Suppression of ventricular premature contractions possibly related to triggered activity by oral diltiazem and atenolol.

The clinical importance of triggered activity as a cause of arrhythmias is uncertain. We assumed that ventricular premature contractions (VPCs) caused by triggered activity could be increased at higher heart rates and be suppressed by calcium channel blockers and beta-adrenoceptor blocker. Thus, we evaluated VPC frequency as a function of underlying heart rate and examined the efficacy of diltiazem and atenolol on VPCs, using 24 hour ECG recording. Plots of VPC frequency vs. heart rate were made at 1-beat/min intervals for all heart rates recorded for at least 5 min during 24 hours. Diltiazem (90-180 mg/day) and atenolol (50 mg/day) were given orally for 4 weeks, respectively in 36 and 16 patients with VPCs of more than 2000/day. Patterns of relationship between VPC frequency and heart rate observed before diltiazem therapy included: an increase of VPCs at higher heart rates (positive correlation) in 16 patients, an increase at low heart rates and a decrease at high heart rates (bidirectional correlation) in 13 patients, an increase at low heart rates and flat curve at high heart rates (positive-flat correlation) in 5 patients, a linear decrease (negative correlation) in 1 patient, and flat curve (flat correlation) in 1 patient. The patterns of correlation in patients treated with atenolol were positive in 6, bidirectional in 7, positive-flat in 2 and negative in 1. Both drugs significantly reduced the VPC frequency per 24 hours for patients with a positive correlation (P group), but induced no significant change for those with the other patterns of correlation (NP group). At the 70% VPC suppression level, diltiazem was effective in 9 of 16 patients of P group and only 1 of 20 patients of NP group (p less than 0.01); atenolol was effective in 5 of 6 patients of P group and only 1 of 10 patients of NP group (p less than 0.05). Both drugs reduced the slope of a positive correlation. These results suggest that: VPCs which increase at higher heart rates may be related to triggered activity, and an evaluation of VPC frequency as a function of heart rate predicts the response of VPCs to diltiazem and atenolol, and probably to other calcium antagonists and beta blockers.