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Short-term rapid ventricular pacing prolongs ventricular refractoriness in patients
M E Krebs1, J M Szwed, T Shinn
1Indiana University School of Medicine, and Roudebush Veterans Administration Medical Center, Indianapolis, USA.
Journal of Cardiovascular Electrophysiology
|November 17, 1998
Summary
Sustained rapid heart rates can prolong ventricular effective refractory period (VERP) in humans, contrary to traditional beliefs. This prolonged VERP may contribute to arrhythmias like torsades de pointes after certain procedures or medications.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Arrhythmias
Background:
- Traditional understanding posits that ventricular refractoriness shortens with rapid pacing.
- Animal studies suggest sustained rapid rates can paradoxically prolong refractoriness, potentially inducing arrhythmias.
Purpose of the Study:
- To investigate the effect of sustained rapid ventricular pacing on ventricular effective refractory period (VERP) in humans.
- To challenge traditional concepts of ventricular refractoriness during and after rapid pacing.
Main Methods:
- Human study involving rapid ventricular pacing (30 min, 400 msec cycle length) from the right ventricular apex or high right atrium.
- Ventricular effective refractory period (VERP) measured using the extrastimulus method.
- Comparison of VERPs immediately post-pacing and 15 minutes post-pacing to baseline and control groups.
Main Results:
- VERPs immediately after rapid pacing showed no significant difference from baseline.
- A significant prolongation of VERPs was observed 15 minutes after rapid pacing compared to baseline (246 +/- 23 msec vs 231 +/- 20 msec).
- Pacing site did not influence VERP prolongation; no time-dependent VERP changes occurred in the control group.
Conclusions:
- Human data demonstrate that sustained rapid ventricular rates lead to a delayed prolongation of VERP.
- This finding contrasts with traditional concepts and may explain arrhythmias observed post-ablation or with Class IA antiarrhythmic drugs.
- The study highlights a potential pro-arrhythmic mechanism related to delayed refractoriness changes.