Morphologic Criteria of Progression and Regression of Cardiac Hypertrophy

Abstract

The heart is able to adapt itself to a demanded load by increasing (hypertrophy) or decreasing (regression of hypertrophy) its muscular mass within a wide range. Overstressing of the ability of adaptation is accompanied by degenerative changes of myocytes. Semiquantitative investigations of endomyocardial biopsies (EMCBs) of patients with dilative cardiomyopathy (DCM) and hypertrophic nonobstructive cardiomyopathy (HNCM) show a fibrosis of the interstitial space, as well as almost similar changes of myofibrils and mitochondria. A reduced number of myocytes in hearts with DCM could explain the decreased functional capacity. Quantitative investigations of endomyocardial biopsies and myectomy specimens in patients with hypertrophic obstructive cardiomyopathy have revealed that hypertrophy and, to a certain extent, hyperplasia of muscle fibers cause asymmetrical thickening of the septum. Experimental investigations of the regression of training-induced hypertrophy in rats have shown that nearly all parameters (cardiac weight, thickness of muscle fibers, myofibrillar mass, interstitial space, and capillary width) returned to the values of controls 14 days after termination of a swimming training regimen. A significantly higher density of capillaries after regression of muscle fiber hypertrophy compared to controls points to a temporal dissociation in the regression of myocyte size and capillary network. Decrease in RNA concentration and an increased number of autophagic vacuoles give evidence for decreased anabolism and increased catabolism may occur during regression. In humans, fibrosis of the myocardium and scar formation explain the irreversibility of cardiac hypertrophy, as observed in some patients with valvular heart disease, despite valve replacement.