Joints recover: Why does the Endocardium fail to do so?
There are in this audience many who have treated cases of acute rheumatism and cases of valvular disease in hundreds of instances. We are all aware that in acute rheumatism, however severe the joint lesion may be, however great the swelling, the pain, the local pyrexia, and the effusion, in the large majority of cases, after the usual treatment all these grave symptoms subside, or if they linger in any joint many of us know how certainly they will vanish if we stimulate the trophic and vasomotor nerves by small blisters applied to the adjacent skin, the final issue in most cases being the restoration of every joint to a normal condition. But, alas, we also know that when the endocardium covering the mitral or aortic valve cusps is in like manner attacked, a like restoration does not take place spontaneously excepting in few and rare instances. When regurgitation through the valve, shown by an apex bruit with accentuation of the second pulmonary sound, has occurred in acute rheumatism, if after treating the rheumatism we leave the affected heart to its own course, and the patient to his, persistent bruit, persistent pulmonary accentuation, hypertrophy, dilatation—in fact, life-long heart disease and its train of attendant evils follow in a large majority of cases, and mar or shorten life. Why should the rheumatic heart be so much more intractable than the rheumatic joint?