To determine whether ventricular short-term enlargement following acute myocardial infarction is related to increased left filling pressures and whether early treatment with captopril alters this process we studied 68 patients with a first acute myocardial infarction. Forty patients with a pulmonary capillary pressure equal or above 17 mmHg were randomized to treatment with conventional therapy plus captopril (n 20) or placebo (n 20), in a double blind fashion. The remaining 28 patients (non-dysfunction group) were treated conventionally. During the first 72 h, afterload showed a prompt decrease in the captopril group as compared to placebo. Changes from baseline to 14 days in end-diastolic and end-systolic left ventricular volume indexes determined by radionuclide ventriculography were: non-dysfunction, 85.6 (+/- 21) vs 88 (+/- 20) and 44 (+/- 17) vs 44 (+/- 17) ml.m-2; captopril (n 20), 96.6 (+/- 18) vs 99 (+/- 19) and 66 (+/- 22) vs 65 (+/- 22) ml.m-2; placebo (n 20), 96 (+/- 25) vs 113 (+/- 19) (P < 0.001) and 63 (+/- 18) vs 74 (+/- 22) ml.m-2 (P < 0.01). This study indicates that short-term ventricular enlargement is related to the degree of ventricular dysfunction and that captopril may improve this process.