Progressive ventricular dilation in experimental myocardial infarction and its attenuation by angiotensin-converting enzyme inhibition.

The extent to which the impaired left ventricle dilates may have important prognostic implications for survival. To determine the influence of infarct size and duration on ventricular dilation, the passive pressure-volume relation of the left ventricle in the rat after coronary artery ligation was obtained. In the early (0.25 to 2 days) phase, the pressure-volume relation was relatively unchanged in all infarct-size groups, except for a rightward shift in the low pressure range for moderate and large infarcts and a leftward shift in the high pressure range for small infarcts. From 2 to 7 days, ventricular dilatation occurred in all groups in relation to infarct size. Thereafter (to 106 days), in rats with moderate and large infarcts, the left ventricle continued to dilate. Associated with this late dilation was a decrease in left ventricular chamber stiffness and an increase in the volume to mass ratio. To determine whether the potentially deleterious progression of ventricular dilation could be attenuated, the angiotensin-converting enzyme inhibitor captopril was given 2 or 21 days after infarction and continued for 3 months. There was a significant overall effect of this treatment in attenuating left ventricular dilation, which was most pronounced in moderate infarcts. Captopril not only attenuated the rightward shift of the pressure-volume relation, but also markedly lowered left ventricular filling pressures so that operating volumes in treated rats were considerably reduced compared with those in untreated rats, even in large infarcts. Therapy with captopril also had an overall effect in prolonging survival, the most benefit being observed in moderate infarcts with lesser dilated left ventricles.