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Department of Medicine, New York Medical College, Valhalla, New York 10595
To establish whether coronary artery narrowing
(CAN) in mice was accompanied by depressed ventricular function, tissue
injury, and modifications in cardiac anatomy, the left coronary artery was constricted in FVB/N mice and the animals were killed 7 days later.
CAN consisted of a 53% reduction in luminal diameter, which resulted
in a twofold increase in left ventricular end-diastolic pressure. Left
ventricular systolic pressure and left ventricular + and
dP/dt decreased 15, 21, and
11%, respectively. Left ventricular weight-to-body weight ratio
increased 33%. This hypertrophic adaptation was characterized by a 9 and 20% increase in the longitudinal and transverse cavitary
diameters, which provoked a 1.5-fold expansion in chamber volume. In
contrast, wall thickness decreased 15%. These anatomic and functional
changes induced a threefold elevation in diastolic stress. Foci of
reparative fibrosis were found in the endomyocardium and epimyocardium,
involving 2-3% of the tissue. Finally, myocyte loss in the
ventricle was 15%, and myocyte hypertrophy was 38%. Impaired
ventricular function, diastolic Laplace overloading, myocyte loss, and
decompensated eccentric hypertrophy in mice after CAN mimic the
ischemic cardiomyopathic heart in humans.
coronary artery stenosis; ventricular dysfunction; myocyte number; replacement fibrosis; decompensated eccentric hypertrophy
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