This section is from the book "A Manual Of Pathology", by Joseph Coats, Lewis K. Sutherland. Also available from Amazon: A Manual Of Pathology.
In this lesion the passage of blood from the left ventricle into the aorta is interfered with. It is, in the great majority of cases, caused by chronic endocarditis. The conditions already described as leading to insufficiency of the valve mostly produce also obstruction Of the orifice, by causing rigidity of the curtains, and this is all the more marked when calcareous infiltration ensues. Where the valve is, in the way already mentioned, converted into a rigid diaphragm, then there must be great obstruction of the orifice as well as insufficiency of the valve. These two forms of lesion are, therefore, usually found associated. In acute endocarditis the roughening of the curtains may to some extent obstruct the flow of blood, but the interference is trivial, and will hardly lead to any of the secondary results of aortic stenosis.
The obstruction at the orifice prevents the blood getting away fully during the systole of the ventricle, and there comes to be an overfilling of the ventricle. The ventricle, as in the previous case, is stimulated to increased exertion, and so here also the primary phenomenon is Hypertrophy of the left ventricle. This may completely compensate for the obstruction, and persons may go about comparatively well with an obstructed orifice and enlarged left ventricle. But this is not so likely as in the previous case, and any need for extra exertion on the part of the heart, or weakness of its muscles, may lead to incomplete compensation. In such a case the ventricle will get abnormally dilated, and the auricle will not be able to empty itself fully into the dilated ventricle. The Pulmonary circulation will become engorged and the Right ventricle overloaded, and so we may have all the evil consequences of mitral disease. It will be observed, however, that, as the left ventricle is much more capable of undertaking additional work than the right, it succeeds much more frequently in bringing about a complete compensation. The hypertrophied left ventricle having to dispose of an increased mass of blood, generally does so slowly, and the pulse is consequently slow and regular.
It will have become apparent that in many cases aortic disease is associated with mitral, and that there is frequently combination and complication of the resulting changes in the heart and circulation.
 
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