ACUTE RHEUMATIC MYOCARDlTlS AT AGE

findings, and the invariant electrocardiograms made it impossible to establish clinically this diagnosis in the case at hand. Exudative mural endocarditis secondarv to bacterial infection. without a similar reaction in the valvular endocardium, is uncommon though Trasoff and Meranze7 mentioned this possibility in association with a Pneumococcal infection. They described a heart with a large thrombus which arose from the left atrial wall slightly beyond the line of attachment of the posterior mitral valve leaflet. The leaflets themselves were moderately thickened. The sequence of events and the significance of the endocardia1 and myocardial lesions, in the evolution of the fully developed abnormality reported herein merit comment 'and speculation. Bacterial invasion of the blood stream, from a septic decubitus ulcer or another site, undoubtedly occurred and produced focal interstitial myocarditis and a large abscess. A solitary abscess of this size, in itself, is an uncommon finding. Shoenfeld et a18 found myocardial abscesses in 0.2-0.5 percent of autopsies while Ryon et ale reported a frequency of 0.181.5 percent. For the most part, these were small abscesses. We believe that this large myocardial abscess initiated the endocardial lesions. The uniform integrity of the endocardium everywhere except over the myocardial lesion, the absence of a demonstrable congenital defect at the infected site, and the rather benign appearance (apart from the inflammatory reaction) of the involved endocardium support this belief. The idea that the vegetations represent a local thrombotic process with subsequent organization and septic degeneration was considered, but the gross and the microscopic features of the involved tissues suggested the mural origin of the vegetations: a ) gentle squeezing of the myocardium, at the diseased area, expressed a thick purulent material which adhered to the surface of the endocardium; b ) microscopic examination of these sites disclosed foci of an interstitial exudative inflammatory process which extended from myocardium to endocardium, disrupted the endothelium, and resulted in the deposition of a necrotic mass of fibrin, bacteria and blood elements on the surface of the myocardium. Focal organization of the process was also present. The isolation of coagulase-negative Staphylococci from the heart, blood and vegetations is another interesting feature of this case. This microorganism rarely causes endocarditis. In a review of the Mayo Clinic records, it was encountered in 1.5-13 percent of patients with bacterial endocarditis.10 All cases hitherto reported described valvular lesions; in our case, this etiologic agent was responsible for a true mural (non-valvular) endocarditis.