[Morphologic findings during regression of heart hypertrophy].
The heart is capable of adapting to widely different loads. Increased load will cause hypertrophy with thickening and elongation of the cardiac muscle cells. Beyond the critical heart weight hyperplasia will develop in man. The volume ratio of mitochondria and myofibrils as well as the volume of interstitial tissue and capillaries depends on the type of hypertrophy (training, volume or pressure overload). Hypertrophy will regress when its cause is removed. Training: In experiments with rats 80% of an increase in heart weight caused by swimming was reduced within 14 days after the training program had been stopped. During this time the size of heart muscle cells and the volume ratio of cell organelles had almost completely normalized. From quantitative morphological and biochemical studies, it is supposed that a reduced synthesis but not an obvious increase of catabolism is important in the regression of cardiac hypertrophy. A significant increase in capillary density during the regression period suggests that more time is needed for the regression of capillary length than is required by muscle cells. Training will cause harmonious growth of the left and right chamber wall. During the regression period no quantitative differences of left and right ventricular wall were observed. Pressure overload: Regression of pressure induced hypertrophy is characterized by a reduction of the muscle cell size but not of the amount of collagen in the interstitium. Preliminary studies on pig hearts with an over 100% increase of the weight of their right chamber wall caused by slowly rising pressure load using ameroid constrictors on the A. pulmonalis have shown a 60% reduction of the weight of the right ventricular wall 10 days after removing the constrictor. A reduced mitochondria/myofibrillar ratio becomes normalized. An incomplete or even lacking reduction of the heart weight in rats with spontaneous hypertension (SHR) after therapeutic depression of blood pressure suggests that other factors besides elevated blood pressure are important for inducing hypertrophy in these rats. Valve replacement: An incomplete reduction of heart weight can be observed in patients even after replacement of damaged cardiac valves. Extensive morphological studies on these hearts disclosed recidive infarction or a high degree of cardiac fibrosis as the cause of irreversible hypertrophy. It is still not known whether a case of hypertropied heart with hyperplasia regression will be accompanied by a reduction of the number of myocytes.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D002306:Cardiac Volume; D006332:Cardiomegaly / Q000473:pathology*; D002311:Cardiomyopathy, Dilated / Q000473:pathology; D002312:Cardiomyopathy, Hypertrophic / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D004727:Endothelium / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D006973:Hypertension / Q000473:pathology; D008929:Mitochondria, Heart / Q000648:ultrastructure; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D009210:Myofibrils / Q000648:ultrastructure; D005082:Physical Exertion; D051381:Rats; D011918:Rats, Inbred SHR
Morphologische Befunde bei Rückbildung einer Herzhypertrophie.