If the heart suffer, it does so for the same reason that a given joint suffers—because its textures are a niclus for the propagation and action of the rheumatic poison. If the heart contain this second factor it does so naturally and before the rheumatic poison gains en trance to the system. It is, therefore, in danger from the very first; and theoretically there is no reason why it should not give evidence of disturbance at as early a period as the joints. Practically, there is very good reason why it should not do so.
The symptoms of rheumatic inflammation of the fibrous textures of a joint are prominent from the commencement of the attack; those of rheumatic inflammation of the fibrous textures of the heart are more tardily developed, and are not apparent till these textures have suffered for some time.
In both joint and heart the fibrous tissue is the part which suffers first. In the joint the inflammation extends from the fibrous textures to the synovial membrane; in the heart from the fibrous rings and valves to the enclocardial lining. Before the synovial membrane be comes affected, there is already pain, tenderness, and all the evidence of inflammation of the fibrous textures. But until the mischief has extended to the endocardium, there is no evidence of its existence and no possibility of diagnosing inflammation of the fibrous textures of the heart; for such inflammation gives rise to no symptoms or signs until the membrane is roughened.
The signs of endocarditis (to which for the present we shall con fine our attention) are those of roughening of the endocardial sur face of a valve; but such roughening is not produced by the direct action of the rheumatic poison on the lining membrane; it results from friction of the valvular surfaces consequent on inflammatory thickening of the subjacent fibrous textures.
It follows from this that there is a stage of the endocarditis which precedes the roughening of the endocardial surface, and precedes, therefore, the earliest evidence of the heart affection. In other words, rheumatic endocarditis cannot be diagnosed till the ailment has existed for one or more clays. An endocarditis whose physical signs first become apparent on a Wednesday has almost certainly begun on Monday or Tuesday, if not sooner. If the rheumatic poison affect a joint and the heart simultaneously, pain, the earliest evidence of joint inflammation, will precede, possibly by some days, the en docardial blow which is the earliest indication of the heart being affected. The rapidity of development of the endocardial murmur will vary with the acuteness of the attack; but in any case its com paratively late development will make the cardiac inflammation ap pear secondary to that of the joints, though the two may in reality have originated simultaneously.
The point is that while rheumatic arthritis is diagnosed as soon as it occurs, rheumatic endocarditis cannot be diagnosed in its earlier stages, for it gives rise to no symptoms and no physical signs before the valvular surface is roughened.
Keeping before us these special peculiarities of rheumatic endo carditis, we are in a position to take up the important question of the action of the salicyl compounds in such inflammation.
The question has naturally two aspects—a prophylactic and a curative: 1. Do the salicyl compounds tend to prevent heart complications in acute rheumatism? 2. Do they have a curative action on these after they have oc curred? We shall first deal with the prophylactic aspect of the question. That a remedy which rapidly cures acute 'rheumatic inflammation of the joints should tend to ward off, if not prevent, the heart com plications which so frequently accompany such inflammation, s a reasonable supposition. And sanguine hopes were at one time en tertained that such an action the salicyl compounds would have. These hopes have not been realized. Numerous cases have been re corded in which heart complications have appeared in the course of acute rheumatism, after the salicyl treatment had been commenced.
How is this to be reconciled with the views advanced, first, as to the pathology of rheumatic inflammation of the heart; and, second, as to the mode of action of the salicyl compounds? If it be the case that rheumatic inflammation of the heart is produced in the same way as rheumatic inflammation of a joint, and if it be the case that the salicyl compounds rapidly cure the joint inflammation by destroying the rheumatic poison, should not these compounds, in virtue of that action, ward off and arrest the course of heart inflammation? The oretically, yes; practically, no. And "no" for the following reasons: The earliest evidence of the existence of endocarditis is the devel opment of an endocardial murmur. But the roughening of the val vular surface which gives rise to this murmur marks a comparatively late stage of the endocarditis; before it can occur there must be : 1. The reproduction of the rheumatic poison in the fibrous struc ture of the valve; 2. Proliferation of the cellular elements of this structure.