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(Circulation. 1999;100:2534.)
© 1999 American Heart Association, Inc.

Basic Science Reports

Induction of Electrical Heterogeneity Impairs Ventricular Defibrillation

An Effect Specific to Regional Conduction Velocity Slowing

Michael R. Ujhelyi, PharmD; J. Jason Sims, PharmD; Allison Winecoff Miller, PharmD

From the University of Georgia College of Pharmacy, Augusta VA Medical Center, and Medical College of Georgia School of Medicine, Augusta.

Correspondence to Michael R. Ujhelyi, PharmD, Medtronic Atrial Fibrillation Research, 7000 Central Ave T203, Minneapolis MN 55432. E-mail michael.ujhelyi{at}medtronic.com

Background—This study determined whether dispersion of conduction velocity, refractoriness, or excitability increases biphasic shock defibrillation energy requirements (DERs).

Methods and Results—Twenty-four swine were instrumented with a mid-LAD perfusion catheter for regional infusion of lidocaine 0.75 mg · kg^-1 · h^-1 (n=7), low-dose d-sotalol (0.16 mg · kg^-1 · h^-1) (n=4), high-dose d-sotalol (0.5 mg · kg^-1 · h^-1) (n=6), or saline (n=7). Effective refractory periods (ERPs) were determined at 5 myocardial sites, and regional conduction velocity was determined in LAD-perfused and -nonperfused regions. Regional lidocaine infusion increased DER values by 84% (P=0.008) and slowed conduction velocity by 23% to 35% (P<0.01) but did not affect ERP. Conversely, regional low- and high-dose d-sotalol infusion did not alter DER values or conduction velocity but increased regional ERP by 14% to 17% (P<0.001). Regional lidocaine increased conduction velocity dispersion by 100% to 200% (P=0.01) but did not change ERP dispersion, whereas d-sotalol increased ERP dispersion by 140% (P<0.001) without affecting conduction velocity dispersion. Lidocaine infusion induced ventricular fibrillation (VF) in 6 of 7 animals, whereas regional d-sotalol was not proarrhythmic. Regional infusion of lidocaine and d-sotalol prolonged VF cycle length by 23% to 41% (P<0.05) in the perfused region and increased VF cycle length dispersion by 85% to 240% (P<0.05). Both agents increased pacing threshold (excitability) in the perfused region by 93% to 116% (P<0.05).

Conclusions—Regional conduction velocity slowing increased DER values, which was probably a result of spatial dispersion of conduction velocity. Increasing refractory period dispersion without changing conduction velocity did not alter DFT values. Thus, dispersion of conduction velocity may be a more likely regulator of defibrillation efficacy than dispersion of refractoriness.

Key Words: fibrillation • defibrillation • electrical stimulation • pharmacology • electrophysiology

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