Vet Clin Equine 18 (2002) 575–589

Cardiac disease in the geriatric horse

Abby M. Sage, VMD, MS
University of Minnesota College of Veterinary Medicine,
225 Veterinary Teaching Hospitals, 1365 Gortner Avenue, St. Paul, MN 55108, USA

Almost all equine cardiac diseases may affect the geriatric horse. This
article focuses on those cardiac diseases that are most common in the older
horse, including degenerative valve disease, aortocardiac fistula, and con-
gestive heart failure. Other cardiac diseases, such as bacterial endocarditis,
pericarditis, and arrhythmias, are seen in all age groups of horses and are
beyond the scope of this article.

Degenerative valvular disease

Any condition that reduces valvular coaptation by means of a change in
the structure of the valve or valve apparatus produces regurgitation. Degen-
erative lesions resulting in regurgitation of the atrioventricular and semi-
lunar valves are the most common cause of valvular disease in the geriatric
horse [1–3]. The etiology of degenerative valve disease is unknown. There is
a degeneration of collagen in the fibrosa of the valve and proliferation of
loose fibroelastic tissue in the spongiosa of the valve [4]. The lesions also
have histiocyte, lymphocyte, and fibroblast infiltration of the superficial
layers of the endocardium [5]. Degenerative lesions appear as either gener-
alized or discrete fibrous thickening and rounding of the free borders of the
valve leaflets, which may form nodules [2,6].
The mitral and aortic valves are more frequently affected than the tricus-
pid and pulmonary valves [2]. The higher pressures and forces on the left
side of the heart may predispose the aortic and mitral valves to develop
lesions [2,6]. Thickening of the valve cusps can interfere with closure and
result in regurgitation [6]. Ruptured chordae tendineae can occur sponta-
neously or secondary to degenerative disease. Chordae tendineae rupture
occurs either at the insertion of the chordae into the papillary muscle or
valve leaflet or within the chordae.

E-mail address: sagex004@umn.edu (A.M. Sage).

0749-0739/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved.
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576 A.M. Sage / Vet Clin Equine 18 (2002) 575–589

Mitral regurgitation
Clinical signs
Mitral regurgitation is the most likely of the acquired valvular lesions to
result in clinical signs. Murmurs of mitral regurgitation are usually holosys-
tolic or pansystolic, plateau (band)-shaped, grade III/VI or louder (but can
be grade I or II), and coarse or honking in quality. The murmurs have a
point of maximal intensity at the left atrioventricular valve or aortic valve
area radiating dorsally and caudally [3,6,7].
Mitral regurgitation may be clinically insignificant at the time of exami-
nation and may remain so in some cases for the life of the horse. Because the
pressure in the left ventricle is higher than that in the right ventricle, mitral
regurgitation is the most likely of the valvular regurgitations to progress to
cause clinical signs. The speed of development of clinical signs is based on
the etiology and severity of the mitral regurgitation [6]. In slowly progressive
regurgitation, the first clinical sign observed is exercise intolerance and pro-
longed recovery from exercise. Excessive exercising respiratory and heart
rates, inability to perform at the previous level of exercise, coughing, and
excessive sweating with exercise are observed. Horses with clinical signs of
mitral regurgitation also have increased respiratory and heart rates and rec-
tal temperatures during recovery from exercise that take longer to return to
normal levels. These horses may not show clinical signs at rest other than a
cardiac murmur.
Severe mitral regurgitation produces elevated left atrial pressures and
pulmonary hypertension. Pulmonary hypertension can lead to pulmonary
edema. Signs of left heart failure and pulmonary edema in the horse may
occur without signs of right-sided failure. The signs may be subtle. Exercise
intolerance, coughing, and an increased respiratory rate at rest may be con-
fused with chronic obstructive airway disease, especially in the older horse.
Thoracic auscultation with a rebreathing bag should always be performed
during cardiac evaluation of the horse. Pulmonary edema presents with
coarse vesicular sounds and crackles in the lung field [3]. Cardiac ausculta-
tion reveals a cardiac murmur consistent with mitral regurgitation, and
tachycardia is usually present [3]. Horses with severe acute mitral regurgita-
tion, such as that which develops secondary to rupture of a major chordae
tendineae, may present with foamy nasal discharge or coughing and may
expel copious quantities of foamy fluid from the lungs [6,8]. Most horses
with pulmonary edema that develops slowly do not have a foamy nasal dis-
charge.
Horses with severe mitral regurgitation may also present with signs of
right heart failure, because the increased left atrial pressure is transmitted
through the lungs to the pulmonary artery and right ventricle. Signs consis-
tent with right heart failure are tachycardia, venous distention, jugular vein
pulsation, and peripheral edema.
 A.M. Sage / Vet Clin Equine 18 (2002) 575–589 577

Elevations in left atrial pressure secondary to mitral regurgitation may

result in an increase in left atrial diameter. Horses with increased left atrial
diameter are at increased risk for the development of atrial fibrillation.
Atrial fibrillation with mitral insufficiency suggests atrial dilation. The most
common pathologic and echocardiographic abnormalities seen in horses
with atrial fibrillation are abnormalities of the mitral valve [2,9].

Electrocardiography
The electrocardiogram is not useful in the horse for evaluating chamber
enlargement because of the explosive nature of the depolarization of the left
ventricle. Arrhythmias like atrial fibrillation may be present as a result of left
atrial enlargement and atrial myocardial disease [3,6]. Other arrhythmias like
ventricular premature beats or ventricular tachycardia may reflect a myocar-
ditis [3]. ST segment depression has been reported in horses with chordae rup-
ture and may indicate myocardial ischemia as is seen in human beings [6].

Pathophysiology
The amount of regurgitation is dependent on the size of the regurgitant
orifice, the gradient of pressure between the left ventricle and left atrium,
and resistance of blood flow in the aorta (afterload). In mitral regurgitation,
the mitral valve is incompetent, and a portion of the left ventricular stroke
volume regurgitates into the left atrium. The increased blood volume in the
left atrium flows into the left ventricle, producing left ventricular volume
overload and dilation [6]. Changes in the position of the papillary muscles
and the chordae tendineae and enlargement of the diameter of the valve
annulus worsen the valve coaptation and increase the regurgitation [6]. In
chronic slowly progressive mitral regurgitation, the left atrium has time to
adjust to the increased blood volume and pressure. As the left atrium
stretches, there is only a small rise in pressure. In cases of acute severe regur-
gitation, the left atrium does not have time to accommodate the high volume
or pressure. The left atrium is noncompliant. The excessive pressure in the
left atrium is transferred retrograde to the pulmonary vasculature, and pul-
monary edema develops quickly [10]. These cases may present with foamy or
frothy nasal discharge. The high pressures may also be transferred to the
pulmonary artery and right heart, resulting in signs of right heart failure.
Signs of right heart failure with few signs of left heart failure are more likely
to develop in horses with chronic and severe mitral regurgitation. Horses
that develop acute severe mitral regurgitation are more likely to present with
signs of left heart failure [3].
The increased volume in the left atrium secondary to mitral regurgitation
flows into the left ventricle in diastole. The third heart sound, S3, audible in
normal horses, is caused by the high diastolic ventricular filling rate. An
increase in the volume and duration of S3 occurs in horses with significant
578 A.M. Sage / Vet Clin Equine 18 (2002) 575–589

mitral regurgitation [3,6,8]. S3 may vary in intensity as blood pressure varies

[6]. Horses with an enlarged left atrium are predisposed to the development
of atrial fibrillation.

Echocardiography
Echocardiography is used to diagnose mitral regurgitation, semiquanti-
tate its severity, and formulate a prognosis. Spectral and color flow Doppler
are used to map the size and location of the regurgitant jet. Doppler echo-
cardiography of the mitral valve is performed from the left parasternal long
axis view [7,11,12]. If the regurgitant jet is small, of brief duration, and lim-
ited to a small area behind the valve leaflets, it is thought to be a normal
physiologic finding and does not represent a manifestation of subclinical
valvular disease [12,13]. The regurgitant jet seen in horses with cardiac mur-
murs compatible with mitral regurgitation seen on color flow Doppler was
longer in duration than that in the normal horse but similar in length, width,
area, and time of onset [12]. The median durations of the high-velocity sig-
nals in horses with clinical signs of mitral regurgitation were five times lon-
ger than the signals recorded in the normal horses. The severity of mitral
regurgitation can be assessed based on the size of the jet in the left atrium.
The jet was considered clinically insignificant (1þ) if it was only detected
immediately behind the valve, mild (2þ) if the jet occupied one third or less
of the left atrial chamber, moderate (3þ) if the regurgitant jet occupied more
than one third or two thirds or less of the left atrium, and severe (4þ) if the
regurgitant jet occupied more than two thirds of the left atrium [3]. The
regurgitant jet may also spread along the walls of the atria rather than in the
center of the atria, making detection of the severity of the jet difficult [7].
In significant mitral regurgitation, both left atrial and ventricular enlarge-
ment is present [3]. The severity of the enlargement is dependent on the
amount and duration of the regurgitation. Rounding of the left ventricular
apex suggests left ventricular volume overload. The left parasternal two-
chamber view of the left atrium provides the best image to measure left atrial
diameter. In this view, the maximal diameter of the left atrium should not
exceed 13.5 cm [7]. The ratio of the aortic root diameter to the left atrial
appendage obtained in the M-mode aortic root view should normally be less
than 1. This measurement is not as sensitive as the maximal atrial diameter
obtained from the left parasternal two-chamber view [3]. Elevated left atrial
pressures are seen as a turgid round appearance of the left atrium and bulg-
ing of the interatrial septum to the right [3].
Dilation of the pulmonary artery is an indicator of pulmonary hyperten-
sion [3]. The pulmonary artery diameter obtained in the two-dimensional
right parasternal view of the right outflow tract should be less than or equal
to the aortic diameter obtained in the right parasternal view of the left out-
flow tract [3]. If the pulmonary artery diameter exceeds the aortic diameter,
pulmonary hypertension is present. Horses with pulmonary hypertension
 A.M. Sage / Vet Clin Equine 18 (2002) 575–589 579

are at risk for sudden death secondary to rupture of the pulmonary artery
[3]. A smaller than normal aortic diameter is compatible with low left ven-
tricular output and left heart failure [3].
Fractional shortening may not be decreased in horses with mitral regur-
gitation [1,3]. In moderate to severe mitral regurgitation, the fractional
shortening should increase to greater than normal because of the increased
left ventricular volume and decreased afterload [1,7]. A normal or less than
normal fractional shortening is indicative of poor myocardial contractility
[1,3,7].

Prognosis
The prognosis for horses with mitral regurgitation is based on the dura-
tion, etiology, and severity of the regurgitation; the extent of chamber
enlargement; myocardial contractility; and clinical signs at the time of pre-
sentation. If the left atrium is normal sized or the degree of left atrial and left
ventricular enlargement is small and the regurgitation is mild to moderate,
the regurgitation is likely to progress slowly [7]. With moderate regurgita-
tion, chamber enlargement, and volume overload, the regurgitation is likely
to progress over several years [7]. Horses with no lesions on the valve leaflets
detected echocardiographically are most likely to have clinically insignifi-
cant to mild mitral regurgitation that remains unchanged or worsens slightly
over years [7]. Degenerative lesions on the mitral valve detected echocar-
diographically are usually associated with clinically insignificant to severe
regurgitation that progressively worsens over several or more years [7]. Flail
valve leaflets and ruptured chordae tendineae are often associated with
degenerative lesions [7]. If a ruptured chordae tendineae involves the septal
or free wall leaflet, acute severe mitral regurgitation and congestive heart
failure often result as a result of sudden volume overload of the left atrium
and ventricle [3,6,8]. If the ruptured chordae tendineae involves an accessory
leaflet, the horse may only have mild to moderate regurgitation initially that
tends to worsen progressively over a few years [8].

Aortic regurgitation
Clinical signs
Aortic regurgitation is most common in horses older than 10 years of age
because it is usually a result of degenerative valve disease [7]. Aortic regur-
gitation is characterized by a grade I to VI/VI holodiastolic decrescendo
murmur with a point of maximal intensity in the left fourth intercostal
space. Aortic regurgitation murmurs often have a musical or honking qual-
ity as a result of vibration of the valve leaflets. They often radiate toward the
cardiac apex [7]. Some horses tolerate even severe regurgitation of the aortic
valve well and do not show clinical signs. Bounding peripheral pulses are
a sign of severe aortic regurgitation and left ventricular volume overload
580 A.M. Sage / Vet Clin Equine 18 (2002) 575–589

[7,14]. The difference in systolic and diastolic pressure is responsible for the
strength of the peripheral pulse. The diagnosis of aortic regurgitation is
often facilitated by palpation of the submandibular artery pulse while simul-
taneously auscultating the heart on the left side. The dramatic fall in pulse
coincides with the murmur, allowing the practitioner to easily differentiate
the diastolic murmur of aortic regurgitation from a systolic murmur. The
left ventricular volume overload produces an elevated systolic blood pres-
sure, and the rapid run off of blood from the aorta in diastole produces
a low diastolic blood pressure.

Pathophysiology
Aortic regurgitation results in an increase in the amount of blood
pumped by the left ventricle. The increased blood volume in the left ventricle
causes an increase in the contractility of the ventricle as explained by the
Frank-Starling principle. Horses with aortic regurgitation with normal myo-
cardial function have a fractional shortening that is greater than normal
[14]. Moderate to severe aortic regurgitation causes left ventricular volume
overload and dilation. If dilation of the left ventricle is severe, contractility
and fractional shortening decrease. At this point, fractional shortening falls
into the normal range (30%–40%) [7,14]. If the aortic regurgitation increases
further, the left ventricle begins to fail and fractional shortening drops below
normal [7,14]. In severe aortic regurgitation, the left ventricular volume
overload may progress enough to cause dilation of the mitral valve annulus
and mitral regurgitation. Severe left ventricular volume overload and dila-
tion may also result in ruptured chordae tendineae. Horses with aortic and
mitral regurgitation have a poor prognosis, because the mitral regurgitation
is usually progressive and often leads to left heart failure.

Echocardiography
Abnormalities of the aortic cusps may not always be detected echocardio-
graphically [14]. If visible, degenerative lesions of the aortic valve cusps
appear thickened with an increase in echogenicity [14].
Moderate to severe aortic regurgitation results in left ventricular volume
overload. The left ventricle is measured in M-mode from the right paraster-
nal, short axis, four-chamber view. An end diastolic left ventricular diameter
greater than 12.5 cm suggests left ventricular dilation [14]. A septal-to–E
point distance greater than 1.0 cm reflects dilation of the left ventricular out-
flow tract [1,7,14]. In left ventricular dilation, the interventricular septum
and left ventricular free wall may become thin [1,7,14]. Fractional shor-
tening should be greater than normal in horses with normal myocardial
function. A normal or decreased fractional shortening is indicative of myo-
cardial dysfunction [7,14]. The aortic root becomes dilated in moderate to
severe aortic regurgitation most likely because of increased blood flow into
the aorta [7,14]. Premature closure of the mitral valve may occur in cases of
 A.M. Sage / Vet Clin Equine 18 (2002) 575–589 581

severe regurgitation as a result of volume overload [1]. In addition, the

septal leaflet of the mitral valve may have high-frequency diastolic flutter
visible on M-mode echocardiography [1,7,14].
Doppler echocardiography of the aortic valve can be performed from the
right parasternal long axis view of the left outflow tract, the right paraster-
nal short axis view of the aorta, or the left parasternal long axis view of the
left outflow tract. The most parallel flow signal is from the left parasternal
window [7]. Aortic regurgitation jets are either directed toward the left apex
or travel laterally toward the left ventricular free wall [13]. A sharp decline
(steep slope) in the continuous wave Doppler spectral tracing of the aortic
regurgitation indicates a rapid increase in left ventricular diastolic pressure
and severe aortic regurgitation [7]. The severity of regurgitation is deter-
mined by the distance the regurgitant jet travels into the left ventricular out-
flow tract and the width of the jet at its origin [7]. A regurgitant jet that
extends into more than two thirds of the left ventricular outflow tract
beyond the septal leaflet of the mitral valve is considered severe [7].

Prognosis
Because most horses do not develop aortic regurgitation until they are
middle-aged and because it usually progresses slowly, it rarely leads to con-
gestive heart failure or death [7]. Severe aortic regurgitation with secondary
mitral regurgitation caused by left ventricular volume overload and dilation
of the mitral valve annulus carries a poor prognosis. The mitral regurgita-
tion is usually progressive and may lead to left heart failure. Horses in left
heart failure with pulmonary hypertension are at risk for sudden death as a
result of pulmonary artery rupture [7].

Tricuspid regurgitation
Clinical signs
Tricuspid regurgitation is characterized by a holosystolic or pansystolic,
band-shaped, grade II/VI or louder, coarse or blowing murmur with a point
of maximal intensity at the right fourth intercostal space [7]. The murmur
often radiates dorsally.
Horses with tricuspid regurgitation rarely show clinical signs. If the tri-
cuspid regurgitation is mild to moderate, most horses do not have exercise
intolerance. Horses with severe tricuspid regurgitation may not be capable
of performing maximal exercise but may be useful as pleasure or show
horses [7]. Tricuspid regurgitation does not usually progress to heart failure,
except when it is secondary to left heart failure and pulmonary hyperten-
sion [7]. Signs of right heart failure as a result of tricuspid regurgitation are
generalized venous congestion, jugular vein pulsation, peripheral edema,
ascites, pleural effusion, and hepatic congestion.
582 A.M. Sage / Vet Clin Equine 18 (2002) 575–589

Echocardiography
Many horses with tricuspid regurgitation do not have valvular lesions
that can be detected echocardiographically [7]. Although ruptured chordae
tendineae and flail valve leaflets occur, they occur less commonly than on
the mitral valve [7]. In the normal horse, the right atrial size should be less
than the left atrial size in the right parasternal four-chamber view [7]. If tri-
cuspid regurgitation is moderate to severe, right atrial enlargement should
be present [1]. Volume overload of the right ventricle presents with right
ventricle enlargement and possible dilation [7]. In horses with normal cham-
ber sizes, the right ventricle is approximately one third the size of the left
ventricle in the right parasternal view of the left outflow tract and aorta
[7]. Paradoxic septal motion occurs when there is severe tricuspid regurgita-
tion and right ventricular volume overload [1].
A regurgitant jet that occupies more than two thirds of the atrium is con-
sidered severe [7]. Doppler echocardiography of the tricuspid valve is best
obtained from the right parasternal angled view, the right parasternal short
axis view of the pulmonary artery, and the right parasternal long axis view
of the aorta [12]. Regurgitant signals in the right atrium occur in normal
horses during systole but are five to eight times longer in duration and larger
in horses with cardiac murmurs associated with tricuspid regurgitation
[11,12].

Prognosis
Tricuspid regurgitation that is not secondary to pulmonary hypertension
and left heart failure usually is not progressive or slowly progresses over years
[7]. Horses with mild to moderate tricuspid regurgitation usually can perform
maximal exercise and show no clinical signs, except cardiac murmur. Horses
with severe tricuspid regurgitation are often useful as pleasure or show horses
but may not be able to perform maximal exercise [7]. Tricuspid regurgitation
that occurs secondary to left heart failure and pulmonary hypertension is pro-
gressive and often leads to right heart failure and death [7].

Pulmonic regurgitation
Clinical signs
Pulmonic regurgitation is rarely a primary valvular disorder but is more
likely to be associated with left heart failure, pulmonary hypertension, and
pulmonary artery dilation [7]. Even when abnormalities of the valve occur, a
characteristic murmur is not always heard presumably because of low right-
sided pressure [7]. Pulmonic insufficiency murmurs are usually holodiastolic,
decrescendo, and grade I to III/VI, with a point of maximal intensity over
the left third intercostal space [7]. Rarely, pulmonic insufficiency murmurs
are louder than a grade III murmur.
 A.M. Sage / Vet Clin Equine 18 (2002) 575–589 583

Echocardiography
In a case of severe pulmonic regurgitation, dilation of the right ventricle,
pulmonary artery dilation, and paradoxic septal motion indicative of right
ventricular volume overload were present [15], Diastolic fluttering of the tri-
cuspid valve may be seen on M-mode echocardiography.
Most horses do not have cardiac murmurs despite demonstration of
pulmonic regurgitant jets on color flow Doppler [7,11,13]. Pulmonic regur-
gitation is best examined with color flow Doppler from the left cranial hemi-
thorax. In severe regurgitation, the regurgitant jet occupies more than two
thirds of the right ventricular outflow tract and occupies a large cross-
sectional area at its origin [7]. A steep slope in the continuous wave Doppler
spectral tracing of the pulmonic regurgitation indicates a rapid increase in
right ventricular diastolic pressure and severe pulmonic regurgitation [7].

Prognosis
Horses with pulmonic regurgitation secondary to left heart failure have a
poor prognosis for life. Severe regurgitation secondary to primary valvular
disease, such as tearing of the valve cusp, also carries a grave prognosis
because of the development of right heart failure [15]. Horses with mild pul-
monic regurgitation and no right ventricular volume overload have a good
prognosis [7].

Aortocardiac fistulas
Aortocardiac fistulas arise after rupture of the right aortic sinus. The
aorta ruptures directly into the right atrium or ventricle or forms a fistu-
lous tract through the aortic ring or ventricular septum to the left or right
ventricle or right atrium. Stallions older than 5 years of age are most com-
monly affected [16]. There is no breed predilection.

Clinical signs
Horses with aortocardiac fistulas are presented in acute distress, often
with signs of abdominal pain. A continuous murmur is heard loudest on the
right. Eighty-five percent of horses experience monomorphic ventricular
tachycardia characterized by a rapid regular rhythm and jugular pulsation
[16]. Ventricular tachycardia most likely results from disruption of the nor-
mal conduction pathway in the interventricular septum by the fistula [16].
Bounding arterial pulses are a result of rapid run off from the aorta.

Pathophysiology
The etiology of the aortocardiac fistula has not been determined in the
horse. In human beings, a congenital defect in the media of the aorta and
584 A.M. Sage / Vet Clin Equine 18 (2002) 575–589

the annulus fibrosis of the aortic valve results in aortic sinus aneurysm rup-
ture [16]. A second presentation in human beings is characterized by an
acquired tearing of the aortic sinus without a previously existing aneurysm
[16]. Sinus of Valsalva aneurysms have been reported in the horse [17,18]. In
one study of seven horses with an aortocardiac fistula, only two horses had
evidence of aneurysmal dilation of the aorta [16].

Echocardiography
The defect in the wall of the aorta and the fistulous tracts can be detected
with echocardiography. Continuous blood flow through the defect into the
left or right ventricle or right atrium can be visualized with color flow Dop-
pler. Volume overload of the left and right ventricles is present. Depending
on the size and duration of the fistula, myocardial failure may be present
[16].

Prognosis
Horses can survive the initial tearing if intracardiac rupture occurs and
the concurrent arrhythmia is not fatal. Most horses survive for weeks to
months, although they may survive for longer than 1 year [16]. The volume
overload of the right and left ventricle leads to heart failure eventually.
Horses that survive have a risk of sudden death.

Congestive heart failure

Etiology
Heart failure in the geriatric horse most likely occurs as a result of
chronic valvular regurgitation as discussed previously. Severe regurgitation
can result in volume overload and subsequent dilation of the cardiac cham-
ber with reduced contractility. Primary myocardial disease may be caused
by nutritional deficiencies like vitamin E and selenium, toxicity (ionophore
or white snakeroot), viral or bacterial infections, or metabolic derange-
ments. Many cases of dilated cardiomyopathy in the horse are idiopathic.

Pathophysiology
In compensated heart failure caused by ineffective myocardial contractil-
ity, adaptive mechanisms of the cardiovascular system occur to sustain
adequate blood pressure and cardiac output. An initial fall in cardiac output
and blood pressure causes an increase in sympathetic activity and with-
drawal of parasympathetic activity. The sympathetic nervous system inner-
vates the myocardium directly, producing an increase in contractility, heart
rate, and cardiac output. Sympathetic innervation of the arteries and arte-
rioles results in vasoconstriction and an increase in blood pressure. Direct
 A.M. Sage / Vet Clin Equine 18 (2002) 575–589 585

sympathetic innervation and a decrease in the solute concentration at the

macula densa of the juxtaglomerular apparatus activate the rennin-angio-
tensin cascade. Angiotensin II acts as a powerful vasoconstrictor. Angioten-
sin II also acts on the adrenal cortex to release aldosterone, which produces
an increase in water and sodium resorption in the kidney. Increased blood
volume decreases venous resistance and increases preload. An increase in
preload increases end diastolic volume and, as explained by the Frank-Star-
ling mechanism, augments an increase in ventricular function and cardiac
output.
In decompensated heart failure caused by ineffective myocardial contrac-
tility, there is little or no further augmentation of stroke volume with
increasing filling pressures. Retrograde transmission of increased pressures
into the systemic and pulmonic vasculature produces edema. Vasoconstric-
tion increases afterload, which further decreases cardiac output. Tachycar-
dia from increased sympathetic drive decreases diastolic coronary blood
flow. Myocardial hypoxia and excessive ventricular wall stress as a result
of increased filling pressure contribute to the decline in stroke volume. The
inotropic and chronotropic responses to sympathetic adrenergic stimulation
and the increased work required to pump against the elevated afterload
increase myocardial energy expenditure and accelerate the rate of cell death.
Edema of the myocardial tissues produced by fluid retention contributes to
poor myocardial function and impairs oxygenation. Oxygenation is also
impaired by pulmonary edema.

Clinical signs
Heart failure associated with left-sided cardiac disease, such as aortic or
mitral regurgitation, may initially only present with signs referable to the left
heart. Left-sided heart failure is characterized by tachycardia, exercise intol-
erance, coughing, and an increased respiratory rate. Coarse vesicular sounds
and crackles in the lung field audible with a rebreathing bag are consistent
with pulmonary edema [3]. Foamy nasal discharge can be seen if pulmonary
edema occurs suddenly [6,8]. Some horses subsequently develop signs of
right heart failure, whereas others do not.
Venous distention, pectoral or ventral abdominal edema, jugular pulses
that extend greater than one third of the way up the neck, and tachycardia
are all signs of right heart failure. Ascites and pulmonary effusion may also
be present and are best assessed with ultrasonography.

Clinical pathology
In horses exhibiting signs of congestive heart failure, elevated creatinine
and liver enzymes reflect prerenal azotemia, poor renal perfusion, and con-
gestion of the liver [3]. The myocardial enzyme fraction of creatine kinase
(CK-MB/CK) and the myocardial isoenzyme of lactate dehydrogenase
586 A.M. Sage / Vet Clin Equine 18 (2002) 575–589

(HBDH) were elevated in 47% and 65% of 17 horses with severe mitral
regurgitation, respectively [3]. Elevation of myocardial isoenzymes suggests
myocardial injury or myocarditis [3]. Troponin has been used recently to
assess myocardial damage [19].

Treatment
The goals in the treatment of heart failure are to decrease fluid retention,
decrease afterload, improve contractility of the myocardium, and decrease
heart rate. Three classes of drugs are used: (1) cardiac glycosides, (2) diu-
retics, and (3) vasodilators.
Digoxin is the most commonly used cardiac glycoside in the horse. It is
relatively inexpensive and easy to administer, and the pharmacokinetics
have been established. The dosage for intravenous maintenance is 2.2 lg/
kg every 12 hours, and the dosage for oral maintenance is 11 lg/kg every
12 hours [20]. An initial maintenance dose (2.2 lg/kg) given intravenously
results in achievement of a therapeutic concentration more rapidly than oral
administration for a portion of the dosing interval. Larger loading doses
increase the chance of toxicity [20]. The therapeutic plasma concentration
of digoxin is between 0.5 and 2.0 ng/mL [21]. Because there is a narrow
safety margin between the therapeutic and toxic levels of digoxin and
because digoxin interacts with many commonly used medications, digitalis
toxicity may occur during treatment. The initial signs of digoxin toxicity are
anorexia, colic, and diarrhea caused by alterations in sympathetic tone. Car-
diac arrhythmias are a common and potentially life-threatening result of
digitalis intoxication. Close monitoring of the clinical response and plasma
digoxin concentration must be performed in treated horses to avoid toxicity.
The level at which clinical symptoms of toxicity show a rapid increase in
prevalence is at greater than 2.0 ng/mL. Some patients may show signs of
toxicity within the ‘‘therapeutic’’ range. Serum levels should be taken 3 days
after initiation of therapy, because individual animals vary in their response
[20,22]. Serum samples should be taken at the time of peak and trough con-
centrations, 2 and 12 hours, respectively, after the last dose is administered
[20]. There are many drugs that may potentially interact with digoxin. H2
blockers, bran, and albuterol may decrease blood levels of digoxin [23].
Propafenone, quinidine, verapamil, erythromycin, omeprazole, phenylbuta-
zone, and tetracycline may increase serum levels of digoxin [23,24]. When
using digoxin with another medication, frequent monitoring of serum levels
should be performed. Hypokalemia, hypomagnesemia, and hypocalcemia
make the patient more sensitive to the toxic effects.
Diuretics are used in the treatment of heart failure to combat water and
sodium retention by the kidneys. Diuretics reduce intravascular volume,
ventricular filling pressures (preload), and wall stress. Although they usually
do not cause a significant increase in cardiac output, diuretics do amelio-
rate the symptoms of congestive heart failure and may decrease the rate of
 A.M. Sage / Vet Clin Equine 18 (2002) 575–589 587

progression of cardiac chamber dilatation by reducing ventricular filling

pressure [25]. Diuretics should be used intermittently as needed because of
the acid-base and electrolyte disturbances that can be attributed to chronic
diuretic therapy.
The most commonly used diuretic in the horse is furosemide, an NAþ,
K , 2CL
symport inhibitor, previously referred to as a loop diuretic. The
þ

effects of furosemide on the cardiovascular system have been well docu-

mented in the normal horse. A decrease in plasma volume, right atrial pres-
sure, stroke volume, and cardiac output and an increase in systemic vascular
resistance occur acutely after administration. Chronic use of furosemide
may induce hypokalemia, hypochloremic alkalosis, hyponatremia, and
hypomagnesemia. These electrolyte disturbances increase the risk for devel-
opment of digoxin toxicity in patients treated with both drugs. Horses
treated with long-term digoxin and furosemide should have serum electro-
lytes monitored routinely. Supplementation with the appropriate diuretic
or change of diuretic is warranted if electrolyte disturbances are detected.
The dosage of furosemide in the horse is 1 mg/kg administered intrave-
nously, intramuscularly, or orally as needed, usually twice daily [24].
As cardiac output falls as a result of ineffective myocardial contractility,
activation of the renin angiotensin aldosterone system and an increase in
sympathetic nervous system activity produce venous and arterial vasocon-
striction. Excessive increases in preload and afterload cause increased energy
expenditure for an already failing heart. Venodilators provide an increase in
venous capacitance and decrease ventricular filling pressures, wall stress,
and preload. Arterial vasodilators provide a reduction in afterload, increas-
ing forward stroke volume. Most vasodilators exhibit activity on both arte-
rial and venous vascular beds, although some vasodilators show specificity
for certain segments of the vasculature [23].
All angiotensin-converting enzyme inhibitors prevent the conversion of
angiotensin I to angiotensin II, thereby attenuating the action of angiotensin
II. They not only produce vasodilatation by decreasing available angioten-
sin II but by increasing available bradykinin. They inhibit the release of
aldosterone from the adrenal cortex and decrease sodium and water ab-
sorption from the kidney, potentiating the effects of diuretics. By decreas-
ing preload wall stress and afterload, myocardial oxygen consumption is
increased. Angiotensin-converting enzyme inhibitors decrease the height-
ened stimulation of the sympathetic nervous system, decreasing heart rate
and vasoconstriction. Pharmacokinetics and dosage for the angiotensin-
converting enzyme inhibitors have not been established in the horse.
The mechanism of action of hydralazine is poorly understood. Hydral-
azine reduces afterload by reducing systemic and pulmonary vascular resist-
ance, resulting in an increase in forward stroke volume and a decrease in
ventricular wall stress [25]. Hydralazine has a direct positive inotropic activ-
ity on cardiac myocytes. It has little effect on venous resistance. Hydralazine
is commonly used for treatment of congestive heart failure in the horse. It is
588 A.M. Sage / Vet Clin Equine 18 (2002) 575–589

available in oral tablets. The recommended dosage in the horse is 0.5 to 1.5
mg/kg given every 12 hours orally [26].

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