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Editorial
Defibrillation remains the only effective therapy against sudden cardiac death, but its side effects necessitate further research into reducing defibrillation energy and understanding its basic mechanisms.
Despite significant research efforts of investigators in academia, medicine, and the pharmaceutical industry, no effective pharmacological alternative to defibrillation by electric shock has been developed. Thus, defibrillation, which is steadily improving its efficacy and safety, has become the only effective therapy against sudden cardiac death. However, despite major improvements over the last several decades, defibrillation is not free of side effects, which may include both contractile and electrical dysfunction.1–3 Furthermore, defibrillation is also associated with psychological side effects.4,5 Therefore, reduction of defibrillation energy is highly desirable, and defibrillation remains a subject of extensive research. The basic mechanisms of defibrillation still remain debatable a century after its inception, which has slowed further improvement of the therapy. In 1899, while studying induction of ventricular fibrillation in the dog heart, physiologists Prevost and Batelli working at the University of Geneva discovered that they could defibrillate a dog heart by applying an appropriate, high-current shock directly to the surface of the myocardium.6 Since they used very high voltage (4,800 V and more), the myocardium was incapacitated after their shocks. Thus, the initial theory of defibrillation was based on “incapacitation ” effects. In 1946, Gurvich
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Igor R. Efimov (2008) studied this question.
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