A system of practical medicine. By American authors. Vol. 3

by Unknown

As a consequence, the rigid valves, whose edges are round and hard, are drawn toward their base, and thus are made to assume a puckered appearance. A similar process in the chordæ tendineæ causes them to become hypertrophied, rigid, and cartilaginous, while they are diminished in length. In this way the valves are not only diminished in depth, but not infrequently have their free edges approximated to the cardiac walls, so that extensive valvular insufficiency is the result. This, however, does not always happen, for a thickened cartilaginous valve may have such abundant fibrinous or papillary excrescences upon it that the onward current is obstructed and extensive stenosis results.

As the thickening and rigidity of the flaps of a valve increase, their mobility is diminished, and adhesions take place between their edges which begin at their bases and progress toward their apices: so thoroughly do they become adherent that in some cases all evidence of a valvular outline is lost, and a fibrinous diaphragm is formed across the valvular orifice having only a small slit at its centre, looking and feeling like a buttonhole; hence the term buttonhole slit. The mitral opening, which will usually admit the ends of three fingers, may be so narrowed that the end of the little finger will scarcely pass through it, and the aortic opening may become so diminished as not to admit a small quill. These retractions and adhesions cause the mitral valves, with their columns and cords, to assume the form of a perforated cone.

Long stringy masses of fibrin, when located on the aortic valve, sometimes form adhesions with the aortic walls, and thus is induced a sudden and extensive regurgitation.

Insufficiency and stenosis are often found at the same valvular orifice as the result of the thickening, adhesion, and retraction.

Changes at the aortic orifice usually occur after middle life, and induce more insufficiency, retraction, and adhesion than those which are limited to the mitral valve. The mitral valves are the most frequent seat of interstitial endocardial changes in early and adult life. These lesions are analogous to those characteristic of endarteritis deformans. The tendency of the lowly-organized tissue which results from interstitial endocarditis is to undergo fatty and calcareous changes.

The minute patches of fatty degeneration in the imperfectly organized tissue underneath the endocardium sometimes form atheromatous masses containing more or less granular débris. The endocardium over these patches may be destroyed, or the patches may soften and ulcerate and cause extensive destruction of the valves. Valvular aneurism may form in the same manner as has been described in exudative endocarditis. The formation of calcareous granules and plates is a very frequent termination of interstitial endocarditis.

The aortic orifice is the most frequent seat of calcareous degeneration. It is rarely associated with mitral stenosis. So extensive may this process be that little beads of chalky material may be seen studding the free edges of the valve and even extending into the cardiac cavities.

When interstitial endocarditis has its seat in the endocardium of the cardiac cavities, the endocardium will undergo changes similar to those of the valves, and the muscular walls of the heart will be the seat of interstitial myocarditis. As a result, the walls of the heart become thinner and less resistant than normal, and depressions are formed on its inner surface. The process is in reality a fibrous overgrowth, which occurs in spots varying in size from half an inch to one inch in diameter. When it extends through the entire heart-wall the columns and cords may be so shortened as to cause valvular insufficiency.

If the cardiac walls yield so that a well-defined pouch is produced, a condition results which is called aneurism of the heart. Cardiac aneurism, thus induced, is usually seated at the apex of the left ventricle; the aneurismal sac may vary in size from that of a marble to that of a closed fist, and may communicate with the ventricle by a funnel-shaped or ring-like aperture. The walls of the sac are solid and rigid; the internal surface is smooth, but it may be anfractuous. In the latter case clots adhere to its wall. Cardiac muscular fibres are found here and there in the aneurismal walls. They are mostly, however, made up of layers of flat cells, their flatness being the result of pressure.

Aneurisms at the base and in the inter-ventricular septum may result from the extension of a valvular aneurism.