Rupture of the chordae tendineas sometimes occurs in the mitral valve when the inflammation happens to extend to these structures. The result will be that during the systole of the ventricle the valvular curtain will be allowed to some extent to pass upwards towards the auricle, and so allow of regurgitation through the orifice.

Aneurysm of the valves is the condition in which a pouch exists, projecting from a valve and with a narrow neck (Fig. 221). It occurs in ulcerative as well as in simple acute endocarditis. With the aid of the accompanying diagram (Fig. 222), the mode of formation of the aneurysm may be illustrated in the case of the aortic valve, which is its most frequent seat. The semilunar curtains which form the valve are each composed of a double fold of endocardium, as represented at a. In acute endocarditis it is the ventricular layer which is principally involved along the line of contact, as indicated at b. The aortic layer is usually smooth and unaltered to the naked eye. At the affected part of the ventricular layer the tissue is softened and during the closure of the valve the single aortic layer may be unable to support the full pressure of the blood. In this way it may be pushed towards the ventricle, carrying before it the softened, ventricular layer, as at c. It will be apparent that, in the case of the aortic valve, the aneurysm will always project into the ventricle. In the case of the mitral valve, on the other hand, the softened layer is on the auricular surface of the valve, and the pressure of the blood during closure of the valve being exercised towards the auricle, the aneurysm consequently projects towards that cavity.

Aneurysms of aortic valve.

Fig. 221. - Aneurysms of aortic valve. There is one to the lift in the form of a pouch, and one to the right which has ruptured.

Diagram of mode of formation of aneurysm of aortic valve.

Fig. 222. - Diagram of mode of formation of aneurysm of aortic valve. The curtain (a) formed of two layers; at (b) its outer layer roughened and softened; at (c) the aneurysm, which has burst at (d), so as to perforate the valve.

As the aneurysm owes its origin to acute endocarditis, its surface is usually covered with vegetations, which are often very abundant, and may so conceal the aneurysm as to lead to its being overlooked. The aneurysm, again, may rupture, and so produce a perforation of the valve. It is sometimes as if the bottom had been blown out of the aneurysm and a short tube left, surrounded by shaggy vegetations (as at d in figure). Even in that case, however, if the neck of the aneurysm be examined, it is often found that the endocardium, as it passes into it, is smooth and unaltered.

(b) Chronic endocarditis commonly follows on the acute form, and, like it, is related to acute rheumatism, chorea, etc, but it may be of more independent origin, not infrequently occurring in the aortic valve along with the similar disease of the aorta, namely, Atheroma. (See further on, under Insufficiency of the Aortic Valve.) It is also stated by Roy and Adami that overstrain of the heart, by acting mechanically on the valvular structures, induces cedema and subsequent thickening. In the ordinary rheumatic form it appears as if the irritation were prolonged in a less intense form, And the changes in the valvular structures extend beyond the localities which we have seen to be mainly affected in acute endocarditis.

The chronic form is chiefly characterized by new-formation of connective tissue. The granulation tissue of the acute stage develops into connective tissue, and the process extends slowly to the remaining structures of the valves. In this way arise great thickenings of the valves (Fig. 223), and, as the connective tissue is of that dense nature common in chronic inflammations, the thickened valvular structures are often exceedingly rigid. The new-formed tissue also contracts, and in this way we may have great retractions of the valves leading to serious deformities (see Fig. 224), as we shall see in studying valvular diseases. Again, it frequently happens that two opposed inflamed surfaces coalesce, and we may have still further deformity from this, as in Fig. 225. We have already seen that the inflammation may extend from the endocardium to the muscular substance, leading to cicatricial transformation of it.

Great thickening of the chordae tendinese of the mitral valve, the result of chronic endocarditis.

Fig. 223. - Great thickening of the chordae tendinese of the mitral valve, the result of chronic endocarditis.

Thickening and shortening of the cusps of the aortic Valve, the result of chronic endocarditis.

Fig. 224. - Thickening and shortening of the cusps of the aortic Valve, the result of chronic endocarditis. Insufficiency of the valve is the result.

Greatly deformed aortic valve seen from the ventricle.

Fig. 225. - Greatly deformed aortic valve seen from the ventricle. The curtains are coalesced into a rigid diaphragm. The rough surface presents calcareous matter.

In the great majority of cases, the endocarditis is limited to, or has its centre in, the valvular structures, but it sometimes happens,that in other parts of the heart an apparently independent endocarditis is set up. This may be along with valvular endocarditis, but separated from it by sound tissue, or it may be without any valvular lesion. We may find an isolated patch of thickening on the surface of the left ventricle,, and we have already seen that the disease may penetrate into the muscular substance.

The thickened and rigid connective tissue frequently becomes the seat of secondary changes. Fatty degeneration may occur. But this is much less frequent than Calcareous impregnation, which may betaken as evidence that the hard, dense, cicatricial connective tissue has, to a great extent, lost its vitality. This condition is so frequent that it may be regarded as a normal occurrence in chronic endocarditis. It sometimes occurs with a very moderate degree of thickening, especially in affections of the aortic valve already referred to as connected with atheroma, and its extent and the date of its occurrence are doubtless determined by individual peculiarities. It may occur in the form of a moderate calcification in the deeper parts of the thickened tissue, or the lime salts may be deposited in a more bulky form so as to give the feeling of considerable stony masses. The occurrence of calcareous infiltration is often of serious import. The valvular structures are rendered still more rigid, and there enters the new element of brittleness. The calcified portion of the valve is exposed very often to mechanical violence in the closure of the valve, and it is common to find that the valve has been broken, as in Fig. 225, and a piece of calcareous matter carried off. So far as the valve is concerned, this is-not very serious, but as the piece carried oft" is usually of some size, the resulting Embolism is frequently of great consequence. Embolism of the cerebral arteries leading to extensive softening is more frequent in chronic than in acute endocarditis, and probably the same applies to-aneurysms of the larger cerebral arteries, which, as we shall afterwards see, may have their origin in embolism. Embolism of the spleen and kidneys is also a frequent result. The rough surface left by the breaking-off of the calcareous piece gets coated with»fibrine, and the fibrine may, by getting detached, form a fresh source of embolism.

It is necessary carefully to distinguish from chronic endocarditis the formation of Opaque patches on the valves with very little thickening. These are due to fatty degeneration and are mentioned at p.

(c) Ulcerative endocarditis (also called Malignant and Infective endocarditis). The special features in this disease are the activity of the destructive process in the heart, its connection with the existence of micrococci, and the virulence of the metastatic processes when emboli are carried to distant parts.