Ventricular fibrillation (VF) is one of the major causes of sudden death in humans. Once VF starts, the heart ceases to function as a pump and death is imminent unless defibrillation is applied within a few minutes. During the past few decades, it has been established that various compounds can be used as so-called defibrillating agents . Pretreatment with one of these drugs supports self-defibrillation of the heart, if VF appears, reverting this lethal arrhythmia into a sinus rhythm. Recent experimental observations have revealed that some class III antiarrhythmics possess a similar defibrillating effect . This effect of sotalol has even been observed clinically.
Tedisamil is an anti-ischemic, antiarrhythmic, brady-cardic compound, with class III antiarrhythmic properties . It prolongs action potential duration (APD) through a blockade of both transient and delayed rectifier potassium ion currents and exhibits a positive inotropic effect . Similar to other class III antiarrhythmic agents with positive inotropic effects, tedisamil has been reported to terminate VF in isolated perfused rat hearts and to help cat hearts to defibrillate spontaneously in vivo (unpublished data). The defibrillating effect of tedisamil, as in other class III compounds, has been related to the prolongation of APD, which interrupts microreentries.
On the basis of extensive examinations of the mechanisms involved in spontaneous ventricular defibrillation, we hypothesized that ventricular defibrillation requires a high degree of intercellular synchronization. Following this hypothesis we postulated that any compound could help the heart to self-defibrillate if it improves intercellular coupling and intracellular cAMP concentration during VF, and exhibits a positive inotropic effect. Although our hypothesis was based on the defibrillating effects of some sympathomimetic compounds , our recent finding that D-sotalol supports the defibrillating process through the same mechanisms led us to include class III drugs in the same criteria.
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