Chronic Rheumatic Fever

2. FACTORS DETERMINING SEQUALAE
 Duration and severity of rheumatic inflammation
 Amount of scarring of valves and myocardium after
inflammation
 Location and severity of haemodynamic lesion
 Frequency of carditis
 Progression of valvular calcification

3. CHRONIC SEQUALAE OF
RHEUMATIC FEVER
 Carditis
 Valvular heart disease
 Chronic rheumatic myocarditis

4. CHRONIC RHEUMATIC
MYOCARDITIS
 Presents as chronic heart failure with physical,
roentgenographic and electrocardiographic features of
mitral and or aortic and sometimes tricuspid
regurgitation.
 It usually occurs as part of a pancarditis
 It may have an intractable course or patient could
recover suddenly with disappearance of the systemic
manifestations of the inflammatory process.

5. VALVULAR HEART DISEASE
 Mitral valve alone 50%
 Mitral and aortic valve 40%
 Mitral,aortic and tricuspid 5%
 Aortic valve alone 2%
 All other combinations 3%

6. MITRAL STENOSIS
 Occurs among 40% 0f patients with rheumatic heart
disease.
 The valve commisures fuse ,the chordae tendinae fuse
and shorten with cusps becoming rigid .
 The funnel shaped valve becomes narrowed.
 Normal valve area is 4-6cm2
 When the valve area is<2cm2,blood flows into the left
ventricle under an elevated pressure gradient between
LA and LV.

7. HAEMODYNAMIC CHANGES
 Elevated left atrial pressure raises pulmonary venous and
capillary pressure thereby reducing pulmonary compliance
and gives exertional dyspnoea.
 Normal left ventricular function and pressures.
 When mitral stenosis is mild or moderate the pulmonary
arterial pressure may be near normal at rest but rise with
exercise.
 When severe, increase of pulmonary vascular resistance
and pulmonary arterial pressure is elevated at rest and may
exceed systemic arterial pressure.
 Right ventricular end diastolic pressure rises, impeding
emptying.

8. CLINICAL FEATURES
 There is a delay between rheumatic carditis and
manifestation of mitral stenosis; up to 20 years in
temperate countries much earlier in developing
countries.
 Asymptomatic
 Dyspnoea,cough during extreme exertion,
excitement,fever,anaemia,pregnancy,sexual
intercourse.
 Symptoms occur with less stress when the stenosis
progresses.

9.  Pulmonary oedema
 Varying degrees of atrial arrhythmias
 Haemoptysis
 Right ventricular failure, fatigue, oedema, hepatic
congestion, pulmonary emboli, pulmonary infections
 Peripheral and facial cyanosis or malar rash
 Small volume pulse or irregularly irregular pulse
 Prominent a waves in JVP
 Tapping apex beat: palpable first heart sound
 Palpable pulmonary closure sound

10.  Diastolic thrill
 Loud 1st heart sound, loud P2
 Opening snap following A2; A2-OS interval varies
inversely with severity of mitral stenosis.
 Diastolic murmur, low pitched best heard at apex in
left lateral recumbent position.
 Graham Steel murmur of pulmonary regurgitation in
pulmonary hypertension.

11. INVESTIGATION
 Roentgenogram
 Straightening of the left border of the
heart(mitralization)
 Prominence of main pulmonary arteries, dilatation of
the upper lobe pulmonary veins.
 Posterior displacement of oesophagus on lateral film
 Left and right atria, right ventricle and SVC are
prominent.
 Kerley B lines.

12. ELECTROCARDIOGRAM
 P mitrale(bifid P wave) in lead II or biphasic in lead V1
 Tall peaked P wave in lead II and upright in V1 when
there’s severe pulmonary hypertension
 Right axis deviation in severe pulmonary hypertension
and right ventricular hypertrophy.

13. ECHOCARDIOGRAM
 M-mode reduced E-F slope
 2-D ECHO shows restriction of valve leaflets,
distortion of sub valvular apparatus ;size of chambers
 Doppler imaging give transvalvular gradient and
mitral orifice size and accompanying regurgitation.

14. TREATMENT
 MEDICAL FOR ASYMPTOMATIC
A. Rheumatic fever prophyllaxis-IM Benzathine
Penicillin
B. Infective endocarditis prophyllaxis: amoxicillin
 Medical treatment for symptomatic
1. Sodium restriction
2. Oral diuretics
3. Digitalis if in Atrial fibrillation or β-blockers
4. Anticoagulants if severe stenosis or if
systemic/pulmonary embolism

15.  Mitral valvulotomy-open or closed commissurotomy:
used in symptomatic individuals with
MVA<1.3cm2.may require re-operation in ten years.
 Percutaneous balloon valvuloplasty for severe mitral
stenosis if there is minimal calcification and poor
operative candidates.
 Valve replacement –success depends on LV function,
team experience and durability of prosthesis.
1. Mechanical
2. Bioprosthetic –older people,reproductive age group,

16. MITRAL REGURGITATION
 This is due to retraction of the rigid ,deformed cusps which
commissures have become fused . The chordae have been
shortened and are fused.
 There is little resistance to LV emptying hence it’s
compressed into LA during ejection with reduced LV
afterload
 LV function gradually deteriorates with increase in LVED
volume.
 LVED pressure only increases minimally
 In acute MR pulmonary oedema is common due to
reduced/normal compliance of LA/Pulmonary capp bed.
 LA/Pulmonary pressures are only slightly increased in
chronic MR

17.  Fatigue, exertional dyspnoea, orthopnoea
 Right sided failure
 Left ventricular failure in acute MR
 SIGNS
A. Normal pulse with sharp upstroke
B. JVP shows prominent A wave ,V wave
C. Apical systolic thrill, displaced apex beat
D. Left parasternal lift when LA is grossly enlarged
E. Soft first heart sound, pansystolic murmur grade 3-
4;third heart sound indicates severe disease

18.  Roentgenogram
1. Enlarged LV,LA
2. Pulmonary venous congestion ,interstitial oedema,
Kerley B lines
 ECG
A. LAE,RAE,LVH,RVH
 Atrial fibrillation
Echocardiogram
Doppler echo and color flow mode are most accurate in
detection and estimation of MR

19. TREATMENT
 Physical restriction
 salt restriction
 Diuretics
 Digitalis increase cardiac output
 Angiotensin converting enzyme inhibitors
 anticoagulants
 Surgery-valve replacement when LV dysfunction
progresses.

20. AORTIC STENOSIS
 Threre’s fusion,thickening and calcification of the
trileaflet aortic valve
 Obstruction to left ventricle emptying leads to LV
hypertrophy and increase in LV pressure
 Relative ischaemia of myocardium,LV
failure,arrhythmias
 Cardiac output fails to rise during exercise
 Preserved LV systolic function

21. CLINICAL FEATURES
 Asymptomatic if narrowing is less than 2/3 of normalvalve
orifice
 Syncope,angina,dyspnoea on exertion
 Small volume pulse,slow rising
 Visible precordial heave ,sustained palpable apical heave,
double apical impulse.
 Crescendo-decrescendo ejection systolic murmur,rough
best heard at aortic area ;the longer the more severe
stenosis.
 Prominent 4th heart sound,soft aortic 2nd heart
sound,systolic ejection click.

22. INVESTIGATIONS
 Roentgenogram- small heart with prominent
ascending aorta
 Electrocardiogram- Left ventricular hypertrophy.left
atrial enlargement,ST segment andT wave inversion
 Echocardiogram—calcified cusps,LV hypertrophy.
Continuous wave doppler can estimate the gradient.
 Coronary angiogram-a prerequisite for surgery.

23. TREATMENT
 Valvotomy for critical stenosis in children and
adolescents
 Valve replacement is the mainstay of treatment.

24. AORTIC REGURGITATION
 During diastole blood refluxes from the aorta into the
left ventricle .
 The LV enlarges in order to maintain cardiac output by
increasing the volume.
 The condition may be initially asymptomatic

25. CLINICAL FEATURES
 Pounding of the heart
 Angina pectoris
 Varying degrees of dyspnoea
 The signs are mostly due to hyperdynamic circulation,
reflux of blood and increased LV size.
1. Quincke’s sign –capillary pulsation
2. De Musset’s sign –head nodding with each heart beat
3. Duroziez’s sign –to and fro murmur over pectoral artery
4. Pistol shots –sharp bang heard over femorals with each
heart beat.

26.  apex beat displace laterally ,downwards and thrusting.
 High pitched diastolic murmur at left sternal edge in
4th left intercostal space .
 A mid-diastolic murmur (Austin Flint).

27. INVESTIGATIONS
 Roentgenogram- enlarged LV,dilated ascending aorta
 Electrocardiogram-LVH ,sinus rhythm
 Echocardiogram- dilated LV ,
 vigorous contraction
 enlarged aortic root
 Diastolic fluttering of anterior mitral leaflets
 CW doppler assesses regurgitation

28. TREATMENT
 Surgery should be carried out before significant
symptoms develop

29. TRICUSPID STENOSIS
 Uncommon lesion
 Commoner in women
 There’s reduced cardiac output
 Increased right atrial pressure
 Systemic venous congestion
 CLINICAL FEATURES
A. Abdominal pain,swelling
B. Insiduous onset of oedema
C. Mild dyspnoea
D. Prominent neck pulsations

30.  Prominent jugular A wave
 Pulsatile liver
 Rumbling mid-diastolic murmur at lower left sternal
border
 Hepatomegaly
 Ascites
 Oedema

31. INVESTIGATIONS
 Roentgenogram –right atrial bulge
 Electrocardiogram –tall peaked P waves in lead II if in
sinus rhythm ,atrial flutter and atrial fibrillation are
common.
 Echocardiogram –thickened immobile valve

32. TREATMENT
 Medical –diuretics, salt restriction, treat arrhythmias.
 Valvotomy
 Valve replacement is often unnecessary.

33. TRICUSPID REGURGITATION
 Incompetent valve
 Presents with features of right sided heart failure
 Examination shows
A. large jugular V wave
B. Pulsatile liver
C. Ascites
D. Left parasternal heave
E. Blowing pansystolic murmur
F. Atrial fibrillation.

34.  Roentgenogram-
 Enlarged cardiac silhouette
 Pleurall effusions
 Elevated dome of diaphragm due to ascites
 Evidence of pulmonary artery and venous
hypertension

35. ECHOCARDIOGRAM
 Right ventricle enlargement
 Paradoxical septal wall motion
 Calcified valves which are rigid
 Continuous doppler evidence of TR
 Color flow doppler showing regurgitation into the
right atrium.

36. TREATMENT
 Medical – salt and fluid restriction
 Surgical if medical therapy does not work and patient
is symptomatic this is by valve replacement.