Acetylstrophanthidin-induced transient depolarizations in Purkinje fibers cause conduction block, providing a potential cellular mechanism for reentry and the transition from ventricular tachycardia to fibrillation.
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Hypothesis-generating for glycoside-induced reentry in Purkinje tissue; should not change clinical arrhythmia management without human validation.
SOUNDERS et al. (1973) studied this question.
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