CORONARY RESERVE IS DEPRESSED IN POSTMYOCARDIAL INFARCTION REACTIVE CARDIAC-HYPERTROPHY

After a myocardial infarction (MI), the remaining myocardium undergoes a compensatory reactive hypertrophy. Although coronary perfusion to the surviving myocardium can be an important determinant of cardiac function in this setting, there are no available data regarding myocardial blood flow in reactive hypertrophy. Accordingly, we measured coronary blood flow and reserve using radioactive microspheres in rats 4 weeks after induction of an MI by ligation of the left coronary artery. Maximal coronary dilation was induced by Carbochrome, a potent coronary vasodilator, infused at a rate of 0.45 mg/kg/min up to a total dose of 12 mg/kg. Sham-operated rats served as controls. All animals in the infarct group had a large MI affecting 30-51% (average, 41%) of the left ventricle. Left ventricular end-diastolic pressure was significantly elevated (30 ± 6.5 vs. 8.0 ± 2.5 mm Hg in sham-operated rats, p < 0.01) and baseline hemodynamic indexes of cardiac performance were significantly (p < 0.01) reduced in this group. Myocyte cross-sectional area measurements were used as an index to quantify the degree of reactive hypertrophy and indicated that the infarcted animals had, on average, a 30% hypertrophic response of the surviving left ventricular myocardium. In the infarcted animals, both coronary flow and vasodilator reserve in the surviving myocardium were depressed. Maximal coronary blood flow in the remaining myocardium was significantly lower than that measured in the sham-operated animals (839 and 1,479 ml/min/100 g, respectively; p < 0.001). Similarly, minimal coronary resistance was significantly higher in the MI group as compared with the sham group (0.12 vs. 0.07 mm Hg/ml/min/100 g, respectively; p < 0.001). There was a significant correlation between minimal coronary resistance and myocyte cross-sectional area (r = 0.65, p < 0.01) or between minimal coronary resistance and left ventricular end-diastolic pressure (r = 0.66, p < 0.01), suggesting that the depression in coronary reserve was related both to the elevated preload and the hypertrophic process itself. Thus, after an MI, the surviving myocardium exhibits a perfusion deficit involving the intramyocardial resistance vessels. This abnormality can render the heart more susceptible to develop ischemia even in the absence of large coronary artery disease.