Acquired heart disease

A. Infective endocarditis
B. Rheumatic heart disease
C. Physiologic/functional murmurs
D. General principle of
management of CHF
• E. Viral myocarditis
Infective Endocarditis

. acute and subacute bacterial

endocarditiS.
. nonbacterial endocarditis caused by
viruses, fungi, and other microbiologic
agents.
• intravenous drug users, survivors of cardiac
surgery, patients taking immunosuppressant
medications, and patients who require chronic
intravascular catheters.
• Many patients get endocarditis on what was
thought to be a previously healthy native
valve.
• endocarditis from oral flora may occur
without a preceding dental procedure.
• ETIOLOGY.
• Viridans-type streptococci (α-hemolytic
streptococci) and Staphylococcus aureus are
the leading causative agents for endocarditis
in pediatric patients.
• In ≈6% of cases, blood cultures are negative
for any organisms ( Many patients with
culture-negative endocarditis have Q fever
(Coxiella burnetii) or Bartonella species.
• No relationship exists between the infecting
organism and the type of congenital defect,
the duration of illness, or the age of the child.
• Staphylococcal endocarditis is more common
in patients with no underlying heart disease;
viridans group streptococcal infection is more
common after dental procedures;
• group D enterococci are seen more often after
lower bowel or genitourinary manipulation;
Pseudomonas aeruginosa or Serratia marcescens
is seen more frequently in intravenous drug
users.
• fungal organisms are encountered after open
heart surgery. Coagulase-negative staphylococci
are common in the presence of an indwelling
central venous catheter.
• Bacterial Agents in Pediatric Infective
Endocarditis
• COMMON: NATIVE VALVE OR OTHER
CARDIAC LESIONS  Viridans group
streptococci (S. mutans, S. sanguis, S.
mitis)  Staphylococcus aureus,  Group D
streptococcus (enterococcus) (S. bovis, S.
faecalis)
• UNCOMMON: NATIVE VALVE OR OTHER
CARDIAC LESIONS  
• Streptococcus pneumoniae 
•  Haemophilus influenzae 
•  Coagulage-negative staphylococci 
•  Coxiella burnetii (Q fever)
• Neisseria gonorrhoeae  
• Brucella
•  Chlamydia psittacli
•  Chlamydia trachomatis
• Chlamydia pneumoniae
•  Legionella
•   Bartonella
• The HACEK group includes
Haemophilus species
• H. paraphrophilus,
• H. parainfluenzae,
• H. aphrophilus
• Actinobacillus
• actino-mycetemcomitans,
• Cardiobacterium hominis,
• Eikenella corrodens, and
• Kingella species.
• Streptobacillus moniliformis
•  Pasteurella multocida
•  Campylobacter fetus  
• Culture negative (6% of cases)
prosthetic valve   
• Staphylococcus epidermidis  
•   Staphylococcus aureus   
• Viridans group streptococcus   
• Pseudomonas aeruginosa
• Serratia marcescens  
•   Diphtheroids  
•   Legionella species 
•   HACEK group  
• Fungi
EPIDEMIOLOGY.
• Infective endocarditis is often a complication
of congenital or rheumatic heart disease but
can also occur in children without any
abnormal valves or cardiac malformations.
• Endocarditis is rare in infancy; in this
age group, it usually follows open
heart surgery or is associated with a
central venous line.
• Vegetations usually form at the site
of the endocardial or intimal erosion
that results from the turbulent flow.
Children with ventricular septal
defects (VSDs)
• In ≈30% of patients with infective
endocarditis, a predisposing factor is
recognized. A surgical or dental
procedure can be implicated in ≈65% of
cases in which the potential source of
bacteremia is identified.
Manifestations of Infective endocarditis
• HISTORY  
•   Prior congenital or rheumatic heart
disease   
• Preceding dental, urinary tract, or
intestinal procedure   
• Intravenous drug use   
• Central venous catheter   
• Prosthetic heart valve
SYMPTOMS   
• Fever, Chills,  Chest and abdominal
pain , Arthralgia, myalgia
• Dyspnea  
•   Malaise
•    Night sweats
•    Weight loss
•    CNS manifestations (stroke,
seizures, headache)
SIGNS   
• Elevated temperature   
• Tachycardia   
• Embolic phenomena (Roth spots,
petechiae, splinter nail bed
hemorrhages, Osler nodes, CNS or
ocular lesions)
• Janeway lesions  
•  New or changing murmur   
• Splenomegaly   
• Arthritis   
• Heart failure   
• Arrhythmias
• Metastatic infection (arthritis,
meningitis, mycotic arterial
aneurysm, pericarditis, abscesses,
septic pulmonary emboli)   
• Clubbing
LABORATORY  
•   Positive blood culture  
•   Elevated erythrocyte sedimentation
rate; may be low with heart or renal
failure  
•   Elevated C-reactive protein  
•   Anemia
• Leukocytosis   
• Immune complexes   
• Hypergammaglobulinemia
•    Hypocomplementemia   
• Cryoglobulinemia
• Rheumatoid factor   
• Hematuria  
•   Renal failure: azotemia, high
creatinine (glomerulonephritis)
• Chest radiograph: bilateral
infiltrates, nodules, pleural effusions
 
•   Echocardiographic evidence of
valve vegetations, prosthetic valve
dysfunction or leak, myocardial
abscess,
• new-onset valve insufficiency
• DIAGNOSIS.
The Duke criteria help in the diagnosis
of endocarditis. Major criteria
include (1) positive blood cultures
• two separate cultures for a usual
pathogen, two or more for less
typical pathogens) and (2) evidence
of endocarditis on echocardiography
(intracardiac mass on a valve or
other site,
 regurgitant flow near a prosthesis,
abscess, partial dehiscence of
prosthetic valves, or new valve
regurgitant flow). Minor criteria
include predisposing conditions,
• fever
• embolic-vascular signs,
• immune complex phenomena
(glomerulonephritis, arthritis,
rheumatoid factor, Osler nodes,
Roth spots),
• a single positive blood culture
• serologic evidence of infection, and
echocardiographic signs not meeting
the major criteria.
• Two major criteria,
• one major and three minor, or five
minor criteria suggest definite
endocarditis.
• minor criteria
• the presence of newly diagnosed
clubbing,
• splenomegaly,
• splinter hemorrhages,
• petechiae;
• high C-reactive protein level;
• microscopic hematuria.
• PROGNOSIS AND COMPLICATIONS.
heart failure caused by vegetations
involving the aortic or mitral valve.
Myocardial abscesses and toxic
myocarditis .
• Systemic emboli,
• Pulmonary emboli
• mycotic aneurysms, meningitis,
osteomyelitis, arthritis, renal
abscess, and immune complex–
mediated glomerulonephritis.
• PREVENTION.
• Antimicrobial prophylaxis before
various procedures and other forms
of dental manipulation may reduce
the incidence of infective
endocarditis.
• Proper general dental care and oral
hygiene are most important in
decreasing the risk of infective
endocarditis in susceptible individuals.
Vigorous treatment of sepsis and local
infections .
•
• Rheumatic Heart Disease
 Acute rheumatic fever (ARF) is a
nonsuppurative sequela that occurs
two to four weeks following group A
streptococcus pharyngitis.
• EPIDEMIOLOGY — In developing
areas of the world, acute rheumatic
fever and rheumatic heart disease
are estimated to affect nearly 20
million people and are the leading
causes of cardiovascular death
during the first 5 decades of life .
Rheumatogenic strains — The
observation in some studies that only
a few M serotypes (types 3, 5, 6, 14,
18, 19, 24, and 29) were implicated in
outbreaks of rheumatic fever in the
United States suggested a particular
"rheumatogenic" potential of certain
strains of GAS [7,14-16]
• PATHOGENESIS — The pathogenic
mechanisms that lead to the
development of acute rheumatic fever
remain incompletely understood.
• Clearly streptococcal pharyngeal
infection is required, and genetic
susceptibility may be present.
• molecular mimicry is thought to play
an important role in the initiation of
the tissue injury .
Streptococcal pharyngitis may be
diagnosed in one of the following
ways:
1.Positive throat culture for group A
beta-hemolytic streptococci
2.Positive rapid streptococcal antigen
test.
3. Elevated or rising antistreptolysin O
antibody titer.
CLINICAL MANIFESTATIONS
Acute illness — Acute rheumatic fever
occurs most frequently in children
from 5 to 15 years of age; it is rare
among children in the first three
years of life and among adults.
Jones Criteria
Acute rheumatic fever is
characterized by group A
streptococcal infection followed by
clinical manifestations outlined
below .
The five major manifestations are:
1.Migratory arthritis (predominantly
involving the large joints)
2.Carditis and valvulitis (eg,
pancarditis)
3.Central nervous system involvement
(eg, Sydenham chorea)
4. Erythema marginatum
5. Subcutaneous nodules
The four minor manifestations are:
Arthralgia
• Fever
• Elevated acute phase reactants
[erythrocyte sedimentation rate
(ESR), C-reactive protein (CRP)]
• Prolonged PR interval
• Mitral insufficiency is the result of
structural changes that usually
include some loss of valvular
substance and shortening and
thickening of the chordae tendineae.
• Clinical Manifestations.
high-pitched holosystolic murmur at
the apex .
The heart is enlarged, with a heaving
apical left ventricular impulse and
often an apical systolic thrill.
Complications.
• atrial fibrillation, or infective
endocarditis.
• right ventricular failure and atrial
and ventricular arrhythmias.
Treatment.
• In patients with mild mitral
insufficiency, prophylaxis against
recurrences of rheumatic fever is all
that is required.
• MITRAL STENOSIS
• Pathophysiology
• Clinical Manifestations.
• AORTIC INSUFFICIENCY.
• TRICUSPID VALVE DISEASE.
• PULMONARY VALVE DISEASE
 functional, normal, insignificant, or
innocent murmur
• Non basal circumstances (high
cardiac output because of fever,
infection, anxiety).
 .
• The most common innocent murmur
is a medium-pitched, vibratory or
“musical,” relatively short systolic
ejection murmur, which is heard best
along the left lower and midsternal
border.
• A venous hum is another example of
a common innocent murmur heard
during childhood. Such hums are
produced by turbulence of blood in
the jugular venous system.
• General principles of management of
CHF
• Diet.
• Digitalis.
• Diuretics.
• After load-Reducing Agents and ACE
Inhibitors.
• Dopamine is a predominantly β-
adrenergic receptor agonist, but it
has α-adrenergic effects at higher
doses.
Viral myocarditis
• adenovirus,
• coxsackievirus B, and other
enteroviruses, although most known
viral agents have been implicated.
PATHOPHYSIOLOGY.
• Acute viral myocarditis may produce a
fulminant inflammatory process characterized
by cellular infiltrates, cell degeneration and
necrosis, and subsequent fibrosis.
• The net final result of chronic viral-
associated inflammation is often
dilated cardiomyopathy.
• CLINICAL MANIFESTATIONS.
• CLINICAL MANIFESTATIONS.
• Signs and symptoms depend on the
patient's age and the acute or
chronic nature of the infection.
• DIAGNOSIS.
• The sedimentation rate, heart
enzymes (creatine phosphokinase,
lactate dehydrogenase), and brain
natriuretic peptide (BNP) may be
elevated in acute or chronic
myocarditis.
• DIFFERENTIAL DIAGNOSIS.
• carnitine deficiency, hereditary
mitochondrial defects, idiopathic
dilated cardiomyopathy, pericarditis,
fibroelastosis of the endocardium,
and anomalous origin of the left
coronary artery
• TREATMENT.
• The approach to treating acute
myocarditis involves supportive
measures for severe congestive
heart failure or cardiogenic shock .
• PROGNOSIS.
• The outcome of symptomatic
neonates with acute viral
myocarditis has been poor. Patients
with lesser symptoms have a better
prognosis, and complete resolution
has been described.