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(Circulation. 2003;108:3149-3156.)
© 2003 American Heart Association, Inc.

Basic Science Reports

Catheter Ablation of Ventricular Fibrillation in Rabbit Ventricles Treated With ß-Blockers

Hui-Nam Pak, MD, PhD; Yong-Seog Oh, MD; Yen-Bin Liu, MD; Tsu-Juey Wu, MD; Hrayr S. Karagueuzian, PhD; Shien-Fong Lin, PhD; Peng-Sheng Chen, MD

From the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center and David Geffen School of Medicine, University of California Los Angeles, Calif, and Division of Cardiology (T.-J.W.), Department of Medicine, Taichung Veterans General Hospital and National Yang-Ming University School of Medicine, Taipei, Taiwan.

Correspondence to Peng-Sheng Chen, MD, Room 5342, Cedars Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048. E-mail chenp{at}cshs.org

Received December 31, 2002; de novo received July 10, 2003; revision received August 11, 2003; accepted August 12, 2003.

Background— A therapeutic implication of the focal-source hypothesis of ventricular fibrillation (VF) is that VF can be terminated by focal ablation. We hypothesize that ß-adrenergic receptor blockade converts multiple-wavelet VF to focal-source VF and that this focal source is located near the papillary muscle (PM).

Methods and Results— We used optical mapping techniques to study the effects of propranolol (0.3 mg/L) on VF dynamics in Langendorff-perfused rabbit hearts. The left ventricular (LV) anterior wall was mapped and optical action potential duration restitution (APDR) was determined at 25 epicardial sites. We performed ablation during VF of the left anterior PM in hearts with (N=6) or without (N=6) cytochalasin infusion, the LV lateral epicardium (Epi group, N=3), and the LV endocardium (Endo group, N=3). The PM was also ablated in 3 hearts without propranolol (control group). Propranolol converted multiple-wavelet VF to slow VF with reentry localized to the PM. Propranolol decreased the maximal slope of the APDR curve (P<0.001) as well as its spatial heterogeneity (P<0.01) and conduction velocity (P=0.01) while increasing the VF cycle length (P<0.001). PM ablation terminated VF during propropranolol infusion with (6 of 6, 100%) or without (4 of 6, 67%) cytochalasin D and significantly reduced inducibility. VF did not terminate in the Epi, Endo, and control groups (P<0.001).

Conclusions— Propranolol flattens the APDR curve and reduces conduction velocity, converting multiple-wavelet VF into VF with a focal source anchored to the PM. Ablation of this focal source may terminate VF.

Key Words: ventricles • fibrillation • catheter ablation • mapping • arrhythmia

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