Sometimes the valves may be covered with thick, warty, irregular excrescences that cause loud murmurs, and yet do not seriously interfere with the outgoing blood-current. At other times stenosis of the aortic orifice may be so extensive as to almost obliterate it. When such is the case, the extent of the lesion will be measured much more by the consequent hypertrophy and its effects on the systemic circulation than by the loudness or harshness of the murmur which it produces.
Very frequently the valves are so rigid that they cannot be pressed back against the wall of the aorta, and these unyielding prominences are greater obstacles to the outgoing current of blood than vegetations on the surface of the valves.
In a few rare cases the outlet may be diminished by constriction of the aorta at the point of insertion of the valves. Adhesion of the aortic valves begins at their bases and extends along their free edges to their tips; sometimes they become fused together into a mass, so that they project into the blood-stream in the form of a funnel irregular in shape and studded with calcareous nodules. The line of attachment of the valves to the aorta frequently becomes entirely obliterated.
In some instances the contraction of the valves between their points of attachment causes them to form a deep pocket or pouch, and their points of attachment may be a quarter of an inch apart.
Obstructions at the aortic orifice are frequently accompanied by atheromatous changes in the aorta, the result of chronic inflammation of its tunics—arteritis deformans.
As a result of aortic stenosis the wall of the left ventricle becomes hypertrophied. This change is a gradual one, and is called compensatory hypertrophy: it is due to the increased force required to propel the blood through the constricted orifice.
After a time insufficiency of the mitral valves is apt to occur, caused either by the extension of endocardial inflammation from the aortic valves or by the forcible pressure of blood upon the ventricular surface of the valves.
A slight thickening or roughening of the aortic valves may cause slight obstruction to the outgoing blood-current, which will interfere but little with the emptying of the ventricular cavity, and which rarely leads to hypertrophy of their walls.
ETIOLOGY.—Aortic obstruction is most frequently met with in early and advanced life, the mean age being forty-seven years. It is not uncommon in children; valvular lesions have been found in children under two years of age. It may be induced where the aorta is defectively developed, and some think that imperfect development of the trachea may lead to imperfect expansion of the chest, and thus induce disease of the aortic valve.6
6 Barlow in Guy's Hospital Reports, S. 1, vol. vi. p. 235.