Aortic Stenosis

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Aortic Stenosis

  1. 1. AORTIC STENOSIS Definition: Aortic stenosis is defined as narrowing of the aortic valve apparatus resulting in a obstruction to the left ventricular outflow of blood. Aortic stenosis can be valvular or non valvular. Non-valvular aortic stenosis can be either supra valvular or infra- valvular. Etiology: Aortic stenosis can be congenital or acquired. Congenital aortic stenosis can be due to bicuspid aortic valve, which develops fibrosis and calcification later in life. Second most important cause of aortic stenosis is chronic rheumatic valvular disease. Valvular damage occurs 5-10 years after the attack of rheumatic fever. Third important cause of aortic stenosis is atherosclerosis of the valve occurring in old age. Infra valvular aortic stenosis is idiopathic hypertrophic subaortic stenosis. The rarer form of aortic stenosis is supra valvular other wise called William’s syndrome. Pathophysiology: There is progressive narrowing of the aortic valve over a period of time resulting in obstruction to blood flow from left ventricle to the aorta. In mild aortic stenosis there is no reduction in cardiac output. In moderate aortic stenosis cardiac output is maintained by the development of a pressure gradient across the aortic valve. As a result the pressure inside the left ventricle is increased through out systole. This produces concentric hypertrophy of the left ventricle. Initially the heart size is not increased. Later there is left ventricular dilatation. The increased pressure in the left ventricle is passively transmitted to the left atrium and the pulmonary veins. When the pulmonary venous pressure rises beyond 25 mm of Hg, plasma may exude into the alveoli and result in acute pulmonary edema. Later the patient can go in pulmonary arterial hypertension. And right sided cardiac failure. Symptoms: Patients with aortic stenosis usually presents with progressive exertional dyspnoea and orthopnoea and paroxysmal dyspnoea. Patients also develop exertional chest pain. The chest pain is typical of angina pectoris. It is not only due to the decreased coronary artery circulation but also sue to increased oxygen demand of the hypertrophied left ventricle. Exertional syncope is another important presenting symptom severe aortic stenosis. Without this symptom diagnosis of severe aortic stenosis should not be made. Later patients with severe aortic stenosis will have features of right-sided cardiac failure with edema and pedal edema. Aortic stenosis caused by rheumatic endocarditis is usually associated with mitral valve disease. Aortic stenosis may also be associated with accompanying aortic regurgitation. In the above circumstances symptoms of aortic stenosis will be earlier and more severe. Signs: The patient is usually moderately built and nourished. There may be pedal edema if there is congestive cardiac failure. The pulse volume is decreased. The character of the pulse is low volume slow rising with a delayed peak. Named as
  2. 2. anacrotic pulse. If there is associated regurgitation of the aortic valve the character of the pulse will be a double peaking pulse called Bisferiens pulse. A double peaking pulse may also occur in case of IHSS, a bifid pulse and a bifid apex may be present in this occasion. The blood pressure in aortic stenosis is normal initially, but later the systolic pressure comes down and the diastolic pressure remains high. Thus the pulse pressure is narrowed. In severe aortic stenosis for example the blood pressure may be 90/70 mm of Hg. The jugular venous pressure is found to be elevated if there is congestive cardiac failure. The ‘a’ wave may be more prominent than the v wave in JVP. The apex beat is normally placed or shifted laterally to the left side. . If there is associated mitral or aortic regurgitation the apex beat may be shifted laterally as well as down wards. The apex beat is heaving in character in other words a sustained and forceful apex. There may be LPH and palpable P2 if there is pulmonary artery hypertension. A thrill may be palpated in the aortic area and along the carotid artery. On auscultation the first heart sound is normal. There may be a sharp ejection click. The normal opening of the aortic valve does not make any sound. But in valvular aortic stenosis the click is usually evident. The ejection click is followed by a medium pitched rasping ejection systolic murmur. The murmur is heard during the middle of the systole and weans off towards the second sound. The murmur is a crescendo decrescendo or diamond shaped murmur. The murmur is conducted along the carotids and often associated with a systolic thrill. In case of supra-valvular aortic stenosis there is a preferential conduction of the murmur towards the right carotid. The ejection systolic murmur itself may sometimes be better heard in the mitral area. The second sound A2 due to the closure of the aortic valve. The softness of the sound is directly related to the severity of the aortic stenosis. It is delayed and may even overlap the pulmonary second sound. There may be even a paradoxical split. Later there may be a third heart sound due to development of left heart failure. This also manifests as tachycardia and basal crepitations over the base of lungs. A palpable and accentuated pulmonary second sound and raised jugular venous pressure are consistent with development of right heart failure Complications: The most dreaded complication of aortic stenosis is sudden cardiac death. This can occur in severe aortic stenosis or sub-aortic stenosis. Left ventricular failure, acute pulmonary edema, atrial fibrillation, pulmonary artery hypertension, congestive cardiac failure are the expected complications. Investigations: ECG will show left atrial enlargement and left ventricular hypertrophy. Chest X ray will show bulging of the left border of heart with or without cardiomegaly, and evidence of pulmonary venous hypertension and pulmonary artery hypertension. Echocardiography is diagnostic and will demonstrate the narrowing of the valve left atrial and left ventricular hypertrophy. Doppler echocardiography will demonstrate the reduced flow across the aortic valve.
  3. 3. Medical Management: Infective endocarditis prophylaxis is indicated in all patients with chronic aortic stenosis. Vigorous exercise and physical activity should be avoided in patients with moderate to severe aortic stenosis. Atrial as well as ventricular arrhythmias occurring in association with aortic stenosis are poorly tolerated and hence must be treated. Patients with heart failure will benefit from digoxin treatment. However it may not be useful in patients with severe aortic stenosis. Diuretics can be used in treating congestive cardiac failure but must be used with extreme caution because reduction in the left ventricular filling pressures can reduce the cardiac output and blood pressure. Nitrates and other vasodilators should also be used with caution in patients with severe aortic stenosis as they may produce severe hypotension and cardiovascular collapse. Asymptomatic patients with mild to moderate aortic stenosis may be closely observed and followed up with serial echocardiography examinations Surgical Management: Symptomatic patients with aortic stenosis should be evaluated for aortic valve replacement. Trans esophageal echocardiography is ideal in preoperative assessment. A coronary angiography should be performed in all patients with aortic stenosis above the age of 50 years as well as in all patients with anginal symptoms. Percutaneous balloon aortic valvuloplasty can reduce aortic valve gradient and improve symptoms and left ventricular function. However restenosi occurs in up to 50% Management of IHSS: Since sudden death often occurs during or just after physical exertion, competitive sports and strenuous activity should be avoided. Dehydration should be avoided, and diuretics should be used with caution. Adrenergic blockers are often used and ameliorate angina pectoris &syncope in one third to half of patients. It does not offer any protection against sudden death.

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