Compensatory hypertrophy in the heart after myocardial infarction in the rat.

Hypertrophy after myocardial infarction would be a very important process for compensation of damaged myocardium and preservation of cardiac function. Fifty-four female Sprague-Dawley rats were studied 5 weeks after randomization to infarct operation, sham operation and control groups. At sacrifice, anteroapical infarcts ranging from 1 to 51% of left ventricle were present in the infarct operated group. When classified according to infarct size, groups with the largest infarcts (greater than 15 to 30% and greater than 30%) had significant (p less than 0.001) cardiac cellular hypertrophy in the noninfarcted myocardium of the septum and anterior walls (fiber diameter 15.9 +/- 2.3 and 14.5 +/- 2.3 microns, respectively) compared with the control group (12.0 +/- 1.8 microns). Because of cardiac hypertrophy, remaining noninfarcted myocardial area, as estimated from serial histologic sections of the heart, was normal in the greater than 15 to 30% infarct group (area 1.35 cm2) compared with the control group (1.43 cm2); however, because hypertrophy plateaued in the greater than 30% infarct group, myocardial area was significantly decreased (1.06 cm2, p less than 0.001), but was still more than expected without hypertrophy. We suggest that hypertrophy accompanies large infarction in the rat and is a compensation for preserving tissue volume lost by infarction. This compensatory response appears to have limitations, such that when very large amounts of myocardium become necrotic, there is not enough hypertrophy to return myocardial volume to normal.