Side-to-side slippage of myocytes participates in ventricular wall remodeling acutely after myocardial infarction in rats.

Abstract

To determine whether acute left ventricular failure associated with myocardial infarction leads to architectural changes in the spared nonischemic portion of the ventricular wall, large infarcts were produced in rats, and the animals were killed 2 days after surgery. Left ventricular end-diastolic pressure was increased, whereas left ventricular dP/dt and systolic pressure were decreased, indicating the presence of severe ventricular dysfunction. Absolute infarct size, determined by measuring the fraction of myocyte nuclei lost from the left ventricular free wall, averaged 63%. Transverse midchamber diameter increased by 20%, and wall thickness diminished by 33%. The mural number of myocytes in this spared region of the left ventricular free wall decreased by 36% and the capillary profiles by 40%. The combination of these functional abnormalities and structural rearrangement of the wall resulted in a 7.8-fold increase in diastolic wall stress. A comparable analysis of the interventricular septum demonstrated a 24% reduction in the number of cells across the septal thickness, whereas capillaries were diminished by 26%. Moreover, a 7.2-fold elevation in diastolic stress was computed in this region of the ventricle. The augmentation in diastolic stress was associated with a 22% and a 16% myocyte cellular hypertrophy in the wall and septum, respectively. In conclusion, side-to-side slippage of myocytes in the myocardium occurs in association with ventricular dilatation after a large myocardial infarction and contributes to ventricular remodeling and the occurrence of decompensated eccentric hypertrophy.