Mechanisms of myocyte and capillary growth in the infarcted heart.
To identify the structural mechanisms of cardiac hypertrophy following myocardial infarction, the changes in the dimensional characteristics of the spared myocytes were measured 40 days after coronary occlusion. Further, to determine whether tissue oxygenation in the hypertrophied ventricle was supported by a proportional growth of the capillary network, morphometric analysis was used to measure capillary luminal volume and surface densities, and the diffusion distance for oxygen. Large infarcts of the ventricle (50%) produced a 10% increase in myocyte diameter and a 38% increase in myocyte length. Small infarcts (23%) induced 6% and 15% expansions of cellular diameter and length. After large infarcts, there was a 22% decrease in capillary numerical density that resulted in an 18% reduction in capillary surface and a 16% increase in the diffusion distance for oxygen. The 15% reduction in capillary numerical density seen with small infarcts was associated with a 10% decrease in surface and a 9% increase in diffusion distance. In conclusion, cardiac hypertrophy following myocardial infarction is consistent with cellular shape changes characteristic of a combination of concentric and eccentric hypertrophic growth. The relatively inadequate adaptation of the capillary vasculature suggests that the injured ventricle is more vulnerable to additional ischaemic episodes.
Anversa
P
P
Department of Pathology, New York Medical College, Valhalla 10595.
Capasso
J M
JM
Sonnenblick
E H
EH
Olivetti
G
G
D000818:Animals; D006332:Cardiomegaly / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology*; D008297:Male; D009203:Myocardial Infarction / Q000150:complications*; D009206:Myocardium / Q000473:pathology*; D010101:Oxygen Consumption; D051381:Rats; D011921:Rats, Inbred WKY; D013318:Stroke Volume