This stouter and more tendinous part it is which suffers in acute rheumatism. The lunula is not affected. The granulations which are formed on the surface of the endocardial lining in the earlier stage of inflammation of that membrane are limited to tke convex surface of the line of fibrous tissue which passes from the attached border of the valve to the corpus Arco/6i, and which bounds the lunula below. Along this line the granulations run like a row of beads. The band of fibrous tissue which forms this line is at once the lowest part of the seat of valvular contact and the highest part of the seat of valvu lar strain. Above it there is no strain; below it there is no contact. It is the chief seat of functional activity, therefore its fibrous tissue is the seat of rheumatic inflammation; it is the lowest line of the seat of contact, therefore its endocardial covering is the seat of friction, when rendered unduly prominent by thickening of the subjacent fibrous tissue.
In the mitral valve there is no lunula; the whole structure is equally strained, and no one part is weaker than the rest. A weak point would be very liable to give way, for the strain on this valve is both greater, and more equally diffused over its surface, than is the strain on the aortic. In the case of the aortic valve there is only the blood pressure to be resisted; but in the case of the mitral there is both the blood pressure and the strain of the tightened chorche tendinem.
The fibrous structure of the whole valve may be the seat of in flammatory thickening; but the evidence of inflammatory change in its endocardial lining membrane is limited to the auricular surface, and to the line of contact of the valvular segments. In other words, in the mitral as in the aortic valve the granulations are formed at that line which is at once the seat of strain and the point of contact. It is the seat of strain, therefore its fibrous tissue is the seat of rheu matic inflammation. It is the point of contact, therefore its endo cardial covering is the seat of friction when rendered unduly promi nent by inflammatory thickening of the subjacent fibrous textures. Normally a valve is So perfectly adapted to the size of the orifice which it is intended to close, that in the act of closing its segments come into perfect and firm contact without any friction. They are firmly pressed against each other, but they do not rub. But if the segments be thickened, it is evident that they must come into contact sooner than they ought. The size of the orifice to be closed being unchanged and the force which closes it remaining the same, these thickened segments must come in contact before the closing force is expended. The continued operation of that force after the segments
of the valve are in full contact, must lead to further movement of the segments. Normally their movement is completed at the moment of perfect and close contact; but with a thickened valve contact takes place too soon, and movement is continued for an appreciable time after that event—with the necessary result of causing the valvular segments to rub against each other at the point of premature contact.
To put it otherwise: The swelling of the deeper fibrous textures of the valves necessarily elevates and makes more prominent the superficial covering of the swollen part. As the segments of the valve close, the unnaturally prominent endocardial covering of each comes into abnormally early contact with the opposing segment. The. con tinuance of the act of closure, and therefore of valvular movement, after such contact is complete necessarily causes these elevated sur faces to rub against each other. This friction produces irritation and inflammation of the endocardial coating of the valves at their line of contact. The point is that the primary action of the rheu matic poison on the valves is to cause thickening of their deeper fibrous structure, and that the roughening of the endocardial surface is a secondary consequence of this, and not a direct result of .the action of the rheumatic poison on it.
The morbid changes which take place in acute rheumatic en docarditis are as follows : 1. There is multiplication of the cellular elements of the fibrous structure of the valves 2. As a consequence of this these fibrous structures are thickened; 3. As a result of this thickening there is undue prominence of the eudocardial covering of the valve; 4. As a consequence of this the surfaces of the valvular segments come into abnormally early contact in the act of closure; 5. This causes them to rub against each other during the latter stage of this act; 6. The friction thus produced causes irritation and roughening of the surface of these valvular segments at the point at which they rub; 7. This roughening it is which produces the physical signs of endocarditis.
It will be seen from this that the changes in the endocardial lining membrane by which we diagnose endocarditis are a comparatively late stage of the disease, and that the earlier changes in the valve give rise to no physical signs and cannot be diagnosed—an important point to bear in mind when considering the action, curative and prophylactic, of remedial agents.