RHEUMATIC

HEART
DISEASE
Presented by
Dr. Thein Tun
2nd Dr.D.Sc (Oral Medicine)

RHEUMATIC HEART DISEASE

Rheumatic fever is a post-streptococcal immunemediated inflammatory disease affect heart and
extra-cardiac sites e.g. joints, skin, brain.
The incidence and mortality of rheumatic fever
has declined over the past 30 years (due to
improved socioeconomic condition and rapid
diagnosis and treatment of strep. pharyngitis).

Pathogenesis
An acute attack of streptococcal pharyngitis by

group A beta-hemolytic streptococci.

Within 2-4 weeks after this attack anti-streptococcal

antibodies are formed and attack the heart and the

extra-cardiac sites.
The mechanism of this immune reaction is not yet

understood, however, the most accepted hypothesis

is antigenic similarity hypothesis.
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The disease passes into two phases;

A. Acute phase
- acute rheumatic pancarditis (inflammation of
endocardium, myocardium and pericardium)
1.
2.
3.

Myocarditis.
Pericarditis: "bread and butter", due to fibrinous
inflammation
Endocarditis: edema, inflammation and fibrin
deposits on valve leaflets (vegetations) along lines
of closure. Mostly mitral and aortic valves.
Aschoff nodules are uncommon in the valves.
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B. Chronic phase
Acute changes may resolve completely or progress
to scarring and development of chronic valvular
deformities many years after the acute disease.

Clinical features of Acute Rheumatic

Fever
Occurs 10 days to 6 weeks after pharyngitis
Peak incidence: 5-15 years.
Cardiac manifestations: pericardial friction rubs, weak heart

sounds, tachycardia and arrhythmias.

Extra-cardiac: fever, migratory polyarthritis of large joints,

arthralgia, skin lesions, chorea.

Pharyngeal culture may be negative, but anti streptolysin O

(ASO) titer will be high.

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CHRONIC RHEUMATIC
HEART DISEASE

Endocarditis heals by progressive fibrosis. Chronic scarring of the

valves constitutes the most important long-term sequelae of
rheumatic fever, and usually becomes clinically manifest decades
after the acute process.
Left sided valves (mitral and aortic) are more commonly

involved than the right.

Fibrosis of valve leaflets --> stenosis.

Fibrosis of chordae tendonae --> regurgitation

(improper closure).

Other cardiac complications:

1.

Subacute bacterial endocarditis.

2.

Arrhythmia.

3.

Chronic heart failure

Mitral valve stenosis:

Leads to left atrial dilatation and failure, chronic

venous congestion of the lung, lung fibrosis,

pulmonary hypertension and chronic right sided heart
failure.

Mitral valve incompetence:

Leads

to left ventricular dilatation and failure, left

atrial dilatation and failure, chronic pulmonary

congestion, lung fibrosis, pulmonary hypertension
and chronic right sided heart failure.

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Infective Endocarditis

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Definition: infection of the cardiac valves or mural

surface of the endocardium, resulting in the
formation septic vegetations (thrombi).
Divided into:
a. Acute infective endocarditis.
b. Subacute infective endocarditis.
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Acute infective endocarditis

Etiology:
Acute suppurative inflammation that affects

healthy valves.

Organisms: Highly virulent as staph. Aureus,

strept.hemolyticus and gonococci.

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Lesions

Mitral & aortic valves are most commonly affected.

Tricuspid is affected in IV drug abusers.

The mural endocardium may be also affected.

The affected valve and mural endocardium show

acute suppurative inflammation + vegetations.

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Complications
1. Embolic complications:
Detached septic vegetations leads to
systemic pyemia.
2. Toxemic complications:
Severe toxemia

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Prognosis
Rapidly fatal due to;
1. Severe toxemia (septicemia).
2. Cusp perforation (acute heart failure).

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Subacute infective endocarditis

Etiology:
Subacute

inflammation that affects abnormal

valves in;

Rheumatic valvulitis
Congenitally abnormal valves.
Prosthetic valves.

Caused

by Less virulent bacteria as

strept.viridans

Lesions

Mitral & aortic valves are commonly affected.

The mural endocardium may be also affected

The affected valve and the mural endocardium

show; the lesion of the corresponding disease (e.g.
rheumatic, congenital) + vegetations.

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Complications
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1. Embolic complications:
Infarctions: in kidney, spleen and brain, retina, heart.
Mycotic aneurysms: mainly in cerebral and mesenteric.
Petechial hemorrhage: in skin, mucous membranes and

serous membranes.
Oslers nodules: small. tender, intracutaneous nodules in
pulps of fingers & toes.

2. Toxemic complications:
Moderate toxemia: fever, anemia, clubbing of fingers,

splenomegaly, petechial hemorrhage and focal

glomerulonephritis (flea bitten kidney)

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Prognosis
Heal by fibrosis leads to valve lesion either stenosis or

incompetence.

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Thank you

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