Aortic stenosis is very often due to disease of the aortic valve cusps but sometimes other causes may obstruct the left ventricular outflow tract, e.g.
All these causes lead to valvar aortic stenosis.
Normal aortic area is 3-4 cm2. Symptoms usually develop when the cross section of the aortic orifice is reduced by 75%, i.e., it becomes 0.8 to 1 cm2. Since flow varies more with the opening than pressure, a large pressure gradient exists across the aortic valve (>50-70 mm of Hg at rest). The resistance is a fixed one. This leads to increased end diastolic pressure,concentric left ventricular hypertrophy, decreased left ventricular compliance and a fixed cardiac output. Left ventricular ischaemia develops and ultimately failure ensues. Left ventricular systolic function is however preserved.
More than 80% cases are males.
The triad of symptoms are:
This may be due to following reasons:
(b) Anginal pain
This is due to low mean aortic blood pressure and low fixed output so that coronary flow cannot be maintained at a level desired by the overworking left ventricle. Sometimes the cause is undermined. Atypical angina may also be seen.
This is due to pulmonary oedema from left ventricular failure due to elevated left ventricular end diastolic pressure. It occurs first on effort, afterwards there is paroxysmal nocturnal dyspnoea leading to orthopnoea.
When this triad of symptoms coexist together the aortic valve area is usually reduced to 0.6 to 0.7 cm2.
Precordial bulging may sometimes be present.
Apical impulse is more down than out, forceful and well sustained (heaving in type). Sometimes apex beat is doubled (double kick) due to hypertrophied left atrial impulse. A basal systolic thrill is felt more over the aortic area and also over the carotids and subclavians. It is best felt in full expiration with the patient leaning forwards. This is present only in severe cases.
Over the aortic area second heart sound (A,) is absent or feeble (depending on the degree of stenosis) and sometimes it may be delayed giving rise to reversed splitting of second sound. A harsh mid-systolic ejection murmur (Grade 3-6) is heard which is well conducted upwards along the carotids and subclavians. Sometimes the murmur may be intensified both at Aortic and mitral area and is less intense in between which is called hour glass conduction. Sometimes the murmur may have a musical character. Sometimes the murmur may be preceded by an ejection click (so long the mobility of the valve is preserved). The first sound over the mitral area may be normal or accentuated and may be preceded by SA. Prominent S4 under 40 years is indicative of severe stenosis. A very soft early diastolic murmur may accompany the systolic murmur which is not due to organic aortic regurgitation. Occasionally the murmur of aortic stenosis may be transmitted to the mitral area particularly the high frequency components specially in association with calcific aortic valve (Gallavardin’s phenomenon).
FEATURES OF SUPRAVALAR STENOSIS:
FEATURES OF SUBVALAR STENOSIS:
4 X-ray shows no post-stenotic dilatation, ascending aorta not dilated, cardiac size is enlarged.
Common in children, ejection click absent, aortic early diastolic murmur is usually common. Angiography reveals a small chamber just under the aortic valve, echocardiogram characteristically shows a mid-systolic closure of aortic valves.
The carotid pulse is normal or jerky, the systolic murmur is better heard at the apex and left border of the heart rather than at the base or over the carotid. Angiography reveals obliteration of left ventricular cavity in its apical part at end systole and echocardiography shows characteristically the same finding as in subaortic stenosis.
Medical management has practically prophylactic penicillin, diuretics, salt-poor diet are all very helpful before surgery and when medical complications arise. Operation is indicated in presence of attacks of syncope, progressive left ventricular failure, recurrent anginal pain not due to coronary disease or where the aortic valve area is less than 1 cm2. In presence of both mitral and aortic stenosis, simultaneous correction should be done. Prosthetic or homograft valve is now usually choiced. The mortality for valve replacement is 2%-5% and it increases with age.
Anticoagulation is required for mechanical prostheses but not for bioprostheses. In patients passed 50 years coronay angiography should be done before surgery and if necessy bypass surgery can also be done simultaneously. Recently Balloon valvuloplasty has been started in many centres. However, the mortality is similar tosurgery and restenosis is often seen within I year. So this procedure is mainly done in very poor-risk surgical candidates.
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