Coronary endarteritis in acute rheumatism.

Krehl1, in 1890, was the first to note the occurrence of fibrous intimal thickening in the smaller arteries of the, heart in chronic valvular disease of rheumatic origin. Later Romberg2 drew attention to this intimal thickening and also reported the finding of hyaline thrombi in many of the small arteries of the heart in two cases of acute rheumatism. No change was found in the walls of the thrombosed vessels nor in the tissues surrounding them, and the presence of fissures between the thrombus and the vessel wall showed that the vascular occlusion was sometimes incomplete. Romberg's comment on the absence of muscle tissue infarction in relation to the occluded arteries was that either the hyaline thrombi formed just before death or that the good collateral blood supply of the myocardium prevented muscle necrosis. Rabe3, in an examination of the heart of a child, aged five, who died of rheumatic fever, found proliferative endarteritis accompanied by medial degeneration (mesarterite) in the small and medium sized coronary arteries. Aschoffl ', who has shown that the walls of the small coronary arteries are sometimes involved in the inflammatory nodules which are named after him, has stated that most of the scars in the rheumatic myocardium are due to ischaemic necrosis caused through the consequent sclerotic narrowing of such vessels. Takayasu6, who examined the heart of a girl, aged eight, dying of acute rheumatism, found what he described as canalized emboli in many of the small coronary arteries at or near the apex. These emboli were considered by Takayasu to have come from the vegetations on the valves of the heart. Geipel7, in 1909, reported a case of acute rheumatism in which there was marked endarteritis of the small and medium sized coronary arteries. Stenosis or complete occlusion, through the presence of fibrin masses and proliferated endothelial and subendothelial cells in the vascular lumen, was frequently noticed and some small infarcts in the myocardium were attributed to this. Geipel considered that the fibrin masses were in the nature of emboli derived from the vegetations on the heart valves and that the intimal changes were secondary to the embolic plugging of the vessel. Coombs8 has described the endothelial and subendothelial cell proliferation which so frequently occurs in the myocardial capillaries and arterioles, and has further remarked on the fibrous intimal thickening so often to be seen in the smaller and some of the larger coronary arteries in rheumatic carditis, an observation recently confirmed by Perry9. Wiitjenl°, in his examination of a case of rheumatic myocarditis, found that all the layers of the coronary artery wall could be involved in the territory of the specific inflammatory nodules, and that nodules occurring in the intima destroyed the internal elastic lamina and involved, more or less strongly, the media. In other instances a diffuse eosinophil cell infiltration of the intima without recognizable nodule formation was observed. The lumen of vessels affected in this way was either