BACKGROUND: Traditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and gradually return to baseline after termination of pacing. Animal data, however, have shown 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 evaluated the effect of rapid pacing (cycle length 400 msec for 30 min from either the right ventricular apex [RVA, 13 patients] or high right atrium [HRA, 11 patients]) on the ventricular effective refractory period (VERP) as measured from the RVA, using the extrastimulus method (drive train 500 msec). A control group of seven patients had serial measurements of VERPs in the absence of pacing. For a given patient, all VERPs were measured at constant stimulus output (twice diastolic threshold) from the same ventricular site and at the same drive train cycle length. VERPs obtained immediately following rapid pacing did not differ from those at baseline (P = 0.46); however, VERPs obtained 15 minutes 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 refractoriness, after the termination of sustained rapid ventricular rates, VERP prolonged. This phenomenon could help explain the observation of torsades de pointes in some patients after atrioventricular junction ablation or the administration of a Class IA antiarrhythmic agent to convert atrial fibrillation with rapid ventricular response to sinus rhythm.
BACKGROUND: Traditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and gradually return to baseline after termination of pacing. Animal data, however, have shown 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 evaluated the effect of rapid pacing (cycle length 400 msec for 30 min from either the right ventricular apex [RVA, 13 patients] or high right atrium [HRA, 11 patients]) on the ventricular effective refractory period (VERP) as measured from the RVA, using the extrastimulus method (drive train 500 msec). A control group of seven patients had serial measurements of VERPs in the absence of pacing. For a given patient, all VERPs were measured at constant stimulus output (twice diastolic threshold) from the same ventricular site and at the same drive train cycle length. VERPs obtained immediately following rapid pacing did not differ from those at baseline (P = 0.46); however, VERPs obtained 15 minutes 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 refractoriness, after the termination of sustained rapid ventricular rates, VERP prolonged. This phenomenon could help explain the observation of torsades de pointes in some patients after atrioventricular junction ablation or the administration of a Class IA antiarrhythmic agent to convert atrial fibrillation with rapid ventricular response to sinus rhythm.
Authors: Aglaia-Angeliki Mantziari; Vassilios P Vassilikos; Yiannis S Chatzizisis; Georgios Dakos; Georgios Stavropoulos; Stelios Paraskevaidis; Ioannis H Styliadis Journal: Open Cardiovasc Med J Date: 2011-02-01