SHORT-TERM RAPID VENTRICULAR PACING PROLONGS VENTRICULAR REFRACTORINESS IN PATIENTS

Background: Traditional concepts suggest that ventricular refractorine ss should gradually shorten during rapid pacing and gradually return t o baseline after termination of pacing. Animal data, however, have sho wn that under certain circumstances sustained rapid ventricular rates can prolong refractoriness and action potential duration and, thereby, promote ventricular arrhythmias, Methods and Results: In humans we ev aluated the effect of rapid pacing (cycle length 400 msec for 30 min f rom either the right ventricular apex [RVA, 13 patients] or high right atrium [HRA, 11 patients]) on the ventricular effective refractory pe riod (VERP) as measured from the RVA, using the extrastimulus method ( drive train 500 msec). A control group of seven patients had serial me asurements of VERPs in the absence of pacing, For a given patient, all VERPs were measured at constant stimulus output (twice diastolic thre shold) from the same ventricular site and at the same drive train cycl e length. VERPs obtained immediately following rapid pacing did not di ffer from those at baseline (P = 0.46); however, VERPs obtained 15 min utes post pacing were prolonged compared with baseline VERPs (231 +/- 20 msec vs 246 +/- 23 msec, P < 0.0026), Pacing site has no impact on VERP prolongation, There was no effect of time on VERP in the absence of pacing. Conclusion: In contrast to traditional concepts of refracto riness, after the termination of sustained rapid ventricular rates, VE RP prolonged. This phenomenon could help explain the observation of to rsades de pointes in some patients after atrioventricular junction abl ation or the administration of a Class IA antiarrhythmic agent to conv ert atrial fibrillation with rapid ventricular response to sinus rhyth m.