Effects of angiotensin-converting enzyme inhibitor therapy on QT dispersion post acute myocardial infarction.

The aim of this study was to determine the effect of an angiotensin-converting enzyme inhibitor (ACEI), initiated within 24 hours of an acute myocardial infarction (AMI), on the QT dispersion (QTd). ACEIs have proven beneficial in improving left ventricular remodeling, following an AMI while contributing to a reduction in sudden cardiac death (SCD). A prolonged QTd is a marker of electrical instability predisposing to ventricular arrhythmias and SCD. No one has looked at the effects on the QTd of ACEI therapy initiated within 24 hours of an AMI. The study included 239 consecutive patients who presented with an AMI between January 1, 1998 and December 31, 1998. A total of 105 patients had never been treated with an ACEI, and 51 patients were started on enalapril within 24 hours of presentation. Patient demographics were similar in both groups. All patients were treated with aspirin and beta-blocker therapy. A baseline QTd was determined and recalculated on days 3-4 and 6-7 following the AMI. There was no significant difference in the baseline QTd, heart rate, QTc(min), and QTc(max) between the two groups. On days 3-4 the QTd in the treatment group (A) was 39.2 +/- 19.4 ms, as opposed to 84.4 +/- 31.2 ms in the control group (B) (P = 1.0E-06). This reduction in QTd was accounted for by a significant difference in the QTc(max). The QTd shortened in both groups on days 6-7 with a QTd of 30.0 +/- 17.5 in group A and a QTd of 54.1 +/- 26.3 in group B (P = 1.0E-05). There was a significant difference in ejection fraction (EF) between the two groups with the ACEI treated group exhibiting a lower EF, (0.403 (A), 0.494 (B), P < 0.043). The mean dose of enalapril was 6.45 mg daily in the treatment group. ACEIs have been previously shown to reduce the QTd after two months of therapy following an AMI. This study shows that the beneficial effects of ACEI occur early following administration of the drug. The authors speculate that the reduction in SCD conferred by ACEI therapy may be attributed to its effect on reducing the degree of ventricular dispersion of repolarization following a myocardial infarction.