Effects of early captopril therapy after myocardial infarction on the incidence of late potentials

Abstract

Background: Late potentials (LP) on signal-averaged electrocardiography (SAECG), recorded 6 to 30 days after an acute myocardial infarction (AMI), identify patients at risk for late arrhythmic events. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce ventricular remodeling and cardiovascular mortality after AMI. Hypothesis: The aim of this study was to investigate the effect of early (<24 h) administration of captopril on the presence of LP on Days 6-30 after AMI. Methods: The study included 117 patients with a first AMI; 63 patients (53 men and 10 women, aged 59 ± 12 years), 35 with an anterior and 28 with an inferior AMI (44 thrombolyzed), received early captopril therapy. The control group consisted of 54 age- matched patients (39 men and 15 women, aged 60 ± 12 years), 19 with an anterior and 35 with an inferior AMI (31 thrombolyzed, p = NS), who did not receive early therapy with an ACE inhibitor. The mean left ventricular ejection fraction was similar in both groups (48 vs. 46%). Time domain analysis of SAECG was performed using a band-pass filter of 40-250 Hz. Late potentials were considered present if any two of three criteria were met: (1) Filtered QRS duration (QRSD) > 114 ms, (2) root-mean-square voltage of the last 40 ms of the QRS complex (RMS) < 20 μV, and (3) duration of low amplitude (< 40 μV) signal of the terminal portion of the QRS (LAS) > 38 ms. Results: In the two groups of patients there were no differences in mean values of SAECG parameters. No patient was receiving any antiarrhythmic drugs. In the captopril group LPs were present in 9 of 63 patients (14%) and in the control group in 17 of 54 patients (31%) (p = 0.046). There was no difference in the number of patients with a patent infarct-related artery in the two groups (76 vs. 59%). Conclusion: Captopril treatment early after an AMI reduces the incidence of LPs recorded on Days 6-30 and may thus favorably affect the arrhythmogenic substrate.