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 venfricuiar 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 electrophysioiogic‐pharmacoiogic testing for VT control were studied. Eighteen of these patients (12 men; meon age = 60.1) both completed ihe 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 (VPGs) 26% from 331 to 245/hour (p < 0.001). During pacing, couplets (pairs, successive VPGs) were reduced from 6.95 to 1.03/hour (p < 0.000001) and VT (≥3 successive VPCs) from 0.89 to 0.045 episodes/hour (p < 0.003). Of 13 patients with couplets, 11 had ≥50% reduction and five had ≥90% reduction. Baseline VT was eliminated in four out of nine patients during pacing. Pacing did not increase VEA significantly in any patient. In this group of patients, reduction of VEA by VVI pacing was significant and was comparable to pharmacologic interventions. Higher forms of VEA fcouplets and VT) appeared to respond better than single VPCs. Further studies may define patients with VEA who can benefit from pacing