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

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 m?V, and (3) duration of low amplitude (< 40 m?V) 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.