Functional infarct expansion, left ventricular dilation and isovolumic relaxation time after coronary occlusion: a two-dimensional echocardiographic study.

Left ventricular dilation and infarct expansion after acute myocardial infarction are associated with an increased morbidity and mortality. The purpose of this study was to determine whether angiotensin-converting enzyme inhibition could reverse left ventricular dilation and improve the diastolic properties of the left ventricle very early after coronary occlusion. The acute time course of left ventricular dilation and infarct expansion (as determined by two-dimensional echocardiography) and early diastolic isovolumic relaxation time were studied in 20 dogs subjected to 3 h of coronary occlusion. End-diastolic area before occlusion was 8.4 +/- 0.5 and 8.9 +/- 0.7 cm2 (p = NS) in the captopril- and the saline-treated group, respectively. At 30 min after occlusion (pretreatment), end-diastolic area increased to 12.6 +/- 0.8 cm2 in the captopril-treated group (p less than 0.01) and 11.3 +/- 0.9 cm2 (p less than 0.05) in the saline-treated group. Three hours after occlusion and after captopril treatment, end-diastolic area decreased to 9.4 +/- 0.6 cm2 (p less than 0.05 versus 30 min after occlusion), whereas it was unchanged in the saline-treated group. Functional infarct expansion (as assessed by end-systolic anterior to posterior endocardial segment length ratio) occurred early after occlusion, and captopril reduced this expansion. Pretreatment values for early diastolic isovolumic relaxation time increased from 29.1 +/- 2.4 to 50.5 +/- 2.9 ms in captopril-treated dogs (p less than 0.01) and from 34.3 +/- 3.4 to 46.9 +/- 2.7 ms in saline-treated dogs (p less than 0.01) after coronary occlusion, implying a worsening of diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)