Ventricular remodeling in global ischemia.
To determine the effects of chronic constriction of the left coronary artery on the function and structure of the heart, coronary artery narrowing was surgically induced in rats and ventricular pump performance, extent and distribution of myocardial damage, and the hypertrophic and hyperplastic response of myocytes were examined. Alterations in cardiac hemodynamics were found in all rats, but the characteristics of the physiological properties of the heart allowed a separation of the animals into two groups which exhibited left ventricular dysfunction and failure, respectively. Left ventricular hypertrophy occurred in both groups and was characterized by ventricular dilatation and wall thinning which were more severe in the failing animals. Multiple foci of myocardial damage across the wall were seen in all animals but tissue injury was more prominent in the endomyocardium and in failing rats. The anatomical and hemodynamic changes resulted in a significant increase in diastolic wall stress which paralleled the depression in ventricular performance. Myocyte cell loss and myocyte cellular hypertrophy were more severe with ventricular failure than with dysfunction. Finally, diastolic overload appeared to be coupled with activation of the DNA synthetic machinery of myocytes and nuclear mitotic division. In conclusion, a fixed lesion of the left coronary artery leads to abnormalities in cardiac dynamics with marked increases in diastolic wall stress and extensive ventricular remodeling in spite of compensatory myocyte cellular hypertrophy and hyperplasia in the remaining viable tissue.
Anversa
P
P
Department of Medicine, New York Medical College, Valhalla, USA.
Zhang
X
X
Li
P
P
Olivetti
G
G
Cheng
W
W
Reiss
K
K
Sonnenblick
E H
EH
Kajstura
J
J
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D017202:Myocardial Ischemia / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D018754:Ventricular Dysfunction / Q000150:complications / Q000473:pathology* / Q000503:physiopathology