Aortic Stenosis.


Definition.—Aortic stenosis is an obstruction at the aortic orifice, due to changes in the segments of the semilunar valves, or arteriosclerosis, or atheromatous deposits. Simple aortic stenosis is very rare, and is nearly always associated with more or less insufficiency.

Etiology.—The stenosis is usually due to a gradual sclerosis of the aortic valves, and this in turn by calcification. These sclerotic changes generally begin in the arch of the aorta and descend to the valves. Occasionally the thickening of the segments may be due to endocarditis, induced by rheumatism. This occurs more frequently in young subjects, older people being more prone to sclerotic changes.

The aorta may undergo these same changes, the leaflets remaining unaffected, though usually both are involved. The rigid and sometimes calcified leaflets narrow the opening, giving rise to stenosis of various grades and forms. Thus adhesions of the edges of the valves mav form a funnel-shaped opening or "buttonhole" slit. The condition is sometimes congenital.

Pathology.—In addition to the changed condition of the valves and orifices, certain compensatory changes take place. To impel the volume of blood received from the auricle through the constricted aortic opening, requires increased power from the left ventricle, and, as a result of this increased work, a gradual hypertrophy follows. As long as compensation is maintained—and in some cases it is to the end—there is no further change in the heart. Finally, however, owing to the great ventricular tension, sclerotic changes occur in the mitral valve, and, compensation giving way, dilatation follows.

Sclerotic changes having already occurred in the mitral valve, mitral insufficiency follows; as a result, there are auricular dilatation, obstructed pulmonary circulation, and increased work is required, with its consequent changes of the right heart.

There are not the marked arterial changes in stenosis as in insufficiency, for the arterial walls do not receive so strong a volume after each systole; in fact, if the stenosis is extreme, a smaller amount than normal flows through the arteries. If compensation is well maintained, however, the pulse will remain normal.

Symptoms.—Since the hypertrophy of the left ventricle keeps pace with the stenosis, there may be few or no subjective symptoms for years, and the patient dies of some other affection, the heart lesion being discovered during an autopsy. As soon as compensation ceases, however, the lesion shows some of the characteristic symptoms. The left ventricle, unable to throw the proper volume of blood, anemia of the brain and peripheral parts of the body occur. This is announced by dizziness, headache, marked pallor, and sometimes fainting.

These symptoms appear upon slight exertion or undue mental disturbance. With the loss of compensation also comes a disturbance of the pulmonary circulation, which is attended by cough, embarrassed respiration, and sometimes by hemoptysis. With the general systemic circulation impaired, dropsy is frequently seen, though usually confined to the extremities.

In some cases warty or cauliflower excrescences are deposited on the valves, and these, becoming loose, float off into the bloodstream, and are conveyed to the brain, kidneys, spleen, and other organs, and give rise to embolism of these organs.

Local symptoms would suggest the organ or organs affected. The pulse is usually small, easily compressed, and does not correspond to the ventricular impulse. In some cases it is irregular or intermittent.

Physical Signs.—Inspection.—The information gained by inspection depends upon the stage of the disease. Thus, before compensation fails, the apex beat is gradually displaced downwards, and is heaving and forceful, not nearly so pronounced, however, as in aortic insufficiency. After compensation fails, the impulse is feeble. In old people, where the chest-walls are firm and unresisting, the apex beat is not seen at any stage.

Palpation.—Unless emphysema be present, palpation reveals a characteristic systolic thrill more pronounced than in any other cardiac lesion, and is felt at the base of the heart and at the second intercostal space. The cardiac impulse is usually strong and heaving, though the apex beat may be imperceptible if pulmonary emphysema be present.

Percussion.—The condition of the lungs determines largely the extent of dullness; for though there is marked hypertrophy of the left ventricle, if emphysema be present, but little increase in dullness will be noticed. If not present, the dullness will be increased downwards and to the left. When compensation fails, and the rest of the heart suffers changes, the dullness is materially increased.

Figure 20. Pulse-tracing of Aortic Stenosis. Auscultation.—A pronounced harsh, systolic murmur, sometimes musical in character, is heard with greatest intensity over the aortic cartilage, the second right intercostal space, and is transmitted to the great vessels of the neck. We are to remember, however, that the roughened aortic valves, and the sclerotic changes of the intima of the aorta, may give rise to the same sound.

If compensation has failed, and there is marked dilatation, the murmur becomes soft and indistinct. The second sound is weak, and may not be recognizable, owing to diminished blood-pressure in the aorta and the inability of the thickened valves to quickly close the orifice. As there is nearly always present aortic insufficiency, a diastolic or regurgitant murmur is associated with the aortic, giving rise to a double bruit.

Dickenson speaks of a musical murmur heard with greatest intensity in the apex region, and due most likely to regurgitation, through the altered mitral valves.

Diagnosis.—If the patient be advanced in years, and a loud, rough, or musical systolic murmur be heard at the aortic cartilage, the second right intercostal, and transmitted to the large vessels of the neck, and if there be evidence of hypertrophy of the left ventricle, and a systolic thrill most marked at the base, with a small, quick, and sometimes irregular pulse, the diagnosis of aortic stenosis would most likely be correct.

The loud, harsh, roughened sound, not musical, that accompanies sclerotic valves, however, may be mistaken for aortic stenosis, though this murmur is not so likely to obscure the second cardiac sound as where there is stenosis. In some cases of chronic Bright's disease with ventricular hypertrophy due to aortic sclerosis, a murmur may be developed whose maximum intensity is heard over the base; the intensification of the second sound, however, together with the characteristic urinary, symptoms, should enable the examiner to make a proper differentiation. We have basic murmurs in anemia, but here the systolic thrill is absent, and also hypertrophy of the left ventricle.

The Eclectic Practice of Medicine, 1907, was written by Rolla L. Thomas, M. S., M. D.