For the segments of the valves to come in contact is natural; but contact does not imply friction. Healthy valves normally come into firm and close contact, without in any way rubbing against and irri tating each other; and this all the valves of the heart do seventy times every minute-100,800 times every day, 36,892,000 every year—and yet there is no evidence of friction or irritation until suddenly some day, after this smooth action has gone on uninterruptedly at this rate for maybe twenty-five years, and after the segments of each set of valves have, without injury and without rubbing, come into close and direct contact more than nine hundred millions of times (922,300,000) suddenly some clay the rheumatic poison gains entrance to the sys tem, and the smooth working of the valves comes to an end—they begin to rub; the friction gives rise to irritation and inflammation of the surface of the valve, and the symptoms and signs of endocarditis are developed. How is this? How can the rheumatic poison cause the segments of the valves to rub against and irritate each other? That they do rub is undoubted. That the rheumatic poison is the cause of the morbid change is equally undoubted. The question which we have to consider is how the friction is produced.
If the inflammation of the endocardial covering of the valve be the result of friction—and there is no reason to doubt that it is so; and if this friction be a result of the action of the rheumatic poison on the valve—and there is no reason to doubt that such is the case— there must be a stage of the valvular lesion which not only precedes the inflammation and roughening of its endocardial covel1ng, but precedes and gives rise to the friction which causes this. Wherein does this stage consist? Structurally a valve consists of two folds of the endocardium en closing between them the fibrous or tendinous material which imparts to the valve its strength, its capacity to resist the pressure of the blood, and to perform the function which it is intended to fulfil. In eudocarditis the inflammation must commence in one of these struc tures, for there is no other structure to be affected ; and there is good reason to believe that the mischief commences in the fibrous structure of the valve and involves its endocardial covering only secondarily.
We have already seen that the rheumatic poison acts chiefly on those fibrous structures which enjoy the highest degree of functional activity. This is why the large joints suffer more than the small, and the valves of the left side of the heart rather than those of the right. The part of the valve which fits it for the work it has to do, and imparts to it its strength and capacity to resist pressure, is not the endocardial covering but the fibrous structures which that en closes. This fibrous structure is the seat of functional activity ; for
that reason it is the part of the valve on which we should expect the rheumatic poison to act primarily and chiefly. And so it is found to be. The stage of rheumatic endocarditis which not only precedes the evidence of inflammation of the endocardial covering of the valves, but also precedes and gives rise to the valvular friction which induces that inflammation, is the stage of inflammatory thickening of their subjacent fibrous texture. The earliest change which takes place in this texture as a result of the inflammation consists in multiplication of its cellular elements. This is the first and earliest result of the action of the rheumatic poison on the valve. Let us see how this would affect the aortic valve. A segment of this valve consists of a duplicature of the endocardial lining membrane, inclosing within it the fibrous structure. At the centre of its free border is an elevated fibre-cartilaginous nodule—the corpus Bands of fibrous tis sue stretch across the valve to its nodule from the border of valvular attachment to the aortic ring. Some of these run along its free sur face; others spread out over the body of the valve, and come to a point, as it were, at the corpus Arantii. Between the fibres of the free margin and those of the body of the valve there is, on each side of the nodule, a small space over which no fibres run. This space, called the lanula, consists simply of a duplicature of the endocardial lining; it is the thinnest part of the valve. In the act of closure the three segments of the valve are thrown together into the middle of the aortic outlet, and the three corpora Aran iii come into contact. at its centre. The three 'unlike also come into contact, and are firmly pressed against each other by the aortic column of blood. They are all equally pressed down by this column; but the pressure. thus ex ercised on each individual segment is counterbalanced by the counter pressure on its other side of the two remaining segments. Thus this thin portion of the valve is freed from strain; for the greater the pressure of the blood column the more perfect is the contact of the lunuhe, and the greater the counter-support which they give each other. The part on which the strain falls is the thicker fibrous por tion of the valve which bounds the lunula below. The strain begins where the counter-pressure of the opposing segments ceases. "The force of the reflux • is sustained by the stouter and more tendinous part of the valve" (Quain).