Chronic Endocarditis.

Synonyms.—Chronic Interstitial Endocarditis; Sclerotic Endocarditis; Fibroid Endocarditis.

Definition.—A chronic inflammation of the endocardium resulting in degenerative changes in the valves and orifices.

Etiology.—In studying the causes of this condition, two classes are to be recognized, the one following acute endocarditis, the other beginning as a chronic inflammation. The great majority of valvular changes follow an attack of acute endocarditis, and all writers and observers are a unit in declaring that over 50 per cent of all such cases can be traced to acute rheumatism; especially is this true where the disease occurs in children and young adults.

A certain number of cases of acute endocarditis are found where the rheumatism was of a vague character, and not recognized as such during- life. Where there is no history of rheumatism. the acute endocarditis may have followed scarlet fever, diphtheria, measles, or pneumonia. Chorea is also responsible for the acute form in children, and which in turn is followed by chronic endocarditis. It will thus be seen that the disease, no matter what the exciting cause, precedes the chronic form in the great majority of cases.

In the second class, the organic changes are frequently the result uf syphilis, malaria, chronic rheumatism, gout, and alcoholism, which is most likely due to the presence of toxins setting up an irritation which develops the disease.

Severe physical exertion, by increasing the arterial tension, provokes an irritation that is followed by endocarditis. This accounts for the number of cases of valvular heart disease found in athletes and laborers whose work necessitates unusual physical exertion, such as molders, boiler-makers, draymen, and soldiers who make long marches.

Arterial sclerosis and Bright's disease give rise to the disease in the same way; namely, by increasing the arterial tension to the point of constant irritation. Traumatism, following a severe blow or crushing injury, has been known to give rise to valvular changes.

Predisposing Causes.—Heredity is generally regarded as predisposing to chronic endocarditis, and the number of heart affections found in some families can hardly be ascribed to mere coincidence, but is in all probability due to the weakened constitution bequeathed to the offspring.

Age determines largely the seat of the interstitial changes. Thus fetal endocarditis affects the right side of the heart, the tricuspid valves being the seat of the disease. In children and early adult life the mitral valve suffers most, while the aortic valve is found affected most frequently in advanced age, though it may be found in early manhood if great physical exertion has been practiced.

Sex.—According to the statistics of F. J. Smith, mitral stenosis occurs more often in women than in men, the ratio being four to one. The reason given for this greater frequency is, that girls and women are more subject to chorea and rheumatism.

Pathology.—The pathological changes are generally confined to the valves, though the entire endocardium may share in the tissue change. The membrane becomes dull, opaque, and covered with an exudate, the membrane losing its elasticity. There is a proliferation of connective tissue-cells in the endothelium, and an infiltration of round cells in the sub-endothelial tissue. These products of inflammation become organized, and give rise to thickening, induration, adhesion, and contraction; and in the advanced stage of the disease, calcification sometimes takes place. As the result of these organic changes the valves and orifices are variously affected.

The tissue changes begin on the surface, where there is the greatest pressure; thus, when the semilunar valves are affected, the primary lesion begins on the ventricular face, the Aurantian body being involved. When the auriculo-ventricular valves are involved, the auricular side is the first impressed.

As progressive changes take place peculiar results follow. At first the base of the valve is involved, to be followed by partial agglutination of the segments. As they contract, they imperfectly close the orifice and we have valvular insufficiency.

The curling of the valves in some cases is so pronounced as to leave mere stubs. These thickened valves offer obstruction to the free flow of blood, and by their failure to completely close the orifice, permit a regurgitation of blood.

When the mitral valve is the one involved, the edges sometimes become adherent, and as the thickened chordae tendineae contract, the valves are drawn into the ventricles, giving it a funnel-shaped appearance.

The more extensive the adhesions, the smaller becomes the opening, and in some cases but a small narrow slit is observed, and is known as the buttonhole slit. Similar changes may take place in the aortic valves, with very similar results. The curling and consequent shortening of the thickened segments permit regurgitation of blood, and where the lining of the orifice becomes involved, a thickened ring lessens the size of the orifice, giving rise to more or less stenosis.

The inflammation may extend a short distance into the aorta, producing sclerosis of its walls. Less rarely we find these same processes taking place at the orifice of the pulmonary artery, the semilunar valves undergoing the same change in varying degrees as the semilunar valves of the aorta.

The tricuspid valves may share in the destructive changes with varying gradation, and give rise to insufficiency of the valves, obstruction to the free flow of blood by their thickened surfaces, and permit regurgitation of blood. These sclerotic valves may finally undergo degeneration and necrosis, following which, atheromatous ulcers may form, which in turn still undergo further change by calcification. These distorted valves are then recognized as cartilaginous or ossified valves.

The diagnosis of these changed conditions, as well as their altered function, will be studied separately under the head of Valvular Lesions.

Endocarditis, separate from valvular lesions, while very rare, may sometimes exist. This does not necessarily imply a uniform thickening, but shows a varied condition. The tissue changes may extend deep into the myocardium, to be followed by necrosis and ulceration.

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