To the practicing physician and to the research investigator alike, the dilated heart has long occupied an enigmatic but challenging role. Transcending etiological diagnosis, ubiquitous to the extent of being commonplace to the pathologist, cardiac dilation, nevertheless, is a major determinant of all functional and therapeutic classification. Even the tempo of the clinical course may be set by the extent to which the heart has become dilated. It follows, then, that in an attempt to elucidate the mechanisms operative in the development of cardiac enlargement, so as better to reverse this process, attention should be directed to that group of myocardial diseases termed myocardoses and myocardites. In many instances, these entities appear to represent a single insult to the myocardium, in contradistinction to the continuing noxious stress of hypertension, congenital defects, valvular deformity, and coronary arterial insufficiency. Even in the case of protracted disturbances, e.g. malnutrition, the areas of disturbed