ANGIOTENSIN-CONVERTING ENZYME-INHIBITION LIMITS DYSFUNCTION IN ADJACENT NONINFARCTED REGIONS DURING LEFT-VENTRICULAR REMODELING

Objectives. We hypothesized that angiotensin-converting enzyme inhibit ors would limit dysfunction in the first 8 weeks after transmural infa rction in adjacent noninfarcted regions, as well as attenuate left ven tricular remodeling. Background. Angiotensin converting enzyme inhibit ion limits ventricular dilation and hypertrophy and improves survival after anterior infarction, but its effect on regional function during remodeling is not well characterized. Methods. Thirteen sheep underwen t coronary ligation to create an anteroapical infarction, At postinfar ction day 2, eight sheep were randomized to therapy with the angiotens in converting enzyme inhibitor ramipril, and five sheep received no th erapy. Animals were studied with magnetic resonance myocardial tagging before and 8 weeks after infarction. Left ventricular volume, mass an d ejection fraction mere measured, as were changes in percent circumfe rential shortening within the subendocardium and subepicardium of infa rcted and noninfarcted myocardium, both adjacent to and remote from th e infarction. Results. Angiotensin-converting enzyme inhibition limite d the increase in end diastolic volume from a mean (+/-SD) of +1.5 +/- 0.7 ml/kg in control animals to +0.5 +/- 0.8 ml/kg in the treated gro up (p < 0.04), Segmental function,within infarcted and remote noninfar cted tissue did not differ between groups, However, angiotensin-conver ting enzyme inhibition limited the decline in function in the adjacent noninfarcted region 8 weeks after infarction, Percent circumferential shortening in the subendocardium decreased by -13 +/- 5% in the contr ol group compared with -5 +/- 5% in the treated group (p < 0.03), Conc lusions. In concert with a reduction in left ventricular remodeling af ter anterior infarction, angiotensin converting enzyme inhibition limi ts the decline in function in the adjacent noninfarcted region, Dysfun ction in adjacent noninfarcted regions may be an important determinant of left ventricular remodeling after infarction.