Endocarditis - Rheumatism

fibrous, inflammation, lining, membrane, heart, valve, seat, fibrin and surface

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Microscopic examination of the affected portion of valve confirms this view of the nature and seat of the morbid change. On making a section of one of these granular nodules, and submitting it to such examination, it is foundthat the seat of swelling is the deep layer of fibrous tissue, and that the superficial lining of the valve is merely raised up by the multiplication of the cellular elements of the sub jacent fibrous texture. "If a valve with these nodules be cut for the microscope across the plane of its curtain, so as to show a section down through one of the small nodules, this will be found to be com posed of a simple cloudy swelling of the tissue of the valve through a multiplication of the cellular elements in its fibrous structure, which here and there by its excess raises the surface into a little hillock. If the hillock takes the form of a distinct projecting grain, you will always find on the top of it a cap of fibrin separated from its sub stance by a line which the microscope defines very clearly. This cap of fibrin differs in composition from the hillock itself, though the difference is more easily seen than described, for the organization in both is very low; but the fibrin is almost structureless, while the hillock of swollen valve substance shows the regularly placed nuclei of fibrous tissue" (Wilks and Moxon).

The cap of fibrin here described is fibrin which is deposited directly from the blood on the roughened surface of the endocardium, just as it would be deposited around any foreigia body. The true seat of the inflammation is the deeper fibrous tissue of the valve.

When rheumatic inflammation attacks the fibrous rings it pro duces there the same multiplication of the cellular elements and the same thickening as it causes in the valves, but thickening of the fibrous textures of the rings is not of so much importance, for it gives rise to no such rubbing as tales place- when the valves are affected. The sole result is thickening of the fibrous rings, and possibly some narrowing of the orifice. There is no friction, and no roughening of the endocardial surface.

Rheumatic endocarditis then is primarily and essentially a disease of the fibrous structures of the heart. It is therefore limited to that portion of the endocardial contents in which these structures exist. The small portion of the lining membrane of the heart which covers the fibrous valves very frequently suffers; the much more extensive portion which lines the heart's cavities remains unaffected. The sole difference between the two is that the one is, and the other is not, in direct contact with the fibrous textures, and that the one is, and the other is not, the seat of friction when these textures are inflamed and swollen.

The lining membrane of the heart differs in structure, in nature, and in function, from that which invests it externally. Error and

misconception have arisen from not recognizing this, and from re garding eudocarditis as bearing to the eudocardial lining membrane the same relation that pericarditis bears to the pericardial invest ment. There is little or no analogy, either physiological or patho logical, between the two membranes. The function of the endo cardial lining is, by presenting a smooth surface to the blood, to facilitate its onward flow. It has exactly the same part to perform as the lining membrane of the great vessels, with which it is structurally continuous. Neither in the heart nor in the arteries does this mem brane tend to take on inflammatory action; and when inflammation does occur in it, it shows no tendency to spread. The irritation pro duced by the rubbing of a valvular vegetation against the lining membrane of the ventricle may be so great as to cause ulceration at the point of contact; but the mischief is limited to this point, and does not spread. There is no such disease as acute general rheu matic inflammation of-the endocardiurn. The membrane has no ves sels, and inflammation cannot spread over its surface, as it does over that of the vascular pericardium.

The symptoms and signs of rheumatic endocarditis vary with the seat of the disease and the severity of the attack. Occurring as it does in the course of acute rheumatism, any febrile disturbance to which it may give rise is apt to be lost in that attributable to the joint in flammation. That endocarditis slightly raises the temperature there can be no doubt, but the invasion of fresh joints has a more marked effect in that way, and as the cardiac complications generally occur at a stage of the illness when fresh joints are apt to suffer, it is sel dom possible to say how much of the abnormal rise is due to the heart affection. Inflammation of the endocardium may cause less general disturbance than inflammation of a joint, while its local ef fects may be so slight as to cause no discomfort to the patient.

The symptoms special to it are subjective and objective. The subjective are not commensurate with the serious nature of the ail ment. They vary with the severity of the attack. Frequently they are altogether absent. In very acute cases there may be pain in the cardiac region; the heart's action may be disturbed and rapid, the breathing accelerated, oppressed, or even labored, and the patient very anxious. If both aortic and mitral orifices and valves are acutely in flamed, such are apt to be the symptoms. But in such acute cases the muscular substance of the heart is generally more or less in volved in the inflammatory mischief, and it is probable that some of the symptoms are due to this, as much as to the endocardial inflam mation. Moreover, the pericardium is also liable to be inflamed in such severe cases.

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