 36 months
following surgery.
DISCUSSION
Pneumothorax is defined as a collection of free air in the pleural space. It
can generally be classified into three groups:
■ Traumatic. Secondary to external trauma such as a bite, rib fracture, etc.
This type of pneumothorax can be closed if a blunt trauma causes rupture
of the bronchial tree when the glottis is closed, or open if there is direct
communication between the exterior and the pleural space.
■ Iatrogenic. It can be open (secondary to surgery, a stab, etc.) or closed
(secondary to bronchoscopy or in cases of tracheal rupture secondary to
intubation, thoracocentesis, lung aspiration, etc.).
■ Spontaneous.
Spontaneous pneumothorax is a closed pneumothorax that occurs when air

enters the pleural space in the absence of any traumatic or iatrogenic cause.
The most common source of air entry is the lung parenchyma and, rarely,
the bronchi, trachea, and oesophagus. Origins are multiple, including
pneumonia, pulmonary abscesses, neoplasia, feline asthma, and, most
commonly, ruptured pulmonary blebs or bullae.
Pulmonary blebs are accumulations of air between the visceral and
parietal pleura, most frequently in the apices of the lungs, and therefore
they are more susceptible to trauma and rupture. Pulmonary bullae are air-
filled spaces within the lung parenchyma that result from rupture or dilation
of alveolar walls. Both blebs and bullae can be small or very large and tend
to occur in healthy, middle-aged, large-breed or deep-chested dogs with no
previous history of pulmonary disease.
The diagnosis of spontaneous pneumothorax is difficult. Although
animals can compensate in case of mild pneumothorax, most of the patients
present with respiratory distress, tachypnoea, coughing, lethargy, and pale
mucous membranes. The clinical signs are more severe when the amount of
trapped air is greater and the presentation is more acute.
Clinical examination usually reveals decreased lung sounds dorsally,
secondary to air accumulation. Thoracic radiographs show the presence and
degree of pneumothorax, and possible blebs or bullae. Transthoracic lung
ultrasonography, an emerging diagnostic tool for lung diseases, reveals the
absence of lung sliding and the presence of the reverse sliding sign in cases
of pneumothorax. CT is more sensitive in detecting bullae or blebs and also
allows better visualisation of the surrounding structures (Fig. 5). However,
as ruptured blebs or bullae are rarely detected in CT scans, exploratory
surgery is recommended to evaluate the pulmonary parenchyma and
remove the source of any possible leak.
FIGURE 5. Transverse CT images of a dog’s chest in lung window showing a moderate, mainly
right-sided, pneumothorax (cross), which causes displacement of the lung parenchyma from the
thoracic wall. Note a round hypoattenuating lesion with a thin hyperattenuating wall (i.e. a bulla) in
the accessory lung lobe (arrows).
Tension pneumothorax is an important subtype and the most severe form

of pneumothorax. It is generally closed and can be due to traumatic and
spontaneous causes. In these cases, the thoracic lesions act as one-way
valves, allowing air into the pleural space during inspiration and preventing
expulsion during expiration. The continued accumulation of air in the
pleural space quickly causes increased intrathoracic pressure and the
collapse of lung lobes and great veins, with the consequent cardiovascular
collapse. These patients deteriorate rapidly and will die if no drainage is
performed promptly. Thoracic radiographs in cases of tension
pneumothorax reveal uni- or bilateral severe pneumothorax, severe collapse
of the lung lobes, and flattening of the diaphragm (Fig. 6).
FIGURE 6. Dorsoventral radiograph of the chest of a dog with a bilateral tension pneumothorax
(crosses). Note the secondary severe retraction and collapse of the lung lobes (arrows).
Treatment of spontaneous pneumothorax depends on the clinical status of

the patient, but stabilisation with strict rest, oxygen therapy, and drainage of
the free air should be the first step, even before radiographs are taken.
Thoracocentesis should be performed as often as necessary to maintain
adequate respiration of the patient.
A mild pneumothorax can resolve spontaneously if there is little damage
to the lung and the bronchial tree is not involved. However, in most cases,
temporary thoracostomy tubes must be placed to drain free air. Surgical
exploration and removal of the affected lung lobe is usually needed to stop
the air leakage into the pleural space.
As medical management of spontaneous pneumothorax is generally not

effective, surgical treatment should be pursued.
The prognosis of spontaneous pneumothorax is good if surgical treatment

is performed promptly. Partial or complete lung lobectomy has been shown
to reduce the rate of recurrence of pneumothorax (from 50 % in cases where
surgery is not performed to 3 % after surgery).
CASE 30. IDIOPATHIC
CHYLOTHORAX
SIGNALMENT
Age: 4 years old
Presenting complaint: Tachypnoea and intermittent cough that has
deteriorated in the last 24 hours
On presentation the cat was bright, alert, and responsive (Fig. 1). Her body
condition score was 3/5 (body weight of 4.5 kg). Her mucous membranes
were pink and moist, with a normal capillary refill time. The heart rate was
150 bpm with regular rhythm and the peripheral pulses were firm. The
respiratory rate was 46 breaths per minute. Thoracic auscultation was
difficult as the heart and lung sounds were muffled. The rest of the clinical
examination was unremarkable.
The results of the complete blood cell count and full biochemistry profile
were normal.
Three projections of the thorax were taken under sedation and revealed a
moderate amount of bilateral pleural effusion, which caused border
effacement of the cardiac and diaphragmatic silhouettes and retraction of
the lung lobes from the thoracic wall. An incidental sternal malformation
was also noted (Fig. 2).
FIGURE 2. Right lateral (a) and dorsoventral (b) radiographs of the thorax showing a moderate
amount of bilateral radiopaque pleural effusion, with retraction of the lung lobes (arrows) and
effacement of the cardiac and diaphragmatic silhouettes.
ECHOCARDIOGRAPHY
A cardiac ultrasound was performed and demonstrated normal systolic and
diastolic functions. No evidence of structural abnormalities or mediastinal
lesions was found.
A moderate amount of bilateral hypoechoic pleural effusion was noted as
well as mild enlargement of the cranial mediastinal lymph nodes (Fig. 3).
A sterile thoracocentesis was performed under ultrasound guidance to
remove 50 ml of milk-coloured fluid (Fig. 4). Fluid analysis in the
laboratory revealed a rich content in triglycerides (fat), thus the presence of
chylothorax was confirmed.
Sampling and examination of the abnormal pleural fluid is needed for the
diagnosis of chylothorax. Chyle has a typical milky appearance.
FIGURE 3. Thoracic ultrasound image showing a moderate amount of hypoechoic effusion (arrow)
and an atelectatic lung lobe (asterisk).
FIGURE 4. Image of the drained pleural effusion with a milky appearance.
COMPUTED TOMOGRAPHY
A whole-body CT scan was performed under general anaesthesia the
following day to identify any possible thoracic abnormalities that could
explain the presence of chylothorax in the patient. It revealed a moderate
amount of dependent pleural effusion and the previously reported mild
mediastinal lymphadenopathy (Fig. 5). No thoracic masses or other
abnormalities that could cause the chylous effusion were detected.
Abdominal CT examination was also unremarkable.
Based on the clinical history, imaging, and clinicopathological results,
the final diagnosis was bilateral idiopathic chylothorax.
FIGURE 5. Postcontrast transverse CT reconstructions of the thorax in soft tissue window at the
level of the heart base (a) and left ventricle (b). Both sections show a large amount of
hypoattenuating dependent pleural effusion (crosses) that produces retraction of the lung lobes
(arrows).
TREATMENT
After drainage of the pleural effusion, medical management included a low-
fat diet, rutin, and repeated drainage of the abnormal fluid to improve the
patient’s breathing. However, as recurrence of the pleural effusion was quite
frequent, surgical intervention was elected and performed 2 months after
initial presentation. Through a left-sided thoracotomy, the thoracic duct was
ligated and a pericardiectomy was performed. The surgery was uneventful
and the patient recovered well. She was discharged from the hospital 3 days
after surgery with broad-spectrum antibiotics and a low-fat diet. No
recurrence of pleural effusion was reported.
DISCUSSION
Chylothorax is an uncommon form of pleural effusion in small animal
practice where lymphatic fluid accumulates in the pleural space due to a
disruption of the thoracic duct. Chyle (lymph) has a typical milky
appearance due to its high content in fat.
After a meal, fat is absorbed by the intestine through the lacteal vessels,
from where it is transported to the regional lymph nodes. Fat then travels
through the lymphatic system to the cisterna chyli, a reservoir located in the
craniodorsal abdomen, and continues to the thorax via the thoracic duct,
which empties its contents into the blood at the level of the cranial vena
cava.
There are numerous causes of chylothorax that result in occlusion or
impedance of flow from the thoracic duct, including increased venous
pressure at the level of the right heart, abnormal organ position (lung lobe
torsion, peritoneopericardial diaphragmatic hernia), neoplasia, fungal
disease, trauma, and cardiac disease. However, most of the times, no
underlying cause can be found and the chylothorax is therefore considered
idiopathic.
Chylothorax is a poorly understood disease.
No age or sex predisposition is suspected, but cats (especially Siamese)

and some dog breeds (e.g. Mastiff, Afghan Hound) seem to have a higher
occurrence of idiopathic chylothorax.
The diagnosis is based on the combination of:

■ Clinical signs and examination:
■ Pale blue mucous membranes may be seen, depending on the
respiratory compromise of the patient.
■ Decreased pulmonary and cardiac sounds due to the dependent pleural
effusion.
■ Diagnostic investigation:
■ Thoracic radiographs reveal the presence of bilateral pleural effusion,
with retraction of the lung lobes from the thoracic walls and
effacement of the cardiac silhouette (depending on the amount of
fluid).
■ Echocardiography identifies any possible cardiac pathology that could
explain the presence of chyle in the thorax.
■ Lymphangiography (mesenteric, percutaneous, or popliteal) is rarely
performed although it can be very useful to identify the path of
lymphatic vessels, the anatomy of the cisterna chyli and thoracic duct,
and any possible chyle leakage into the cranial thorax.
■ Fluid examination is needed for a definitive diagnosis. Cytology of the
fluid reveals mainly lymphocytes, and nondegenerate neutrophils in the
more chronic cases. A Sudan stain can be used to identify the presence of
lipids. However, the detection of higher triglyceride levels in the fluid
than in serum is pathognomonic of a chyle effusion.
Treatment of idiopathic chylothorax is challenging, but it should be

attempted as the chronic presence of chylous fluid in the pleural space can
cause life-threatening fibrosing pleuritis and pericarditis.
Medical management is usually not successful and consists of effusion
drainage, dietary modification (low-fat diet to decrease flow through the
thoracic duct), and rutin, an oral nutritional supplement that helps to break
down proteins and remove them from the lymphatic system.
If detected, treating the primary cause of chylothorax may resolve the
effusion. In most cases of idiopathic chylothorax, surgery is required and
involves the ligation of the thoracic duct in combination with either subtotal
pericardiectomy to decrease venous pressure or ablation of the cisterna
chyli to relieve the pressure on the thoracic duct. Surgical treatment with
thoracic duct ligation has been shown to successfully resolve idiopathic
chylothorax in 15–50 % of feline cases, which improves to 80–100 % if it is
combined with pericardiectomy or ablation of the cisterna chyli.
Most cases of idiopathic chylothorax require surgical intervention.
MEDIASTINAL DISEASE
The mediastinum is the central space between the lungs and extends from
the thoracic inlet to the diaphragm. It communicates cranially with the
cervical fascial planes and caudally with the retroperitoneal space. In most
animals, the mediastinum is fenestrated.
The mediastinum is divided in three parts: cranial, middle, and caudal.
The cranial part contains the thymus, lymph nodes, mediastinal vessels,
trachea, oesophagus, and cranial mediastinal reflection; the middle part
contains the oesophagus, trachea, lymph nodes, aorta, azygos vein, and
heart; and the caudal part contains the caudal oesophagus, caudal vena cava,
aorta, azygos vein, and caudal mediastinal reflection.
In general, plain radiology is the first diagnostic tool for mediastinal
disease in veterinary medicine, and ultrasound can be useful in some cases.
The size of the mediastinum depends on the species. In dogs, the width of
the mediastinum should be less than twice the width of the vertebral
column, with the exception of obese or brachycephalic dogs, in which the
mediastinum can be wider. In cats, the mediastinum should be no wider
than the width of the thoracic vertebrae at the same level. It is important to
remember that the thymus is a mediastinal structure that regresses at around
4–6 months of age, and its silhouette is generally identified in young
patients on the cranioventral aspect of the thorax. In most cases, the thymus
disappears completely by about 1 year of age.
Due to the anatomy of the thoracic cavity, mediastinal disease generally
involves the space between the pleural layers. Depending on the location of
the lesions, the possible cause can be identified.
The most common mediastinal abnormalities seen in veterinary practice

are:
■ Mediastinal shift. Though not a disease, it helps to identify several
thoracic abnormalities and narrow the differential diagnoses list. Due to
the midline position of the mediastinum, any deviation of the mediastinal
structures towards one side or the other produces changes in the volume
of one hemithorax. This finding can only be identified on dorsoventral or
ventrodorsal radiographic views.
Lung atelectasis or previous lobectomy, for example, cause mediastinal
shift towards the pathological hemithorax. Shifting of the mediastinal
structures towards the nonpathological hemithorax can occur in cases of
pleural or lung masses, unilateral pneumothorax or pleural effusion,
unilateral lobar emphysema, or diaphragmatic hernia/rupture.
■ Mediastinal masses. Most mediastinal masses are located in the
cranioventral aspect of the thoracic cavity. They can be neoplastic in
origin or consistent with an enlarged lymph node, abscess, cyst,
haematoma, or granuloma. Less common localisations of mediastinal
masses include:
■ Craniodorsal. Oesophageal disease, tumours of neural or
neuroendocrine origin, paravertebral/vertebral masses, aortic lesions.
■ Perihilar. Heart base neoplasia, perihilar lymph node enlargement
(lymphoma, metastatic or fungal disease), oesophageal masses or
foreign bodies.
■ Caudodorsal. Oesophageal/mediastinal lesions, hiatal hernias.
■ Caudoventral. Peritoneopericardial hernias, diaphragmatic rupture or
mass.
Mediastinal neoplasms are common in dogs and cats, particularly
thymoma and lymphoma. They can be variable in size but generally
occupy most of the cranial aspect of the thoracic cavity when the patient
shows clinical signs. Due to their cranioventral location, these masses
displace the rest of mediastinal structures caudodorsally, including the
heart and the lung parenchyma.
Diagnostic imaging techniques are necessary for the diagnosis, and the
imaging appearance depends on the size and type of mass. Radiology is
not sensitive enough to differentiate between different structure densities;
however, ultrasound or CT can help in that regard as well as being a
useful guide for sampling. CT is also extremely helpful prior to any
surgical treatment to evaluate the extension of the changes and identify
any possible vascular invasion or metastatic spread.
It is not uncommon to have pleural effusion in cases of mediastinal
disease, which can make the diagnosis more challenging.
■ Mediastinal effusion. Rare condition that can be secondary to blood
accumulation (coagulopathies), inflammation (feline infectious
peritonitis), or oesophageal rupture or trauma.
■ Pneumomediastinum. Presence of free gas in the mediastinum. It can
be secondary to:
■ Extension of air from the fascial planes of the neck. This is frequent in
cervical bites, tracheal or oesophageal rupture, or recent cervical
surgery.
■ Retroperitoneal gas.
■ Intrathoracic tracheal or oesophageal rupture.
■ Spontaneous after severe cough or respiratory disease.
Gas in the mediastinum provides an excellent radiographic contrast
media and helps in the diagnosis, as it allows differentiation of
mediastinal structures (mainly the cranial vena cava, brachiocephalic
trunk, and aorta).
CASE 31. THYMOMA
SIGNALMENT
Age: 10 years old
Presenting complaint: Chronic history of lethargy and dyspnoea
The cat was quiet but alert and responsive on presentation. Her mucous
membranes were pink and moist, but she had significant dental disease. Her
respiratory rate was 74 breaths per minute, and she had a mild increased
respiratory effort. Cardiac auscultation was difficult and cardiac sounds
were only audible in the right hemithorax. Lung sounds were reduced
cranially and ventrally. Abdominal palpation was unremarkable.
The results of the complete blood cell count and full biochemistry profile
were within reference values and FELV/FIV tests were negative.
Thoracic radiographs were taken under sedation and revealed the presence
of a large soft tissue mass in the cranioventral thorax, which occupied most
of the left hemithorax. The mass was mediastinal in origin and was causing
marked mass effect, with a mediastinal shift and displacement of the cardiac
silhouette to the right and caudodorsal displacement of the carina to the 6th
intercostal space (Fig. 1). The pulmonary parenchyma was also compressed
and displaced caudodorsally by the mass.
FIGURE 1. Right lateral (a) and dorsoventral (b) radiographs of the chest showing a large cranial
mediastinal mass (star) with marked right caudodorsal displacement of the cardiac silhouette
(arrows).
THORACIC ULTRASONOGRAPHY
A thoracic ultrasound was performed and revealed a heterogeneous but
mainly hypoechoic mass in the cranial mediastinum, which was partially
vascularised on colour Doppler mode (Fig. 2). Ultrasound-guided
transthoracic fine needle aspirations were performed and cytological
examination of the samples showed a large amount of amorphous epithelial
cells (Fig. 3). Clinical, imaging, and cytological findings were consistent
with a mediastinal thymoma.
FIGURE 2. Ultrasound images of the mediastinal mass. Note the mainly hypoechoic mass around
the cranial mediastinal vessels (a). The mass appears partially vascularised on the colour Doppler
scan (b).
FIGURE 3. Cytological image of the mediastinal mass showing amorphous epithelial cells and
multiple small lymphocytes. Image courtesy of Maciek R. Antoniewicz.
COMPUTED TOMOGRAPHY
With the cytological diagnosis of thymoma, the owners elected surgery, and
a CT scan of the chest was recommended to identify any possible vascular
invasion as well as distant metastases.
The CT scan was performed under general anaesthesia (Fig. 4) and
showed the large and heterogeneous mass in the cranioventral mediastinum,
occupying most of the left cranial hemithorax. It was displacing the heart
and the surrounding main vessels (Fig. 5). No signs of vascular invasion or
pulmonary nodules were identified.
FIGURE 4. Image of the anaesthetised patient undergoing a CT scan in sternal recumbency.

FIGURE 5. Precontrast transverse (a), dorsal (b), and sagittal (c) CT reconstructions of the thorax.
Postcontrast image in transverse plane at the level of the cranial mediastinum (d). The large mass
(star) is heterogeneous with small areas of mineralisation, and produces a marked mediastinal shift
with right-sided displacement of the heart (H).
TREATMENT
As the CT images showed no spread of the disease, surgical intervention
with a median sternotomy was performed to remove the mass. The surgery
was uneventful and the patient recovered well from the anaesthesia. She
was sent home 4 days after surgery with broad-spectrum antibiotic therapy
(amoxicillin–clavulanic acid).
The cat had a small amount of bilateral pleural effusion a week after the
surgery that resolved with no further treatment.
Surgical removal of thymomas is the treatment of choice in those cases

where the mass is noninvasive.
DISCUSSION
Mediastinal masses are common in general practice in dogs and cats, and
have also been described in rabbits, horses, pigs, and cattle.
The most common localisation of mediastinal masses in small animals is
the cranioventral mediastinum; however, they can be located anywhere in
the mediastinum (craniodorsal, caudodorsal, caudoventral, or perihilar).
The possible differential diagnoses of cranioventral mediastinal masses are:

■ neoplasia (lymphoma, thymoma, ectopic thyroid carcinoma)
■ cyst
■ thymic branchial cyst
■ lymph node enlargement
■ haematoma
■ abscess.
The major differential diagnoses of cranial mediastinal masses in small

animals are lymphoma and thymoma.
Thymomas are uncommon neoplasms that derive from thymic epithelial

cells and have some lymphocytic infiltration. Thymomas occur mainly in
middle-aged to old cats, unlike lymphomas, which tend to occur in younger
animals. They progress slowly, expand from the cranial mediastinum, and
displace the surrounding structures. Most of them are encapsulated, but they
can also be invasive and reach the main cranial mediastinal vessels, as well
as cause distant metastases. A cystic component of the mass is common.
The clinical signs of cranial mediastinal thymomas usually depend on the
size of the lesion. It might be an incidental finding when it is small, but the
most common clinical signs include coughing, dyspnoea, anorexia, exercise
intolerance, and vomiting, which worsen when the lesion becomes larger
and compresses the lungs. Muffled cardiac sounds and decreased
compressibility of the cranial mediastinum are also typical clinical findings
in these cases. Secondary exfoliative dermatitis and the presence of
paraneoplastic syndromes such as myasthenia gravis, megaoesophagus,
hypercalcaemia, and cranial vena cava syndrome have also been reported.
The main radiographic findings are the presence of a soft-tissue mass in
the mediastinum, which displaces the trachea dorsally and causes a
secondary mediastinal shift, best seen on dorsoventral or ventrodorsal
projections. Ultrasound helps to distinguish between different types of
lesions, determine the consistency of the mass, and obtain a sample.
Thymomas generally have heterogeneous echogenicity and can have a
cystic appearance, whereas lymphomas are more likely to be solid. If a
surgical intervention is considered, a CT scan should be performed to
identify any possible metastases and the presence of vascular invasion.
Discriminating between mediastinal lymphomas and thymomas can be
challenging. Flow cytometry may help to differentiate thymic lymphocytes
from thymic lymphoblasts (lymphoma cases), and this is crucial for the
treatment of the patient.
A combination of the imaging techniques and fine needle

aspiration/biopsy of the mass allows a definitive diagnosis.
Surgical excision is the treatment of choice if the mass is resectable.

Thymomas have a good prognosis if they are noninvasive and surgical
intervention is possible, with a low incidence of recurrence (median
survival 41 months). However, cases with associated paraneoplastic
syndromes or patients with unresectable thymomas have a more guarded to
poor prognosis.
CASE 32. VASCULAR RING
ANOMALIES. PERSISTENT
RIGHT AORTIC ARCH
SIGNALMENT
Breed: German Shepherd Dog
Age: 4 months old
Sex: Female, intact
Presenting complaint: Chronic history of regurgitation since she started
eating solid food
The dog was bright, alert, and responsive on presentation at the referral
hospital. She was evidently underweight (body condition score of 3/9) and
small in size. Thoracic auscultation, abdominal palpation, and rectal
temperature were normal.
Thoracic radiographs were taken under mild sedation (butorphanol 0.2
mg/kg IV) and revealed a marked focal dilation of the cranial aspect of the
thoracic oesophagus, which caused a widening of the cranial mediastinum.
The dilated oesophagus was located on the left side of the trachea and was
air-filled on the right lateral view and fluid-filled on the left lateral view.
There was a small amount of mineralised material in the ventral aspect of
the oesophageal dilation, consistent with some degree of gravel sign. The
oesophagus was markedly narrowed at the level of the carina, with
moderate dilation caudal to the constriction (Fig. 1). No signs of aspiration
pneumonia were identified.
The clinical history and radiographs were strongly suggestive of a
vascular ring anomaly (VRA), likely a persistent right aortic arch (PRAA).
However, the position of the aortic arch was unclear and therefore a CT
angiogram was requested prior to surgery.
FIGURE 1. Thoracic radiographs (dorsoventral [a], right lateral [b], and left lateral [c] projections)
showing a marked focal dilation of the oesophagus cranial to the carina (arrows). Note the mild
dilation of the caudal oesophagus (arrowheads).
COMPUTED TOMOGRAPHY
The CT angiogram was performed under general anaesthesia and revealed a
right-sided aortic arch with a left brachiocephalic trunk and a right
subclavian artery. The presence of a ligamentum arteriosum was also
detected, which caused extramural compression and secondary dilation of
the cranial aspect of the cervical oesophagus (Fig. 2).
Findings were consistent with a PRAA and a left-sided ligamentum
arteriosum (type 1 VRA), as this is the most likely vascular anomaly with
no additional dorsal compression of the oesophagus by major vessels.
FIGURE 2. Postcontrast transverse views of the thorax in the soft tissue window showing a dilated
air- and fluid-filled oesophagus (Oe) cranial to the heart base (a) and a right-sided location of the
aorta (Ao) at the heart base (b). T, trachea.
TREATMENT
Surgical intervention was scheduled for the following day. A left-sided
thoracotomy was performed to allow access to the base of the heart. The
ligamentum arteriosum and other fibrous tissue were identified, ligated, and
transected, which resolved the oesophageal constriction (Fig. 3).
Surgery is the treatment of choice in cases of persistent right aortic arch.

FIGURE 3. Surgical image showing the ligated and transected ligamentum arteriosum.
After placing a chest drain, the patient recovered from the anaesthesia
without any incidents. She was hospitalised for a week for pain
management (methadone 0.2 mg/kg every 6 h for 1 day and then
buprenorphine 0.01 mg/kg every 8 h), as well as nonsteroidal anti-
inflammatory (meloxicam 0.1 mg/kg every 24 h) and broad-spectrum
antibiotic therapy (amoxicillin–clavulanic acid 12.5 mg/kg every 12 h). She
developed a small amount of chylous pleural effusion. Once the effusion
had resolved, the chest drain was removed and the patient was discharged.
At recheck 1 week after discharge, the owners reported that she had only
had mild nausea. One month after discharge, the owners did not report any
recurrence of the dog’s clinical signs in a telephone conversation.
DISCUSSION
VRAs are developmental abnormalities of the thoracic vessels. Several
have been reported in dogs, including PRAA, persistent left aortic arch with
right ligamentum arteriosum, aberrant left/right subclavian artery, and
double aortic arch.
The characteristics of these VRAs are as follows:

■ Persistent right aortic arch. The ligamentum arteriosum stretches
between the pulmonary trunk and the right-sided aorta, causing
compression of the oesophagus (Fig. 4). It is the most common type and
causes rightward displacement of the aorta and leftward displacement of
the trachea.
■ Persistent left aortic arch with right ligamentum arteriosum. The
abnormal ligament extends between the right pulmonary arch and the
normal aortic arch.
■ Aberrant left subclavian artery (generally seen with PRAA). The
abnormal left subclavian artery arises from the left aortic arch making a
dorsal constriction of the oesophagus.
■ Aberrant right subclavian artery (associated with a normal left aortic
arch). The abnormal right subclavian artery arises distal to the left
subclavian artery and passes to the right, compressing the oesophagus
dorsally. It can be associated with oesophageal signs, but in some cases it
may be an incidental finding.
■ Double aortic arch. Both sides of the aortic arch persist, and the
oesophagus is compressed bilaterally (Video 1).
FIGURE 4. Three-dimensional CT reconstructions of the heart in a cat with persistent right aortic
arch. The aorta (Ao) arises from the heart and is located to the right of its usual position. The left
subclavian artery originates from the ascending aorta (arrow), and the carotid trunk and right
subclavian artery arise separately from the arch. The ring which constricts the oesophagus is best
seen from a cranial aspect (dashed line) and is formed by the ligamentum arteriosum (solid line),
which connects the right aortic arch to the pulmonary artery (PA). The ligamentum is partially patent
in this case, and its origin can be identified as a dilation of the aorta at its ventral aspect (asterisk).
Video 1
Three-dimensional reconstruction of CT images from a dog with a double aortic arch. The ring
effect is clearly identified where oesophageal constriction would occur.
PRAA is the most common VRA in dogs and accounts for approximately
95 % of VRA cases. Although German Shepherd Dogs and Irish Setters
have a higher prevalence of PRAA, other breeds and species can also be
affected.
Persistent right aortic arch is the most commonly seen vascular ring
anomaly in dogs.
During embryonic development, six pairs of aortic arches connect the aortic
sac with the dorsal aorta. These arches are located around the trachea and
oesophagus and evolve as follows:
■ The first two pairs of arches atrophy.
■ The third arches form the common carotid arteries.
■ The right fourth arch forms the right subclavian artery, and the left fourth
arch forms the definitive aortic arch.
■ The fifth arches are not present in mammals.
■ The sixth arches form the pulmonary trunk.
PRAA occurs when the right fourth aortic arch fails to regress normally and
entraps the oesophagus, which causes oesophageal dilation cranial to the
narrowing.
The main clinical sign in patients with PRAA is postprandial
regurgitation, generally noted shortly after weaning onto solid food.
Radiographic changes are usually quite consistent and include focal
dilation of the oesophagus cranial to the carina and a leftward curvature of
the trachea near the cranial border of the cardiac silhouette. Contrast studies
can be used to differentiate generalised megaoesophagus from a VRA and
to highlight the abnormal oesophagus. Contrast-enhanced CT imaging can
help to identify the exact cause of the oesophageal constriction as well as to
assess other possible congenital abnormalities.
Aspiration pneumonia secondary to frequent regurgitation is a common
complication in patients with PRAA. In these cases, clinical signs
consistent with respiratory distress (dyspnoea and tachypnoea), fever, and
lethargy can occur. The radiographic finding of aspiration pneumonia is
increased pulmonary opacity, usually located ventrally in the lung lobes
(Fig. 5).
It is important to look for signs of aspiration pneumonia or dilation of the

caudal aspect of the oesophagus during diagnostic investigations, as they
affect the prognosis.
Surgical treatment with a left-sided thoracotomy should be performed to

relieve the constriction caused by the ligamentum arteriosum. A proportion
of dogs have residual blood flow through the ligamentum, so ligation
should always be performed before transecting the structure. Broad-
spectrum antibiotic therapy is recommended in animals with secondary
pneumonia.
Surgical correction of the stenosis does not guarantee a complete

resolution of the clinical signs.
The prognosis is generally very good if surgery is carried out early and if
there is no dilation of the caudal oesophagus or secondary aspiration
pneumonia. However, the literature indicates that complete resolution of the
oesophageal dilation is rarely achieved despite the disappearance of clinical
signs in the majority of cases.
FIGURE 5. Oesophagram (left lateral [a] and dorsoventral [b] projections] of a puppy showing a
marked barium-filled dilation of the oesophagus cranial to the carina. Note the focal, ill-defined
increase in opacity present in the right caudoventral lung field (circle), consistent with pneumonia.
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Case 27. Pneumocystic pneumonia. Pneumocystis

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Case Studies in Cardiothoracic Medicine

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Case Studies in Cardiothoracic Medicine

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CASES STUDIES IN

First printing: March 2021

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All rights reserved.

And to my patients and their owners,

To my veterinary colleagues and my mentors

And to my family, friends, and partner for always being there.

Raquel Salgüero Fernández

Raquel Salgüero Fernández wishes to thank:

Kieran is an American, European, and RCVS recognised specialist in

RAQUEL SALGÜERO FERNÁNDEZ

Raquel is a Diplomate of the European College of Veterinary Diagnostic

Dr Peter Darke BVSc PhD DVR DVC MRCVS DipACVIM

01 CARDIAC CASE STUDIES

Congenital heart disease

02 RESPIRATORY CASE STUDIES

CONGENITAL HEART DISEASE

A 2019 consensus statement on the assessment and treatment of MVD in

Consensus guidelines on the diagnosis and management of cardiomyopathy

Stage B is divided in B1, cats with no left atrial dilation on

Echocardiographic findings of left atrium-to-aortic root ratio >1.6 and

Screening for dogs likely to be affected by myxomatous mitral valve

Pimobendan has been proven to benefit dogs in stage B2 MMVD. Since

Sudden death is not uncommon in dogs with myxomatous mitral valve

FIGURE 1. Echocardiographic 2D images of the heart. Subjectively, wall motion appears to be

Pimobendan helps to reduce heart size and prolong symptom-free

Dilated cardiomyopathy (DCM) in dogs is mostly caused by primary

In dogs with DCM, treatment with pimobendan in the preclinical phase

THORACIC ULTRASONOGRAPHY AND

Focused ultrasonographic assessment is preferable over thoracic

Left atrial size is a crucial part in the echocardiographic assessment in

It is possible that combining clopidogrel with low-dose aspirin, or the use

FIGURE 1. Six-lead electrocardiogram showing a background sinus rhythm with ventricular

Arrhythmogenic right ventricular cardiomyopathy is diagnosed by a

Sotalol is the first-line anti-arrhythmic drug to control ventricular ectopy,

Dogs with arrhythmogenic right ventricular cardiomyopathy may present

Genetic studies in the USA initially suggested a causative gene (the

ARVC has been described in three stages in the Boxer dog:

FIGURE 2. Right parasternal short-axis echocardiographic view confirming pericardial effusion

FIGURE 5. Image of a different patient undergoing pericardiocentesis. The procedure is performed

The cause of 50 % of all cases of pericardial effusion in dogs is

In this case, a haemangiosarcoma was strongly suspected based on

In dogs with pericardial effusion but no echocardiographic evidence of a

Palliative treatment for heart base tumours, for example pericardiectomy

The anaesthetised dog was positioned in right lateral recumbency. After

Although most heart base tumours cause clinical signs of pericardial

In this patient, CT imaging illustrated collateral blood flow bypassing the

Clinical and echocardiographic findings were diagnostic of endocarditis,

Diagnosis of endocarditis should be made using the modified Duke

■ Echocardiographic valve lesion with typical

■ Pyrexia of unknown origin*

Endocarditis is a challenging diagnosis to make, and cases often present

Blood cultures may be negative in dogs with endocarditis owing to recent

Sinus rhythm originates in the sinoatrial node, located at the junction

Arrhythmias can occur because of four main mechanisms:

Commonly encountered arrhythmias in veterinary practice are:

Arrhythmias are a common complication of heart disease but may also be

FIGURE 1. Sixty-second electrocardiographic strip in lead II showing a background sinus rhythm

No further syncope had occurred, and the patient was no longer

Holter electrocardiography should be used as a monitoring tool to assess

Although ventricular tachycardia is a common feature of dilated

The decision to treat with anti-arrhythmic drugs should be taken based on

Up to 90 % day-to-day variability in the frequency of ventricular