In these patients, verapamil treatment may offer a possibil¬ ity for secondary prevention and improve quality of life.

Deedwania and Carbajal also describe diltiazem as an established treatment after non-Q-wave infarction. They do not comment on verapamil for secondary prevention, although the arguments for verapamil compared with dil¬ tiazem are more obvious from a scientific point of view. The non-Q-wave diltiazem reinfarction study recorded 15 reinfarctions in 287 diltiazem- and 27 reinfarctions in 289 placebo-treated patients in the 2-week trial period (P=.06, two sided); 11 patients in the diltiazem group and nine pa¬ tients in the placebo group died.5 Verapamil, 360 mg/d, has been tested in two large postinfarction trials. In the Danish Verapamil Infarction Trial I (DAVIT I),6treatment started immediately after admission; in the 6-month trial period, the mortality rate was 12.9% in the 717 verapamiltreated and 14.0% in 719 placebo-treated patients (not sig¬ nificant); the corresponding first reinfarction rates were 7.9% and 9.2% (not significant). In DAVIT II,7-8 treatment started in the second week after the acute myocardial infarction and continued for at least 12 months (mean, 16 months). End points were total death and the first major event, ie, the first rein¬ farction or death. Mortality rate after 18 months was 11.1% in the verapamil group (n=878) and 13.8% in the placebo group (n=897) (hazard ratio, 0.80; 95% confidence interval [Cl], 0.61 to 1.05; P=. 11); the first major event rates were 18.0% and 21.6%, respectively (hazard ratio, 0.80; 95% CI, 0.64 to 0.99; P=.03); and the 18-month first nonfatal reinfarction rate was 7.2% in verapamil- and 9.4% in placebo-treated patients (hazard ratio, 0.70; 95% CI, 0.50 to 0.99; P=.03). Deedwania and Carbajal also use results of meta-analysis to document effect of treatment. When the method proposed and used by Yusuf et al3 for evaluation of the effect of s-blocker treatment is applied to results of DAVIT I and DAVIT II, mortality was reduced with 22% (odds ratio, 0.78; 95% CI, 0.63 to 0.99 ; P=. 04) ; first maj or events with 21 % (odds ratio, 0.79; 95% CI, 0.65 to 0.96; P=.02); and first rein¬ farctions with 27% (odds ratio, 0.73; 95% CI, 0.57 to 0.94; P=.02) in verapamil group compared with placebo group.8 It is important to note that (1) verapamil significantly reduced the incidence of angina pectoris; (2) the most pro¬ nounced effect of verapamil is found in patients without heart failure priorto randomization, mortality rates of 7.7% in the verapamil group and 11.8% in the placebo group (hazard ratio, 0.64; 95% CI, 0.44 to 0.94; P=.02), and no deleterious effect was observed in patients treated for heart failure prior to randomization (hazard ratio, 1.05; 95% CI, 0.72 to 1.54; P=.79); and (3) during follow-up, verapamil,7"9 contrary to diltiazem10 did not provoke new heart failure. The results of DAVIT I and DAVIT II support the view