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(Circulation. 2003;108:2298.)
© 2003 American Heart Association, Inc.

Review: Current Perspective

A Tale of Two Fibrillations

Peng-Sheng Chen, MD; Tsu-Juey Wu, MD, PhD; Chih-Tai Ting, MD, PhD; Hrayr S. Karagueuzian, PhD; Alan Garfinkel, PhD; Shien-Fong Lin, PhD; James N. Weiss, MD

From the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif (P.-S.C., H.S.K., S.-F.L.); the Division of Cardiology, Department of Medicine, Taichung Veterans General Hospital and Institute of Clinical Medicine, Cardiovascular Research Center, National Yang-Ming University School of Medicine, Taipei, Taiwan (T.-J.W., C.-T.T.); and the Cardiovascular Research Laboratory and Division of Cardiology, Department of Medicine, Center for Health Sciences, David Geffen School of Medicine at UCLA, Los Angeles, Calif (A.G., J.N.W.).

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

Key Words: death, sudden • heart arrest • electrophysiology • arrhythmia • drugs

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Sudden cardiac death remains a major public health problem in the United States. Ventricular fibrillation (VF) is the most common arrhythmia that directly leads to sudden cardiac death. However, the mechanisms of VF are unclear. Recently,¹ 2 different types of VF have been demonstrated in isolated, perfused rabbit hearts linked to the electrical restitution properties of the heart (ie, the dynamic dependence of action potential duration [APD] or conduction velocity [CV] on the previous diastolic interval). Type I (fast) VF is associated with a steep APD restitution, flat CV restitution, and multiple wandering wavelets. Type II (slow) VF is associated with flat APD restitution, broad CV restitution, decreased excitability, and spatiotemporal periodicity in activation maps. Our goal in this article is to explain how this new knowledge about the 2 types of VF can account for seemingly contradictory experimental findings by different investigators, and to speculate on the relevance to patient care.

	Four Stages of VF

 
In normal hearts, physiological triggers such as premature ventricular contractions (PVCs) usually do not have the ability to generate an initial wavebreak causing sustained ventricular reentry. If such an event occurs, however, practically all normal hearts can fibrillate.² In contrast, physiological triggers can sometimes induce wavebreak, initiating reentry in diseased hearts, as a result of increased structural and electrophysiological heterogeneity caused by the disease. Wiggers et al² reported that VF occurred in 4 distinct stages visible by cinematography. The first (tachysystolic) stage lasts no more than a few seconds, characterized by either a single spiral wave or a . . . [Full Text of this Article]

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