Heredofamilial factor as a cause of myocardial damage.
The existence in an inbred strain of Syrian hamster (BIO 14.6) of a genetically transmitted cardiomyopathy (CM) that results in congestive heart failure offers unique opportunities to study causes of myocardial damage and the sequence of events leading to cardiac insufficiency. It is well known that the clinical course and pathologic aspects of the cardiac condition of the CM hamster resemble a type of idiopathic CM in man. This paper presents the findings obtained from light- and electron-microscopic observations of the CM heart muscle of the BIO 14.6 hamster. The investigation included qualitative X-ray micro-analysis of intra- and extracellular calcific deposits in the damaged myocardium, biochemical data of calcium-activated neutral protease in cardiomyolysis, and morphometric analysis for cardiac hypertrophy. It is concluded that the myocardial damage is due to disturbed biosynthesis of contractile components and the cellular membrane system. This defect, being accompanied by persistent hypoxia together with a large amount of Ca2+ and Ca-activated protease, leads progressively to necroses and scar formation with calcification in the cardiomyopathic heart muscle of the left (and later also the right) ventricle. It also leads to hypertrophy as a compensatory mechanism of unaffected cardiomyocytes and ultimately to fatal heart failure.
D000367:Age Factors; D000818:Animals; D002118:Calcium / Q000378:metabolism; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology; D009202:Cardiomyopathies / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D006224:Cricetinae; D004195:Disease Models, Animal; D004577:Electron Probe Microanalysis; D008647:Mesocricetus; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*
D002118:Calcium