VALVULAR HEART DISEASES

 Include a diverse group of congenital and

acquired lesions.
 Some occur in isolation while others in
association with other heart diseases.
Deformed cardiac valves may cause disease
by two mechanisms;
 Major haemodynaemic burden (stenosis
or regurgitation & sometimes a
combination
 Abnormal valves more susceptible to
infection and its complications
Causes:
1. Rheumatic heart diseases- already
covered
2. Connective tissue disorders
3. Bacterial endocarditis
4. Non-bacterial endocarditis
5. Calcific aortic stenosis
6. Mitral valve prolapse.
Lupus erythematosus
 Heart involved in systemic lupus
erythematosus (SLE)
 Most common lesion is fibrinous
pericarditis and myocarditis
 Endocarditis , most striking lesion,
producing verrucous vegetations(Libman-
Sacks endocarditis) found on mitral valve
 Usually heals without scarring
Scleroderma
 Involvement of the heart is second to
renal disease as a cause of death
 Myocardium shows intimal sclerosis of
small arteries, leading to small infarcts and
patchy fibrosis.
 Rarely may valves be involved.
Infective endocarditis
 Infection of cardiac valves or mural
surface of endocardium, with formation of
thrombotic mass with organisms
(vegetations)
 By far bacteria are the commonest
organisms.
 Divided into acute and sub-acute
endocarditis.
Acute endocarditis
 Infection of normal cardiac valves by
highly virulent , suppurative organisms.
◦ Staphylococcus aureus and streptococcal
pyogenes
 Cause rapidly progressive infection with
little accompanying local host reaction.
Subacute endocarditis
 Caused by less virulent organisms:
◦ Streptococcus viridans or Staphyloccus
epidermidis colonizing deformed valves
previously damaged.
 The infection tends to progress slowly
Epidemiology:
 The majority of children developing
endocarditis have underlying cardiac lesion
Congenital heart disease
Rheumatic heart disease .
 In adults mitral valve prolapse and congenital
heart disease are common causes
 Intravenous drug users at risk
 Prosthetic valves also a risk
Pathogenesis
 How virulent organisms infect normal
valves - mechanism not known.
 Infection by less virulent organisms:
 Haemodynaemic factors
Formation of initially sterile platelet and fibrin
thrombus
Adherence properties of microorganisms.
Pathology
 Most commonly involves the mitral ,
aortic or both valves
 In rheumatic carditis, mitral valve is
affected in more than 85 % by bacterial
endocarditis.
 Congenital heart diseases predisposing to
endocarditis include PDA, Tetralogy of
Fallot and VSD
Acute infective endocarditis
Acute Bacterial Endocarditis
(destroying aortic valve)

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 Vegetations:
◦ composed of platelets,
◦ fibrin,
◦ cell debris,
◦ and masses of organisms form on the valve
surface at point of closure of leaflets
Low power view –note colonies and
fibrin deposition
Blue colonies into myocardium
 Underlying valve becomes oedematous
and inflamed.
 Infected thrombo-emboli may cause
systemic embolism, with infarction and/or
abscesses in various organs
Clinical features
 Many patients manifest early symptoms
within a week of bacteraemic episode.
◦ Heart murmurs are heard, with a changing
pattern during course of the disease.
 Serious complication is CCF
 Splenomegaly, petichiae, clubbing of fingers
 Embolic phenomena to the brain in some.
NONBACTERIAL THROMBOTIC
ENDOCARDITIS ( MARANTIC
ENDOCARDITIS)
 The presence of sterile vegetations on
apparently normal cardiac valves
 Almost always in association with
advanced cancer or some wasting disease.
 Affects mitral and aortic valves equally
 Similar to infective endocarditis but does
not destroy affected valves.
 Microscopically no inflammation of
organisms demonstrated.
 Cause of disorder poorly understood, but
attributed to increased blood coagulability
or immune complex deposition.
 Commonly a paraneoplastic condition
seen in ;
◦ adenocarcinomas of lung and pancreas
◦ haematologic malignancies
 May also be part of DIC syndrome
accompanying debilitating nonneoplastic
diseases hence the synonym “marantic
endocarditis”= wasting away.

 Danger: embolization to brain, kidneys,

intestine and spleen
CALCIFIC AORTIC STENOSIS
 Narrowing of aortic valve as a result of
deposition of calcium in cusps and valve
ring.
 Occurs in a number of situations:
Elderly patients as a degenerative process
As a result of healed rheumatic heart disease
Congenital bicuspid aortic valve
Severe atherosclerosis of aorta.
 The dystrophic calcification produces
nodules in the lower half of the cusps.
 Severe aortic stenosis results in
concentric hypertrophy of left ventricle
 Later on the heart fails leading to CCF.
Calcified aortic stenosis-aortic valve
MITRAL VALVE PROLAPSE
 A condition where mitral valve leaflets fail
to approximate during systole, resulting in
mitral regurgitation.
 Caused by several factors, leading to
excessive mobility of mitral valve allowing
the valve to prolapse into the left atrium
during systole
Pathogenesis
 Has hereditary component- autosomal
dominant inheritance
 There is striking accumulation of
myxomatous connective tissue in centre
of valve leaflets
Grossly:
 Mitral valve redundant and deformed
 C/S gelatinous appearance
 Myxomatous proliferation involves valve
leaflets in addition to annulus and chordae
tendineae
 Chordae may severely be damaged with
rupture
Prolapse Mitral
Valve

Note long, thin chordae

tendinae

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Clinical features
 Majority entirely asymptomatic
 Endocarditis, both infective and
nonbacterial may occur
 Embolic phenomenon and mitral
regurgitation may occur.
End