CORRELATION BETWEEN CARDIAC REMODELING, FUNCTION, AND MYOCARDIAL-CONTRACTILITY IN RAT HEARTS 5 WEEKS AFTER MYOCARDIAL-INFARCTION

Early after infarction, ventricular dysfunction occurs as a result of loss of myocardial tissue. Although papillary muscle studies suggest t hat reduced myocardial contractility contributes to this ventricular d ysfunction, in vivo studies indicate that at rest, cardiac output is n ormal or near normal, suggesting that contractility of the remaining v iable myocardium of the ventricular wall is preserved. However, this h as never been verified. To explore this further, 100 rats with various -sized myocardial infarctions had ventricular function assessed by Lan gendorff preparation or by isolated papillary muscle studies 5 weeks a fter infarction. Morphologic studies were also done. Rats with large i nfarctions (54%) had marked ventricular dilatation (dilatation index f rom 0.23 to 0.75, p < 0.01) and papillary muscle dysfunction (total te nsion from 6.7 to 3.2 g/mm(2), p < 0.01) but only moderate left ventri cular dysfunction (maximum developed tension from 206 to 151 mmHg (1 m mHg = 133.3 Pa), p < 0.01), a decrease less than one would expect with an infarct size of 54%. The contractility of the remaining viable myo cardium of the ventricle was also moderately depressed (peak systolic midwall stress 91 to 60 mmHg, p < 0.01). Rats with moderate infarction s (32%) had less marked but still moderate ventricular dilatation (dil atation index 0.37, p < 0.001) and moderate papillary muscle dysfuncti on (total tension 4.2 g/mm(2), p < 0.01). However, their decrease in v entricular function was only mild (maximum developed pressure 178 mmHg , p < 0.01) and less than one would expect with an infarct size of 32% . The remaining viable myocardium of the ventricular wall appeared to have normal contractility (peak systolic midwall stress = 86 mmHg, ns) . We conclude that in this postinfarction model, in large myocardial i nfarctions, a loss of contractility of the remaining viable myocardium of the ventricular wall occurs as early as 5 weeks after infarction a nd that papillary muscle studies slightly overestimate the degree of v entricular dysfunction. In moderate infarctions, the remaining viable myocardium of the ventricular wall has preserved contractility while p apillary muscle function is depressed. In this relatively early postin farction phase, ventricular remodelling appears to help maintain left ventricular function in both moderate and large infarctions.