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Cardiovascular Research 2004 61(1):9-10; doi:10.1016/j.cardiores.2003.11.004
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Why shocking might be not shocking enough

Joris R de Groot*

Experimental and Molecular Cardiology Group, Department of Clinical and Experimental Cardiology, Academic Medical Center, PO Box 22700, Meibergdreef 9, Room MO-54, 1100 DE Amsterdam, Netherlands

* Tel.: +31-20-566-3266; fax: +31-20-697-5458. j.r.degroot@amc.uva.nl

Received 31 October 2003; accepted 7 November 2003

The first 10% of the full text of this article appears below.

See article by Chattipakorn et al. [10] in this issue.

Sudden cardiac death remains the single most frequent cause of mortality in the industrialized world [1]. Indeed, approximately every 100 s somebody dies suddenly in the United States alone [2]. Most frequently, ventricular fibrillation (VF) associated with acute myocardial ischemia or infarction is the cause of circulatory collapse [1].

When untreated, VF is lethal within minutes because the arrhythmia precludes coordinated contraction of the ventricles and thus causes circulatory arrest. The electrophysiologic mechanism of VF is reentry. Reentrant activation was first described by George Ralph Mines who showed in 1914 that an impulse can travel around a ring of excitable heart tissue and can . . . [Full Text of this Article]


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