Studies on the pathogenesis, therapy, and prevention of congestive heart failure are greatly hindered by the lack of easily reproducible disease models. There is presently no standardized and generally accepted method for the induction of heart failure in laboratory animals, although a number of techniques have been devised. 1-lO Pertinent literature indicates that the type of failure which develops during persistently increased stress produced by overload, when the mechanical demand is enhanced in proportion to the active mass of the heart (eg failure caused by aortic stenosis or by aortic valve insufficiency), has been the most intensively investigated because its primary causes are the least complicated and because it can readily be imitated by experimental procedures. Although theoretically an analogous situation prevails when, conversely, the active contractile mass of the heart is diminished (eg by an infarct or other degenerative myocardial lesion), this type of failure is difficult to induce experimentally. Studies on dogs, rats, and other laboratory animals suggest that, if the survival time following extreme destruction of the myocardium (by coronary artery ligature or electrocautery) is sufficient, the remaining contractile ventricular mass is able to compensate for the nonfunctioning portion of the heart over a long peri0d.*~-14 In fact, some investigators believe that as little as 15-20% of the total ventricular mass is sufficient to maintain adequate systemic circulation. 15 Nevertheless, it should be noted that a single injury to the heart muscle was produced in all the afore-mentioned studies, whereas spontaneous pathological processes in man often cause intermittent and graded injuries to the myocardium.

The existence in an inbred strain of Syrian hamsters of a genetically transmitted (or conditioned), degenerative cardiomyopathy that terminates in congestive heart failure offers unique opportunities to study the sequence of events leading to cardiac insufficiency and to analyze the importance of extracardiac factors in the mechanism of generalized venous congestion. This hereditary disease, which has a 100% incidence in the pedigreed BIO 14.6 strain of hamsters, is apparently a primary myopathy. The degenerative lesions that occur in all striated muscles are definitely noninflammator. y in nature. 16-lQ The gross and histopathological abnormalities seen in the middle-aged or older myopathic hamsters, except those of the cardiac and skeletal muscles, are consistent with long-standing passive venous congestion, and this progressive cardiovascular insufficiency may be regarded as the ultimate cause of death. 20 Although our earlier studies, briefly summarized above, largely characterized the morphogenesis and, at least in some respects, the enzyme histogenesis of the cardiac-and skeletal-muscle lesions of the myopathic animals, several important questions remained unanswered. We were especially interested in estab-