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Am J Physiol Heart Circ Physiol (January 24, 2002). doi:10.1152/ajpheart.00867.2001
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Articles in PresS, published online ahead of print January 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00867.2001
Submitted on October 5, 2001
Accepted on January 21, 2002

Action Potential Duration Restitution and Ventricular Fibrillation due to Rapid Focal Excitation

Moshe Swissa1, Zhilin Qu2, Toshihiko Ohara1, Moon-Hyoung Lee1, Shien-Fong Lin3, Alan Garfinkel2, Hrayr S Karagueuzian1, James N Weiss2, and Peng-Sheng Chen1*

1 Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA
2 Departments of Medicine (Cardiology), Physiology and Physiological Science, UCLA School of Medicine, Los Angeles, CA, USA
3 Department of Physics and Astronomy, Vanderbilt University, Nashville, TN, USA

The focal source hypothesis of ventricular fibrillation (VF) posits that rapid activation from a focal source, rather than action potential duration (APD) restitution properties, is responsible for the maintenance of VF. We injected aconitine (100µg) in normal isolated-perfused swine right ventricles (RVs) stained with di-4-ANEPPS for optical mapping studies. Within 97±163 sec, aconitine induced ventricular tachycardia (VT) with mean cycle length 268±37 ms, which accelerated before converting to VF. Drugs that flatten APD restitution slope, including diacetyl monoxime (10-20 mM, n=6), bretylium (10-20 µg/ml, n=3), verapamil (2-4 µg/ml, n=3), reversibly converted VF to VT in all cases. In two RVs, VF persisted despite of the excision of the aconitine site. Simulations in 2D cardiac tissue showed that once VF was initiated, it remained sustained even after the "aconitine" site was eliminated. Conclusion: In this model of focal source VF, the VT to VF transition occurred due to wavebreak outside the aconitine site, and drugs that flattened APD restitution slope converted VF to VT despite continuous activation from aconitine site.




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