Antiarrhythmic effects of VVI pacing at physiologic rates: a crossover controlled evaluation.

Ventricular pacing can prevent bradycardia-dependent ventricular ectopic activity (VEA) and is helpful in some cases of drug-refractory ventricular tachycardia (VT). This study is a prospective evaluation of VVI pacing for the control of VEA not related to underlying bradycardia, drug side-effects, or prolonged QT interval syndromes. Twenty-nine patients undergoing serial electrophysiologic-pharmacologic testing for VT control were studied. Eighteen of these patients (12 men; mean age = 60.1) both completed the protocol and had sufficient VEA for analysis. Coronary disease was present in 13 patients, cardiomyopathy in two patients, and one patient each had myocarditis, mitral valve prolapse, and no structural heart disease. Ambulatory (Holter) monitor recordings during VVI pacing were compared with control recordings made in the absence of pacing. VVI pacing rates were 10-15 bpm above the mean daily heart rate (mean = 92 bpm; range = 63-110). Hours from paced recordings were paired with hours from control (prior to analysis) according to time of day to reduce the effects of spontaneous variability in VEA frequency. Overall, VVI pacing reduced ventricular premature complexes (VPCs) 26% from 331 to 245/hour (p less than 0.001). During pacing, couplets (pairs, successive VPCs) were reduced from 6.95 to 1.03/hour (p less than 0.000001) and VT (greater than or equal to 3 successive VPCs) from 0.89 to 0.045 episodes/hour (p less than 0.003). Of 13 patients with couplets, 11 had greater than or equal to 50% reduction and five had greater than or equal to 90% reduction. Baseline VT was eliminated in four out of nine patients during pacing. Pacing did not increase VEA significantly in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)