Short-Term Rapid Ventricular Pacing Prolongs Ventricular Refractoriness in Patients

Rapid Ventricular Rates Prolong VERP. 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...

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Published inJournal of cardiovascular electrophysiology Vol. 9; no. 10; pp. 1036 - 1042
Main Authors KREBS, MARK E., SZWED, JOSEPH M., SHINN, TIMOTHY, MILES, WILLIAM M., ZIPES, DOUGLAS P.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.10.1998
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Abstract Rapid Ventricular Rates Prolong VERP. 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 IRVA, 13 patients] or high right atrium [HRA, II 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.
AbstractList Rapid Ventricular Rates Prolong VERP. 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 IRVA, 13 patients] or high right atrium [HRA, II 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.
BACKGROUNDTraditional 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 RESULTSIn 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. CONCLUSIONIn 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.
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. 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. 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.
Rapid Ventricular Rates Prolong VERP. 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 IRVA, 13 patients] or high right atrium [HRA, II 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.
Author KREBS, MARK E.
MILES, WILLIAM M.
SZWED, JOSEPH M.
ZIPES, DOUGLAS P.
SHINN, TIMOTHY
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Snippet Rapid Ventricular Rates Prolong VERP. Background: Traditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and...
Traditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and gradually return to baseline after termination of...
Rapid Ventricular Rates Prolong VERP. Background: Traditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and...
BACKGROUNDTraditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and gradually return to baseline after...
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StartPage 1036
SubjectTerms Adult
Aged
arrhythmia
Cardiac Catheterization
Cardiac Pacing, Artificial
electrophysiology
Electrophysiology - methods
Female
Heart Conduction System - physiopathology
Heart Ventricles - physiopathology
Humans
Male
Middle Aged
Myocardial Contraction
tachycardia
Tachycardia - physiopathology
Tachycardia - therapy
Title Short-Term Rapid Ventricular Pacing Prolongs Ventricular Refractoriness in Patients
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https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1540-8167.1998.tb00881.x
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https://search.proquest.com/docview/70045086
Volume 9
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