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European Heart Journal 1993 14(12):1692-1700;
Copyright © 1993 by the European Society of Cardiology.
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© 1993 The Europen Society of Cardiology

The effects of early captopril treatment on left ventricular volumes and function in patients with and without depressed global ejection fraction after acute myocardial infarction

M. K. KYRIAKIDIS, P. N. PETROPOULAKIS, E. K. GEORGIOU, S. A. MARAKAS, D. A. MICHALOPOULOS, A. A. ANTONOPOULOS, C. C. PROUKAKIS and P. K. TOUTOUZAS

Department of Cardiology and Department of Medical Physics, Hippokration Hospital, University of Athens Athens, Greece

Received 4 February 1993; revised 17 May 1993; .

Correspondence Michael Kyriakidis, MD, 139 143 Karaiskou Street, 185 35 Piraeus, Greece

Abstract

To determine the effects of captopril on left ventricular volumes and function in patients with and without depressed ventricular function following acute myocardial infarction (AMI) we studied 78 patients with a first Q wave AMI and no clinical evidence of heart failure. All patients underwent radionuclide ventriculography (RVG) on the 4th day after admission and were then randomly assigned to receive conventional treatment alone (36 patients, control group) or with the addition of oral captopril, 25 mg three times daily (42 patients, captopril group). RVG was repeated one month after the baseline examination. After one month the left ventricular ejection fraction (LVEF) significantly increased in the captopril group (from 43.2±1.3 to 50.9±1.6%, P<0.001) and remained relatively unchanged in the control group (from 47±1.3 to 49.2±1.7%, P=ns). In the captopril group the subgroup of patients with a baseline LVEF <45% demonstrated a significant decrease in end-systolic volume index (ESVI) (from 53.3 ±3.2 to 42.4±2.8ml.m–2, P<0.002) and a highly significant improvement in LVEF (from 36.3±1.3 to 49.6±1.8%, P<0.00005). In the control group, LVEF also increased in those in whom it was <45% (from 38±1.4 to 42±2.4%, P<0.01), but the increase was less than that in the captopril group (P<0.01), mainly due to an increase in end-diastolic volume index (EDVI) (from 78.2±4.6 to 84.6±12.3 ml.m–2, P=ns). In both the captopril and control subgroups of patients with a baseline LVEF ≥45% there was no significant change in LVEF (from 50.1±0.8 to 52.1±2.6% and 53.4±1.5 to 54.2±2.1% respectively), but there was a trend for both left ventricular volumes to increase (EDVI: from 81.4±4.7 to 91.1±9.9ml.m–2 and 76±5.7 to 90.3±9.2 ml.m–2; ESVI: from 40.6±2.6 to 45.2 ±3.4 ml.m–2 and 32.1±2.6 to 40.1 ±3.8 ml.m–2 respectively, all P=ns).

In conclusion, our study confirmed the beneficial effect of captopril on left ventricular size and function in patients with depressed global LVEF after AMI, but there was no evidence of a similar effect in patients with preserved global LVEF, at least during the first month of treatment.

Key Words: Captopril treatment • acute myocardial infarction • left ventricular function


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