CHAPTER IX

CHRONIC ENDOCARDITIS

Pathogenesis-Morbid Anatomy—Effects on the Functions of the Valves—Effects on the Heart and Circulation-Effects on other organs.

CHRONIC endocarditis is commonly the sequel of an acute or subacute inflammation of the endocardium, but in a large number of instances the morbid process develops gradually and insidiously, and is chronic from the beginning.

Rheumatism is by far the most common cause of chronic endocarditis in persons under middle age. During and after this period of life chronic inflammation of the endocardium (which gradually merges into and becomes indistinguishable from the morbid condition known as atheroma or arterio-sclerosis) usually depends on the strain imposed on the valves and walls of the heart by longcontinued or recurrent high blood pressure in the aorta. The walls of this vessel suffer in common with the heart, and in many instances are the primary seat of the inflammatory or degenerative changes. Excessive blood pressure in the aorta is most commonly due to the protracted high arterial tension that is associated with renal disease, gout, chronic poisoning by lead or alcohol, excessive eating and drinking, and the defective elimination of the waste products of metabolism, old age, and other conditions. It is also produced by muscular strain, more especially when the effort is made in a constrained position or is accompanied by fixation of the chest and closure of the glottis, as in the case of miners, colliers, navvies, wharfingers, etc. Here, although the stress is intermittent, it acts at times with great intensity, and frequently obtains over a considerable number of years.

Syphilis, chronic alcoholism, and excessive eating and drinking, etc., which are potent factors in the causation of atheroma, no doubt frequently co-operate with strain in the production of degenerative or chronic inflammatory lesions of the cardiac valves. It is probable, too, that both gout and syphilis occasionally act as direct exciting causes of endocarditis.

The influence of chlorosis in the causation of chronic valvular changes must be ascribed to the high arterial tension which is sometimes found in association with this disorder.

Mental excitement or worry, and prolonged acceleration of the

heart's action, when combined with strain, may also be mentioned as occasional causes of chronic valvular changes.

In some instances endocarditis has followed external violence in the shape of a blow or fall on the chest.

Rupture of a valve and subsequent valvulitis is occasionally produced by sudden muscular effort.

PATHOLOGY AND MORBID ANATOMY

As in the acute form of the disease, the valvular structures on the left side of the heart are the parts most commonly affected. Right-sided valvular lesions are seldom observed, except as the result of diseases of the lungs or left heart, and in some instances of fœtal endocarditis, or congenital malformation. The rarity of post-natal inflammatory affections of the pulmonic and tricuspid valves has already been accounted for under the pathology of acute endocarditis.

Chronic endocarditis of the mitral valve is usually of rheumatic origin.

The aortic valve, on the other hand, suffers more commonly from the effects of strain. In any event, strain tends to perpetuate and aggravate chronic inflammatory or degenerative changes affecting either the mitral or aortic valve.

The morbid process in chronic endocarditis consists primarily in a gradual fibrosis of the valves and their attachments, which, in consequence, become thickened, hard, and rigid. The subsequent contraction of the newly formed fibrous tissue leads to a variety of issues, among which are narrowing of the valvular orifices, puckering, retraction, and distortion of the curtains of the valves, and shortening of the chorda tendineæ.

The thickened endocardium is very liable to be attacked by atheroma, or the disease may have been originally of an atheromatous nature, and in either event the affected structures are commonly the seat of ulceration and calcification.

Ulcerative lesions lead to thinning, or even to perforation of the valvular curtains, and it sometimes happens that the flap of a valve becomes partially or wholly destroyed by the extension of this process. In other instances the aortic orifice, less commonly the mitral opening, is converted into a calcareous ring, and the segments of the valves not infrequently undergo a similar transformation.

The aortic valve is especially liable to atheromatous changes, owing to the frequent extension of the morbid process from the root of the aorta. The disease may in like manner spread from the aortic to the mitral valve.

Acute endocarditis often attacks the sclerosed and degenerated tissue, and may give rise to vegetations which are sometimes a source of embolism.

M

The endocardial changes in chronic endocarditis are not necessarily confined to the cardiac valves.

Patches of thickened tissue are often found in other parts of the lining membrane of the heart, and these may become atheromatous, and in some instances ulcerate, or undergo a calcareous transformation.

EFFECTS ON THE FUNCTIONS OF THE

VALVES

The effect of chronic endocarditis is to impair to a greater or less extent the functional efficiency of the valvular apparatus of the heart, and thus to interfere with the normal circulation of blood through the organ.

The valvular inefficiency may take one of three directions, i.e. the damaged cusps may be unable to completely close the orifice which they guard, or the orifice itself may be narrowed, or, as most commonly happens, the two conditions are combined in varying proportions.

In the first event the valve permits the backward flow of blood, and is said to be incompetent; in the second the onward flow of blood is hindered, and the term "stenosis" or obstruction is applied to the condition of the opening.

Incompetence of a valve may occur without obstruction at the orifice which it guards, as the result either of retraction or ulceration of the valvular curtains.

Obstruction at an orifice, on the other hand, is very commonly attended by some degree of incompetence of its valve, owing to the usual inability of the valvular cusps, whether damaged or not, to adequately close the narrowed opening.

EFFECTS ON THE HEART AND CIRCULATION

Organic valvular disease of the heart, whether obstructive or regurgitant, tends to produce anæmia in front and congestion behind the seat of the lesion. This result is, however, seldom very obvious at first, except in cases where incompetence of a valve is suddenly produced, owing to the establishment of compensatory changes, which temporarily, at least, restore the balance of the circulation.

Compensatory changes always entail some degree of enlargement of the heart, and the effect of any particular lesion in this respect depends on the following general considerations:

1. The valve affected, and the nature and tendency of the morbid process which is concerned in the production of the valvular defect.

2. The suddenness and extent of the lesion.

3.

The age, sex, occupation, habits, and general condition of the patient.

These points will be considered in detail under the account of the prognosis of valvular affections.

Enlargement of the left side of the heart is very commonly accompanied by hypertrophy of the right ventricle, which, by keeping up the blood pressure in the pulmonic circulation, comes to the assistance of the left ventricle.

Disease at any cardiac orifice tends in course of time to produce an increase in size of the openings situated behind the seat of the lesion. As a rule, regurgitant lesions are more effective in this respect than obstructive disease in the same situations. Indeed, according to Professor Hamilton, stenosis of the mitral or aortic opening causes little or no enlargement of the pulmonic and tricuspid orifices, but this view is opposed to the opinion of the majority of writers on diseases of the heart. Nevertheless, an increase in size of the pulmonic opening is hardly ever observed, and incompetence of the pulmonic valve is one of the rarest of cardiac lesions.

EFFECTS ON OTHER ORGANS

Valvular disease of the heart leads, sooner or later, in the large majority of cases, to congestion of the pulmonic and systemic circulations, and is, in consequence, attended by disturbance of function of the various organs throughout the body.

Moreover, long-continued venous congestion of the viscera induces organic changes which are most marked in the lungs, liver, stomach, spleen, kidneys, brain, and heart.

The pulmonic lesions most commonly found are-congestion and oedema of the lungs, dilatation and rupture of the pulmonic capillaries, pulmonary apoplexy, brown induration of the lungs, bronchitis, and lobar pneumonia.

In the early stages of valvular disease the liver becomes enlarged and congested. Atrophy and fatty degeneration of the hepatic cells ensue, and ultimately the fibrous tissue of the organ is increased. On section the viscus presents the typical "nutmeg" appearance.

The mucous membrane of the stomach and intestines is congested, and may show hæmorrhages. Catarrhal inflammatory changes are commonly observed throughout the alimentary tract.

The spleen is enlarged and firm. It shows on section a dark purple colour owing to congestion. Infarcts may be seen, and the fibrous stroma of the organ is increased.

The kidneys are usually enlarged and indurated. On section the medullary portions are seen to be engorged with blood, and there may be signs of old or recent infarction. The kidneys sometimes

show cirrhotic changes.

The vessels of the brain are usually congested, and the organ itself may be shrunken. Signs of embolism may be seen.

The myocardium is not uncommonly the seat of pigmentary,

Relative insufficiency (as the condition is usually termed) of the pulmonic valve is practically unknown.

Mitral regurgitation is not uncommonly due to dilatation of the orifice of the valve, whereby the proper adaptation of the flaps is prevented.

The enlargement of the mitral opening is, in the large majority of cases, part of a general dilatation of the left ventricle, and the muscular constriction of the orifice, which takes place during systole, is insufficient to enable the valvular curtains to come into apposition. Defective muscular closure of the valve is in some instances the sole cause of its insufficiency.

Tricuspid incompetence is, mutatis mutandis, brought about in a similar way.

5. Congenital malformation of the valves and intra-uterine endocarditis. Pulmonic stenosis, which is frequently associated with some other structural or valvular defect of the heart, is the most common congenital malformation of the cardiac valves.

Intra-uterine endocarditis usually affects the right side of the heart, and the pulmonic valve suffers more frequently than the tricuspid.