Cellular basis of ventricular remodeling in hypertensive cardiomyopathy.
This review summarizes the effects of long-term pressure overload hypertrophy on the right and left ventricular myocardium. In particular, the role that the fundamental processes of myocyte growth plays in the remodeling of the wall is analyzed quantitatively. Moreover, emphasis is placed on the observation that the duration of the overload is an important component of the onset, development, and progression of time-dependent myocardial dysfunction associated with hypertensive cardiomyopathy. The deterioration in ventricular pump function is postulated to be accompanied by myocyte cellular hyperplasia and capillary proliferation in an attempt to increase the thickness of the ventricular wall and, consequently, to decrease the magnitude of systolic and diastolic stress generated by the elevation in ventricular systolic and end-diastolic pressures. Myocyte cellular hyperplasia constitutes an essential growth reserve mechanism of the heart. Regeneration of damaged and lost myocardium may be accomplished by hyperplasia of myocytes, a phenomenon considered not feasible for several decades.
Anversa
P
P
Department of Medicine, New York Medical College, Valhalla 10595.
Capasso
J M
JM
Olivetti
G
G
Sonnenblick
E H
EH
D009202:Cardiomyopathies / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D002452:Cell Count; D006321:Heart / Q000503:physiopathology; D006352:Heart Ventricles; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D006976:Hypertension, Pulmonary / Q000150:complications; D006977:Hypertension, Renal / Q000473:pathology / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000209:etiology; D009206:Myocardium / Q000473:pathology; D016277:Ventricular Function, Left