Aortic Regurgitation


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Aortic Regurgitation

  1. 1. AORTIC REGURGITATION Definition: Aortic Regurgitation is defined as leakage or incompetence of the aortic valve apparatus or the dilatation of the valve ring. Etiology: Aortic regurgitation can be chronic or acute in origin. Causes of Chronic Aortic regurgitation are: • Chronic rheumatic valvular heart disease • Bacterial endocarditis of bicuspid aortic valve • Syphilitic aortitis with aortic root dilataion • Acquired connective tissue disorders like rheumatoid arthritis and ankylosing spondylitis • Congenital connective tissue disorders like Marfan’s syndrome and Ehlers Danlos syndrome Causes of acute Aortic regurgitation are: • Blunt trauma to the chest • Acute bacterial endocarditis • Dissection of ascending aorta • Rupture of ascending aorta aneurysm • Rupture of sinus of valsalva aneurysm Pathophysiology: In chronic rheumatic valvular disease the aortic valve is usually damaged by chronic inflammation of the valve cusps, leading to in approximation of the valve and resultant leakage of blood from the aorta to the left ventricular chamber. In connective tissue diseases myxomatous degeneration of the valves results in increased pliability of the valves and also excessive redundancy of the chordae tendinae and the papillary muscles. Aortic regurgitation may also occur due to dilatation of the valve ring that might occur as a dilatation of the root of aorta as in syphilitic aortitis, aneurysm of ascending aorta and left ventricular hypertrophy. Hemodynamics: Leakage of blood from aorta to the left ventricle occurs only during the early phase of diastole. This is because of the fact that, the left ventricle gets filled up by the blood received normally from the left atrium thorough the mitral valve during diastole, and the blood received from the aorta during the AR leak. Thus the pressure in the aorta and the left ventricle gets equalized during mid- diastole, earlier than the normal persons; hence the leak also diminishes during the late diastole. All these lead to a volume overload of the left ventricle and increasing its end diastolic volume. Most of this blood is pumped back into the aorta during the next systole there will be an increase in the stroke volume. This may cause an ejection systolic murmur even in the absence of any aortic valve stenosis. The volume over load of the left ventricle leads to left ventricular hypertrophy, left ventricular dilatation, passive congestion of the left atrium and the pulmonary veins. Rarely left ventricular failure, pulmonary artery hypertension and right heart failure may occur late in the course of the disease. In acute aortic 1
  2. 2. regurgitation compensatory mechanisms are not active and therefore the increase in end diastole pressure is marked and left ventricular failure also occurs early. Symptoms: Patients with chronic aortic regurgitation may remain asymptomatic for along time. Moderate degree of aortic regurgitation presents with palpitation, increased fatigability, exertional dyspnoea, and some times chest pain. . Cardiac failure symptoms are unusual as the initial presentation. If aortic regurgitation coexists with aortic stenosis or mitral valve disease, the patient may present with more symptoms at an earlier date. Signs: Patients with isolated aortic regurgitation are moderately built and moderately nourished. If the regurgitation is due valvular endocarditis the patient may also present with evidence of pallor, clubbing and other peripheral signs of endocarditis. The pulse rate and rhythm are usually normal. The character of the pulse is typically high volume and collapsing. This character is due to three pathophysiological mechanisms which are present simultaneously a) an increased stroke volume, b) rapid run off of blood from the aortic circulation and c) peripheral vasodilatation. On must also remember that high volume collapsing pulse may also occur in conditions like persistent ductus arteriosus, arteriovenous fistulas and Paget’s disease of the bone. The blood pressure is also suggestive of aortic regurgitation. The systolic pressure is markedly elevated and the diastolic pressure is grossly reduced and hence the pulse pressure is very high. A typical instance of blood pressure in aortic regurgitation will be 180/40 mm of Hg. When there is coexisting aortic stenosis the systolic blood pressure is not elevated to the same extent as in case of aortic regurgitation. Jugular venous pressure is not elevated in case of aortic regurgitation unless there is congestive heart failure. The jugular venous wave pattern is uncharacteristic. Apex beat is shifted laterally and downwards due to ventricular dilatation. The character of the apex is forceful due to the volume overload. A diastolic thrill is unusual. Left parasternal heave and palpable shock of second heart sound are present only if there is significant pulmonary artery hypertension. On percussion of heart borders the cardiomegaly will be evident. On auscultation the first heart sound is usually normal and the second heart sound also unaltered. No S3 is heard; S4 may be present. The characteristic murmur is an early diastolic murmur of grade2-4 intensity, which is high pitched decrescendo best heard in the second aortic area conducted along the right sternal border. In syphilitic aortic regurgitation, the murmur is best heard in the aortic area and conducted along the right sternal border. The aortic regurgitation murmur is better heard when the patient is sitting up and leaning forward with the breath held in expiration An ejection systolic murmur not associated with an ejection click or conduction to the carotids is heard because of the increased stroke volume due to increased flow across the aortic valve even without any valvular stenosis. But if any mount of aortic stenosis coexists with aortic regurgitation, the 2
  3. 3. characteristics of the systolic murmur will also differ including a thrill and conduction to the carotids. The third murmur, which may occur in aortic regurgitation, is an Austin Flint murmur. This is a mid diastolic rumble heard in the mitral area, due to the displacement of the anterior mitral valve leaflet by the blood regurgitating from the aortic valve obstructing the blood flow from left atrium to the left ventricle. Patients with moderate to severe aortic regurgitation may also have peripheral signs of aortic regurgitation. These are: Alfred de Musset’s sign (head nodding), Muller’s sign (pulsations of uvula), Corrigan’s sign (dancing carotids), Dancing brachial, Traube sign (pistol shot sounds), Durozeiz murmur (diasolic murmur on compression of femoral artery proximally) Hills sign difference in systolic Blood pressure between upper limb and lower limb >20 mm of Hg. Investigations: ECG will show evidence of left ventricular enlargement and left ventricular hypertrophy, but without evidence of strain pattern asymmetrical T inversion and ST depression in V5 and V6 Chest X ray PA view will show cardiomegaly with displacement of apex downward and outward. Pulmonary venous congestion and pulmonary artery hypertension may also be present. Echocardiography will show dilated left atrium and left ventricle. And Doppler echo will demonstrate the aortic valve leak. ECHO will also demonstrate the presence of vegetations in case of infective endocarditis. Cardiac catheterization is diagnostic. Differential Diagnosis: Aortic regurgitation needs to be differentiated from pulmonary regurgitation in which case signs of pulmonary arterial hypertension and right ventricular hypertrophy. On has to look for evidence of acquired connective tissue disorders like rheumatoid arthritis and ankylosing spondylitis. Also look for evidence of congenital connective tissue disorders like Marfan’s syndrome and Ehlers Danlos skin. More commonly a rheumatic etiology will be evident if there is a positive rheumatic history. In that situation the mitral valve is also usually involved Syphilitic aortic regurgitation is suggested by the conduction of the murmur along the right sternal border and a positive VDRL and Khan test. Medical Treatment: • This includes treatment of cardiac failure like diuretics, vasodilators and ACE inhibitors and digoxin. • Restriction of strenuous physical activities and • Salt restriction. • Infective endocarditis as a cause of aortic regurgitation requires treatment for 4-6 weeks given after culture and sensitivity test. Surgical Treatment: Aortic valve replacement is recommended for all patients with severe chronic aortic regurgitation who develop signs and symptoms of cardiac failure, either with bioprosthetic valve or a metallic prosthesis. These patients will require life long anticoagulation. 3
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