Left ventricular remodeling after myocardial infarction is closely related to the prognosis of the patients with infarction and can be modified by angiotensin converting enzyme inhibitor. In experimental transmural infarction rat model, captopril decreases the ventricular compliance and simultaneously decrease the ventricular volume, but its effects on the nontransmurally infarcted heart are not elucidated.

Female Sprague-Dawley rats underwent 45-minute left coronary artery occlusion followed by reperfusion to produce nontransmural myocardial infarction. At 5 days after infarction, rats were randomized into two groups : untreated(n=8) and captopril-treated(captopril 2g/liter drinking water)(n=8). After 21 days of treatment, the hearts were arrested at diastole and excised. Passive pressure-volume curve of the left ventricle was plotted, and the stiffness modulus and mean compliance were calculated in the range of 5 to 30mmHg of pressure. Infarct size was also measured to confirm each group has similar size of lesion. The extent of fibrosis(relative area of fibrosis to randomly-selected peri-infarcted zone) was quantified on Masson's trichrome-stained ventricular slices by automatic image analysis software.

Compared with untreated group, captopril-treated rats showed significantly decreased ventricular weight-to-body weight ratio(2.60±0.18mg/g vs. 2.84±0.20, p<0.05), decreased ventricular stiffness modulus(7.24±0.61 vs. 8.28±0.57, p<0.005), increased mean compliance(9.71±0.75 1/mmHg vs. 7.55±0.67, p<0.0001), and decreased fibrosis extent(0.82±1.49% vs. 5.53±5.33, p<0.01).

These findings suggest that captopril increases the compliance of nontransmurally-infarcted left ventricle at least partly by the suppression of fibrosis, in contrast with previous findings that captopril decresed the passive compliance of transmurally-infarcted ventricle.