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CLINICAL STUDY: DIAGNOSIS AND TREATMENT OF ARRHYTHMIAS

Upstream stimulation versus downstream stimulation

arrhythmogenesis based on repolarization dispersion in the human heart

Frank Bode, MD^*, Pamela Karasik, MD, FACC^*, Hugo A. Katus, MD, FESC and Michael R. Franz, MD, PhD, FACC^*,*

^* Veteran Affairs and Georgetown University Medical Centers, Washington, DC, USA
Medizinische Klinik II, Universitaetsklinikum Luebeck, Germany

Manuscript received November 14, 2001; revised manuscript received March 26, 2002, accepted May 20, 2002.

^* Reprint requests and correspondence: Dr. Michael R. Franz, Cardiology Division, VAMC, 50 Irving Street, NW, Washington, DC 20422, USA.
michael.franz{at}med.va.gov

OBJECTIVE: The purpose of this study was to test the hypothesis that a ventricular tachycardia (VT) induction site has a shorter action potential duration (APD) and effective refractory period (ERP) than a noninducing site, resulting in collision against longer ERP ("upstream") as opposed to shorter ERP ("downstream," no collision).

BACKGROUND: Induction of sustained VT is often feasible at one stimulation site while application of an identical pacing protocol to another site fails to provoke VT.

METHODS: Sixty-nine patients undergoing programmed stimulation for VT inducibility had monophasic action potential recording/pacing catheters placed in the right ventricular outflow tract (RVOT) and right ventricular apex (RVA) simultaneously. Up to three extra-stimuli were introduced in 5 to 10 ms decrements until ERP was reached. Upon completion of a drive cycle at one stimulation site, it was repeated at the other.

RESULTS: Thirty-eight patients had inducible VT, nine exclusively by RVA pacing and nine exclusively by RVOT pacing. Action potential duration and ERP at the induction site were significantly shorter (12 ± 15 ms, p <0.05 and 22 ± 14 ms, p < 0.01, respectively, at 600 ms basic cycle length) than at the noninduction site. Dispersion of repolarization between corresponding APD at the two sites was 58 ± 41 ms during baseline stimulation (S1) at the inducing site but only 37 ± 23 ms at the noninducing site (p < 0.05). Dispersion increased during extra-stimulus application (p < 0.05), reaching a maximum of 75 ± 45 ms during VT induction, but only 53 ± 33 ms during extra-stimulation at the noninduction site.

CONCLUSIONS: Site specificity of VT induction underscores the role of dispersion of repolarization and refractoriness in facilitating re-entry arrhythmias. Upstream stimulation at a site with short repolarization produces larger dispersion and facilitates VT induction.

Abbreviations and Acronyms   APD   action potential duration   BCL   basic cycle length   ERP   effective refractory period   MAP   monophasic action potential   RVA   right ventricular apex   RVOT   right ventricular outflow tract   VT   ventricular tachycardia

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