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The heart, 500g in weight, with subacute myocarditis associated with granulomatous myocarditis may be a good model for the study on the pathophysiologic mechanism of cardiac failure. Furthermore, the clinical data of this case is enough to clarify his all clinical course from admission to death due to cardiac failure. So, we analyzed the clinical data, histologic findings, and morphometric pattern of histologically intact myocardial cells and inflammatory reaction to investigate the pathophysiologic mechanism of the cardiac failure. The results were summarized as follows. 1. Clinically, the heart showed cardiac failure of diastolic phase and abnormal conduction system related to sudden cardiac death. However, it might be adapted to the relatively stable wital signs due to pericardial positive pressure by slowlyprogressed pericardial effusion. 2. The distribution pattern of area of intact myocardial cell area and inflammtion reaction showed relatively even spread of inflammatory reaction and extremely decreased area of myocardial cells to about 21% of total heart. So, its contractility might be decreased below to the 21% of the normal cardiac contractility. 3. The mechanism of the cardiac failure in myocarditis may be sudden inflammatory involvement of conduction system and/or extremely decreased myocardial cell volume due to inflammatory destruction. 4. Morphometric analysis may be a useful objective method to grading the severity of old and recent form of myocarditis. From the above results, the cardiac failure of myocarditis is influenced by the adaptability at the inflammatory abnormality of the conduction system, contractility of injured myocardial cells, and compensation activity of pericardial effusion.
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