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The present study was a prospectively planned subset of the postinfarction, double blind, randomized, multicenter, placebo controlled trial of verapamil, DAVIT II. Patients had 24 hours of Holter monitoring before randomization, i.e., second week after infarction (placebo, n=122; verapamil, n=128), after 1 month (placebo, n=108; verapamil, n=94) and after 16 months (placebo, n=75; verapamil, n = 63) of treatment. The purpose was to evaluate the effect of verapamil on the prevalence and changes over time of arrhythmias and heart rate. In patients monitored twice, a significant increase of average ventricular premature complexes (VPC) per hour from before to 1 month (p=0.0007) and 16 months (p=0.02) after was demonstrated in the placebo group, and from before to 1 months (p=0.01) after in the verapamil group. Average VPC/hr did not change from 1 to 16 months of treatment. A significant increment of >10 VPC/hr was found after 1 (p=0.03) and 16 months (p=0.05) compared to prerandomization in the placebo, but not in the verapamil group. A significant increase of supraventricular arrhythmias after 1 month compared with prerandomization was found in the placebo group (p=0.003) but not in the verapamil group. The prevalence of VPC and supraventricular tachycardia was significantly lower in the verapamil compared with the placebo group after 1 month of treatment. At 16 months no significant difference was found between the two groups. The 24 hour mean heart rate was significantly lower, 3 beats/min, in the verapamil compared with placebo after 1 and 16 months of treatment. Thus a significant increase of ventricular and supraventricular arrhythmias during the first postinfarction month, without change the following year, was seen in the placebo group. Verapamil significantly lowered heart rate, prevented supraventricular tachycardia, and reduced VPC early after an AMI. This rather limited effect of verapamil on postinfarction arrhythmias cannot explain the beneficial effect of verapamil on mortality and major events in patients without heart failure.

The purpose of this study was to examine the 24-hour antiischemic efficacy of once-a-day anipamil compared to placebo in the treatment of patients with stable angina. The study was designed as a double-blind, placebo-controlled crossover study with an initial 3 week single-blind placebo period. The patients received anipamil 80 mg once daily, anipamil 160 mg once daily, and placebo in a randomized order. At the end of each treatment period the patients underwent 24-hour ambulatory ECG recording. Nineteen patients were included, all with typical stable angina pectoris for at least 2 months, exercise test withor = 0.10 mV horizontal or down-sloping ST-segment depression and limited by angina pectoris, and at least 10 attacks of angina pectoris in the initial single-blind placebo period. During the placebo period, a total duration of transient myocardial ischemiaor = 0.10 mV during the 24-hour ambulatory ECG monitoring period was 2263 minutes, 75% of which were asymptomatic. Anipamil 80 mg and 160 mg significantly reduced the duration of episodes to 712 minutes (p0.001), with 87% asymptomatic, and to 913 minutes (p0.001), with 92% asymptomatic, respectively. In conclusion, anipamil given once a day is an effective 24-hour antiischemic drug in the treatment of transient myocardial ischemia.