Rheumatic fever can cause inflammation of the heart valves, known as rheumatic heart disease. Repeated attacks can lead to scarring of the valves over time, most commonly affecting the mitral and aortic valves. The main manifestations include mitral stenosis, mitral insufficiency, aortic insufficiency, and tricuspid valve disease. Symptoms vary depending on the severity of valve involvement and complications such as heart failure or pulmonary hypertension. Treatment involves medications to prevent future rheumatic fever attacks as well as surgical interventions like valve repair or replacement for severe cases.

1. RHEUMATIC HEART DISEASE

2.  Rheumatic involvement of the
valves and endocardium is the most
important manifestation of
rheumatic fever .
 The valvular lesions
Begin as small verrucae composed of
fibrin and blood cells along the borders
of one or more of the heart valves
As the inflammation subsides, the
verrucae tend to disappear and leave
scar tissue.

3.  With repeated attacks of rheumatic
fever, new verrucae form near the
previous ones, and the mural
endocardium and chordae tendineae
become involved
Valves involved
The mitral , followed by the aortic
valve;
Right-sided heart manifestations are
rare

4. Patterns of valvular disease
 MITRAL INSUFFICIENCY
 MITRAL STENOSIS
 AORTIC INSUFFICIENCY
 TRICUSPIDVALVE DISEASE
 PULMONARYVALVE DISEASE

5. MITRAL INSUFFICIENCY
Pathophysiology
 Mitral insufficiency is the result of some loss
of valvular substance and shortening and
thickening of the chordae tendineae.
 heart failure is caused by a combination of
mitral insufficiency coupled with
inflammatory disease of the pericardium,
myocardium, endocardium, and epicardium.
 Because of the high volume load and
inflammatory process, the left ventricle
becomes enlarged.
 The left atrium dilates as blood regurgitates
into this chamber.

6.  Increased left atrial pressure results
in pulmonary congestion and
symptoms of left-sided heart
failure.
 Spontaneous improvement usually
occurs with time, even in patients in
whom mitral insufficiency is severe
at the onset.
 The resultant chronic lesion is most
often mild or moderate in severity,
and the patient is asymptomatic.

7.  More than half of patients with acute
mitral insufficiency no longer have
the mitral murmur 1 yr later.
 In patients with severe chronic mitral
insufficiency, pulmonary arterial
pressure becomes elevated, the right
ventricle and atrium become
enlarged, and right-sided heart
failure subsequently develops

8. Clinical Manifestations
 The physical signs of mitral
insufficiency depend on its
severity.
 With mild disease,
 No signs of heart failure ,
 the prericordium is quiet,
 a high-pitched holosystolic murmur
at the apex that radiates to the
axilla.

9.  With severe mitral insufficiency,
 signs of chronic heart failure .
 The heart is enlarged,
 heaving apical left ventricular impulse
 an apical systolic thrill.
 accentuated 2nd heart sound if
pulmonary hypertension .
 A holosystolic murmur at the apex with
radiation to the axilla.

10. Investigation
Mild disease
 Normal electrocardiogram and roentgenograms
With more severe insufficiency,
 ECG
 prominent bifid P waves,
 signs of left ventricular hypertrophy,
 right ventricular hypertrophy if pulmonary
hypertension is present.
 CXR,
 prominence of the left atrium and ventricle
 Congestion of perihilar vessels,.
 Calcification of the mitral valve
 Echocardiography

11. Complications.
 cardiac failure
 precipitated by
 progression of the rheumatic process,
 the onset of atrial fibrillation,
 infective endocarditis.
The effects of chronic mitral
insufficiency may become manifest
after many years
 right ventricular failure
 atrial and ventricular arrhythmias

12. Treatment.
 Medical treatment
 In patients with mild mitral insufficiency,
 prophylaxis against rheumatic recurrences .
 Treatment of complicating
 heart failure ,
 arrhythmia
 infective endocarditis .
 Afterload-reducing agents (ACE inhibitors) may
 reduce the regurgitate volume
 preserve left ventricular function.
 Surgical treatment
 annuloplasty
 valve replacement

13. MITRAL STENOSIS
Pathophysiology.
 Mitral stenosis of rheumatic origin results from
 fibrosis of the mitral ring,
 commissural adhesions, and
 contracture of
 the valve leaflets,
 chordae, and
 papillary muscles over time.
 It takes 10 yr or more for the lesion to become
fully established, although the process may
occasionally be accelerated.

14.  Rheumatic mitral stenosis is seldom
encountered before adolescence and is not
usually recognized until adult life.
 Significant mitral stenosis results in
increased pressure and enlargement and
hypertrophy of the left atrium, pulmonary
venous hypertension, increased pulmonary
vascular resistance, and pulmonary
hypertension.
 Right ventricular and atrial dilatation and
hypertrophy ensue and are followed by
right-sided heart failure

15. Clinical Manifestations.
 The correlation between symptoms and
the severity of obstruction is good.
 Patients with mild lesions are
asymptomatic.
 More severe degrees of obstruction are
associated with exercise intolerance and
dyspnea.
 Critical lesions can result in
 orthopnea,
 paroxysmal nocturnal dyspnea,
 pulmonary edema,
 atrial arrhythmias.

16.  pulmonary hypertension
manifested by,
 functional tricuspid insufficiency,
 hepatomegaly,
 ascites,
 edema.
 Hemoptysis caused by
 rupture of bronchial and pleurohilar
veins
 pulmonary infarction

17. clinical manifestations (continued)
 increased Jugular venous pressure in
severe disease
 with heart failure,
 tricuspid valve disease,
 severe pulmonary hypertension.
 In mild disease, heart size is normal .
 moderate cardiomegaly is usual with severe
mitral stenosis.
 Cardiac enlargement can be massive when
atrial fibrillation and heart failure supervene.
 A parasternal right ventricular lift is palpable
when pulmonary pressure is high.

18.  Clinical manifestations (Continued)
 The principal auscultatory findings are
 a loud 1st heart sound,
 an opening snap of the mitral valve, and
 a long, low-pitched, rumbling mitral diastolic
murmur with presystolic accentuation at the apex.
 The mitral diastolic murmur may be virtually
absent in patients who are in heart failure.
 A holosystolic murmur secondary to tricuspid
insufficiency may be audible.
 In the presence of pulmonary hypertension, the
pulmonic component of the 2nd heart sound is
accentuated.
 An early diastolic murmur may be caused by
associated aortic insufficiency or secondary
pulmonary valvular insufficiency

19. Treatment.
Surgical valvotomy
 balloon catheter mitral
valvuloplasty .
 indicated for symptomatic, stenotic,
pliable, noncalcified valves of
patients without atrial arrhythmias
or thrombi

20. AORTIC INSUFFICIENCY
 In chronic rheumatic aortic insufficiency,
sclerosis of the aortic valve results in
distortion and retraction of the cusps.
 Regurgitation of blood leads to volume
overload with dilatation and hypertrophy
of the left ventricle.
 Combined mitral and aortic insufficiency is
more common than aortic involvement
alone

21. Clinical Manifestations.
 palpitations
 Excessive sweating
 heat intolerance
 Dyspnea on exertion
 orthopnea
 pulmonary edema;
 angina precipitated by heavy exercise.
 Nocturnal attacks with
 sweating,
 tachycardia,
 chest pain, and
 hypertension .

22. Clinical manifestations (continued)
 wide pulse pressure
 bounding peripheral pulses.
 Elevated Systolic blood pressure.
 In severe aortic insufficiency, the heart is
enlarged, with a left ventricular apical
heave.
 A diastolic thrill may be present.

23. The diastolic murmur heard over the upper
and mid left sternal border with radiation to
the apex and the aortic area.
 high-pitched blowing ,easily audible in full
expiration.
A systolic ejection murmur is frequent
because of the increased stroke volume.
An apical presystolic murmur (Austin Flint
murmur) resembling that of mitral stenosis
is sometimes heard and is a result of the
large regurgitant aortic flow in diastole that
prevents the mitral valve from opening fully

24. Investigations
 CXR
 show enlargement of the left ventricle and aorta.
 ECG
 may be normal,
 but in advanced cases it reveals signs of left
ventricular hypertrophy and strain with prominent P
waves.
 The echocardiogram
 shows a large left ventricle and diastolic mitral valve
flutter or oscillation caused by regurgitant flow hitting
the valve leaflets.
 Doppler studies demonstrate the degree of aortic
runoff into the left ventricle.

25. Treatment
 medical
 afterload reducers (ACE inhibitors)
and
 prophylaxis against
 recurrence of acute rheumatic fever and
 the development of infective endocarditis.
 Surgical intervention
 valve replacement

26. PULMONARY VALVE DISEASE
 Pulmonary insufficiency usually occurs on
a functional basis secondary to pulmonary
hypertension
 a late finding with severe mitral stenosis.
 The murmur (Graham Steell murmur) is
similar to that of aortic insufficiency, but
peripheral arterial signs (bounding pulses)
are absent.
 The correct diagnosis is confirmed by two-
dimensional echocardiography and
Doppler study

27. TRICUSPID VALVE DISEASE
 Primary tricuspid involvement is rare after
rheumatic fever.
 Tricuspid insufficiency is more common
secondary to right ventricular dilatation
resulting from unrepaired left-sided
lesions.
 The signs of tricuspid insufficiency
 prominent pulsations of the jugular veins,
 systolic pulsations of the liver,
 and a blowing holosystolic murmur at the
LLSB that increases in intensity during
inspiration

28.  Concomitant signs of mitral or aortic valve
disease, with or without atrial fibrillation, are
frequent.
 Signs of tricuspid insufficiency decrease or
disappear when heart failure produced by the
left-sided lesions is successfully treated.
 Tricuspid valvuloplasty may be required in
rare cases.