Valvular Heart Disease

1. Valvular Heart Disease Dr. Randa Al-Harizy Prof. of Internal Medicine

2. Tricuspid Valve

3. Valvular Heart Disease MITRAL STENOSIS Almost all mitral stenosis is due to rheumatic heart disease. It is much more common in women. Other causes include: Lutembacher's syndrome, which is the combination of acquired mitral stenosis and an atrial septal defect, carcinoid tumours and SLE.

4. Valvular Heart Disease PATHOPHYSIOLOGY When the normal valve orifice area is reduced to 1 cm2, severe mitral stenosis is present. To maintain cardiac output, the left atrial pressure increases and left atrial hypertrophy and dilatation occur. Consequently, pulmonary venous, pulmonary arterial and right heart pressures also increase, followed by pulmonary oedema. Pulmonary hypertension leads to right ventricular hypertrophy, dilatation and failure resulting in tricuspid regurgitation.

5. Valvular Heart Disease COMPLICATIONS OF MITRAL STENOSIS Atrial fibrillation Systemic embolization Pulmonary hypertension Pulmonary infarction Chest infections Infective endocarditis (rare) Tricuspid regurgitation Right ventricular failure

6. Valvular Heart Disease SYMPTOMS Usually there are no symptoms until the valve orifice is moderately stenosed (i.e. has an area of 2 cm2). Because of pulmonary venous hypertension and recurrent bronchitis, progressively severe dyspnoea develops. A cough productive of blood-tinged, frothy sputum and occasionally frank haemoptysis may occur. Right heart failure and its symptoms of weakness, fatigue and abdominal or lower limb oedema. Atrial fibrillation, giving rise to palpitations. Atrial fibrillation may result in systemic emboli.

7. Valvular Heart Disease SIGNS Face: mitral facies or malar flush. Pulse: a small-volume pulse, may be an irregularly irregular pulse. Jugular veins: Distension of jugular veins in right heart failure. Palpation: There is a tapping impulse felt parasternally on the left side (palpable first heart sound). A sustained parasternal impulse due to right ventricular hypertrophy may also be felt. Auscultation: loud first heart sound, and 'opening snap'. This is followed by a low-pitched 'rumbling' mid-diastolic murmur at the apex with presystolic accentuation.

8. Valvular Heart Disease INVESTIGATIONS Chest X-ray: small heart with an enlarged left atrium, Pulmonary venous hypertension, a calcified mitral valve, signs of pulmonary oedema or pulmonary hypertension. ECG: shows a bifid P wave or AF, features of right ventricular hypertrophy (right axis deviation and perhaps tall R waves in V1) Echocardiogram: assessment of the mitral valve apparatus and calculation of mitral valve area, also determines left atrial and right ventricular size and function. Estimate of pulmonary artery pressure Cardiac catheterization

9. Valvular Heart Disease TREATMENT Mild mitral stenosis may need no treatment other than prompt therapy of attacks of bronchitis. Antibiotic prophylaxis for infective endocarditis. Mild dyspnoea is treated with low doses of diuretics. Atrial fibrillation requires treatment with digoxin and anticoagulation to prevent atrial thrombus and systemic embolization. If pulmonary hypertension develops, surgical relief of the mitral stenosis is advised. Surgical treatment includes; Trans-septal balloon valvotomy, Closed valvotomy, Open valvotomy or Mitral valve replacement.

10. MITRAL REGURGITATION • CAUSES • The most common cause is rheumatic heart disease (50%) • and a prolapsing mitral valve. • Other causes include; aortic valve disease, acute rheumatic fever, myocarditis, dilated cardiomyopathy, hypertensive heart disease, ischaemic heart disease, infective endocarditis, hypertrophic cardiomyopathy, SLE, Marfan's syndrome, Ehlers-Danlos syndrome, rupture of the chordae tendineae (e.g.due to myocardial infarction).

11. MITRAL REGURGITATION • PATHOPHYSIOLOGY • Regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure. • With acute mitral regurgitation the left atrial v wave is greatly increased and pulmonary venous pressure rises to produce pulmonary oedema. • Since a proportion of the stroke volume is regurgitated, the stroke volume increases to maintain the forward cardiac output and the left ventricle therefore enlarges.

12. MITRAL REGURGITATION • SYMPTOMS • Mitral regurgitation can be present for many years before any symptoms occur. • The increased stroke volume is sensed as a 'palpitation'. • Dyspnoea and orthopnoea develop owing to left ventricular failure. • Fatigue and lethargy develop because of the reduced cardiac output. • In the late stages of the disease the symptoms of right heart failure also occur and eventually lead to congestive cardiac failure. • Cardiac cachexia may develop. • Thromboembolism is less common than in mitral stenosis, but subacute infective endocarditis is much more common.

13. MITRAL REGURGITATION • SIGNS • Laterally displaced (forceful) diffuse apex beat and a systolic thrill (if severe). • Soft first heart sound. • Pansystolic murmur, radiating widely over the precordium and into the axilla. • Prominent third heart sound. • The signs related to atrial fibrillation, pulmonary hypertension, and left and right heart failure develop later in the disease.

14. MITRAL REGURGITATION INVESTIGATIONS Chest X-ray: left atrial and left ventricular enlargement. There is an increase in the CTR, and valve calcification is seen. ECG shows the features of left atrial delay (bifid P waves) and left ventricular hypertrophy as manifested by tall R waves in leads I and V6 and deep S waves in the right-sided precordial leads V1 and V2. Atrial fibrillation may be present. Echocardiogram: dilated left atrium and left ventricle. There may be specific features of chordal or papillary muscle rupture. Cardiac catheterization.

15. MITRAL REGURGITATION TREATMENT Mild mitral regurgitation in the absence of symptoms can be managed conservatively by following the patient with serial echocardiograms. Prophylaxis against endocarditis is required Any evidence of progressive cardiac enlargement generally warrants early surgical intervention by either mitral valve repair or replacement. In patients who are not considered appropriate for surgical intervention, management usually involves treatment with ACE inhibitors, diuretics and possibly anticoagulants.

16. AORTIC STENOSIS CAUSES Congenital aortic valve stenosis. Rheumatic fever; In rheumatic heart disease the aortic valve is affected in about 40% of cases and there is usually associated mitral valve disease. Calcific valvular disease is the commonest cause of aortic stenosis and mainly occurs in the elderly.

18. AORTIC STENOSIS PATHOPHYSIOLOGY Obstructed left ventricular emptying leads to increased left ventricular pressure and compensatory left ventricular hypertrophy. In turn, this results in relative ischemia of the left ventricular myocardium, and consequent angina, arrhythmias and left ventricular failure.

19. AORTIC STENOSIS SYMPTOMS There are usually no symptoms until aortic stenosis is moderately severe (when the aortic orifice is reduced to one-third of its normal size). At this stage, exercise-induced syncope, angina and dyspnoea develop. When symptoms occur, the prognosis is poor - on average, death occurs within 2-3 years if there has been no surgical intervention.

20. AORTIC STENOSIS SIGNS Pulse: small volume and is slow-rising or plateau in nature. Precordial palpation: The apex beat is not usually displaced because hypertrophy (as opposed to dilatation) does not produce noticeable cardiomegaly. However, the pulsation is sustained and obvious. A double impulse is sometimes felt because the fourth heart sound or atrial contraction ('kick') may be palpable. A systolic thrill may be felt in the aortic area. Auscultation The most obvious auscultatory finding in aortic stenosis is an ejection systolic murmur that is usually 'diamond-shaped' (crescendo-decrescendo). The murmur is usually rough in quality and best heard in the aortic area. It radiates into the carotid arteries and also the precordium.

21. AORTIC STENOSIS INVESTIGATIONS Chest X-ray reveals a relatively small heart with a prominent, dilated, ascending aorta. This occurs because turbulent blood flow above the stenosed aortic valve produces so-called 'post-stenotic dilatation'. The aortic valve may be calcified. The CTR increases in heart failure. ECG shows left ventricular 'strain' pattern due to 'pressure overload' (depressed ST segments and T wave inversion in leads I, AVL, V5, V6). Echocardiogram readily demonstrates the thickened, calcified and immobile aortic valve cusps. Left ventricular hypertrophy may be seen. Cardiac catheterization.

22. AORTIC STENOSIS TREATMENT In patients with aortic stenosis, symptoms are a good index of severity and all symptomatic patients should have aortic valve replacement. Asymptomatic patients should be under regular review for assessment of symptoms and echocardiography. Antibiotic prophylaxis against infective endocarditis is essential.

23. AORTIC REGURGITATION CAUSES The most common causes of aortic regurgitation are rheumatic fever and infective endocarditis complicating a previously damaged valves. Acute aortic regurgitation: Acute rheumatic fever, Infective endocarditiS, Dissection of the aorta, Ruptured aneurysm, Failure of prosthetic heart valve. Chronic aortic regurgitation: Rheumatic heart disease, Syphilis, Arthritides (Reiter's syndrome, Ankylosing spondylitis, Rheumatoid arthritis), Hypertension (severe), Bicuspid aortic valve, Aortic endocarditis, Marfan's syndrome And Osteogenesis imperfecta.

24. AORTIC REGURGITATION Pathophysiology Aortic regurgitation is reflux of blood from the aorta through the aortic valve into the left ventricle during diastole. Consequently the left ventricular size must enlarge. Because of the aortic run-off during diastole, diastolic blood pressure falls and coronary perfusion is decreased. Cardiac ischaemia develops.

25. AORTIC REGURGITATION SYMPTOMS In aortic regurgitation, significant symptoms occur late and do not develop until left ventricular failure occurs. As with mitral regurgitation, a common symptom is 'pounding of the heart' because of the increased left ventricular size and its vigorous pulsation. Angina pectoris is a frequent complaint. Varying grades of dyspnoea occur depending on the extent of left ventricular dilatation and dysfunction. Arrhythmias are relatively uncommon.

26. AORTIC REGURGITATION SIGNS Pulse: bounding or collapsing. Signs of hyperdynamic circulation: Quincke's sign (capillary pulsation in the nail beds), De Musset's sign (head nodding with each heartbeat), Duroziez's sign (a to-and-fro murmur heard when the femoral artery is auscultated with pressure applied distally-it is a sign of severe aortic regurgitation), pistol shot femorals. Apex beat: is displaced laterally and downwards and is forceful in quality. Auscultation: a high-pitched early diastolic murmur best heard at the left sternal edge in the fourth intercostal space with the patient leaning forward and the breath held in expiration. Commonly an ejection systolic flow murmur. The regurgitant jet can impinge on the anterior mitral valve cusp, causing a mid-diastolic murmur (Austin Flint).

27. AORTIC REGURGITATION INVESTIGATIONS Chest X-ray: left ventricular enlargement and possibly dilatation of the ascending aorta. The ascending aortic wall may be calcified in syphilis, and the aortic valve may be calcified if valvular disease is responsible for the regurgitation. ECG: appearances are those of left ventricular hypertrophy due to 'volume overload' - tall R waves and deeply inverted T waves in the left-sided chest leads, and deep S waves in the right-sided leads. Echocardiogram: vigorous cardiac contraction and a dilated left ventricle. The aortic root may also be enlarged. Cardiac catheterization.

28. AORTIC REGURGITATION TREATMENT The underlying cause of aortic regurgitation (e.g. syphilitic aortitis or infective endocarditis) may require specific treatment. The treatment of aortic regurgitation usually requires aortic valve replacement. Because symptoms do not develop until the myocardium fails and because the myocardium does not recover fully after surgery, operation is performed before significant symptoms occur. Antibiotic prophylaxis against infective endocarditis is necessary.

29. Mechanical Valve

30. Porcine Valve

31. TRICUSPID STENOSIS CAUSES This uncommon valve lesion, which is seen much more often in women than in men, is usually due to rheumatic heart disease. It is frequently associated with mitral and/or aortic valve disease. It is also seen in the carcinoid syndrome.

32. TRICUSPID STENOSIS PATHOPHYSIOLOGY Tricuspid valve stenosis results in a reduced cardiac output, which is restored towards normal when the right atrial pressure increases. The resulting systemic venous congestion produces hepatomegaly, ascites and dependent oedema.

33. TRICUSPID STENOSIS SYMPTOMS Usually, patients with tricuspid stenosis complain of symptoms due to associated left-sided rheumatic valve lesions. Abdominal pain (due to hepatomegaly) and swelling (due to ascites) and peripheral oedema.

34. TRICUSPID STENOSIS SIGNS Prominent jugular venous a wave. Presystolic pulsation may also be felt over the liver. Rumbling mid-diastolic murmur, heard best at the lower left sternal edge and is louder on inspiration. A tricuspid opening snap may occasionally be heard. Hepatomegaly, abdominal ascites and dependent oedema may be present.

35. TRICUSPID STENOSIS INVESTIGATIONS Chest X-ray: prominent right atrial bulge. ECG: enlarged right atrium manifested by peaked, tall P waves (> 3 mm) in lead II. Echocardiogram: thickened and immobile tricuspid valve, but this is not so clearly seen as an abnormal mitral valve. Cardiac catheterization.

36. TRICUSPID STENOSIS TREATMENT Medical management consists of diuretic therapy and salt restriction. Tricuspid valvotomy is occasionally possible, but tricuspid valve replacement is often necessary. Other valves usually also need replacement because tricuspid valve stenosis is rarely an isolated lesion.

37. TRICUSPID REGURGITATION CAUSES Functional tricuspid regurgitation may occur whenever the right ventricle dilates, e.g. in cor pulmonale, myocardial infarction or pulmonary hypertension. Organic tricuspid regurgitation may occur with rheumatic heart disease, infective endocarditis, carcinoid syndrome, Ebstein's anomaly (a congenitally malpositioned tricuspid valve) and other congenital abnormalities of the atrioventricular valves.

38. TRICUSPID REGURGITATION SYMPTOMS and SIGN Symptoms of right heart failure. Physical signs include a large jugular venous cv wave and a palpable liver that pulsates in systole. Usually a right ventricular impulse may be felt at the left sternal edge, and there is a blowing pansystolic murmur, best heard on inspiration at the lower left sternal edge. Atrial fibrillation is common.

39. TRICUSPID REGURGITATION TREATMENT Functional tricuspid regurgitation usually disappears with medical management. Severe organic tricuspid regurgitation may require operative repair of the tricuspid valve or valve replacement.

40. PULMONARY STENOSIS CAUSES This is usually a congenital lesion, but it may rarely result from rheumatic fever or from the carcinoid syndrome. Congenital pulmonary stenosis may be associated with an intact ventricular septum or with a ventricular septal defect (Fallot's tetralogy). Pulmonary stenosis may be valvular, subvalvular or supravalvular.

41. PULMONARY STENOSIS SYMPTOMS and SIGNS Fatigue, syncope and the symptoms of right heart failure. Physical signs: harsh mid-systolic ejection murmur, best heard on inspiration, to the left of the sternum in the second intercostal space. This murmur is often associated with a thrill. The pulmonary closure sound is usually delayed and soft. There may be a pulmonary ejection sound if the obstruction is valvular. A right ventricular fourth sound and a prominent jugular venous a wave are present when the stenosis is moderately severe. A right ventricular heave (sustained impulse) may be felt.

42. PULMONARY STENOSIS INVESTIGATIONS Chest X-ray: prominent pulmonary artery owing to post-stenotic dilatation. ECG: both right atrial and right ventricular hypertrophy, although it may sometimes be normal even in severe pulmonary stenosis. Echocardiogram Doppler is the investigation of choice. Cardiac catheterization.

43. PULMONARY STENOSIS TREATMENT Treatment of severe pulmonary stenosis requires pulmonary valvotomy (balloon valvotomy or direct surgery).

44. PULMONARY REGURGITATION This is the most common acquired lesion of the pulmonary valve. It results from dilatation of the pulmonary valve ring, which occurs with pulmonary hypertension. It is characterized by a decrescendo diastolic murmur, beginning with the pulmonary component of the second sound, that is difficult to distinguish from the murmur of aortic regurgitation. Pulmonary regurgitation usually causes no symptoms and treatment is rarely necessary.

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