作者: E. Vanoli , P. J. Schwartz , S. G. Priori , A. Zaza
DOI: 10.1007/978-3-642-85624-2_13
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摘要: The repeated failures of a variety antiarrhythmic drugs in preventing sudden cardiac death, particularly among post myocyardial infarction (MI) patients, have eventually turned the interest toward arrhythmogenic interactions that often not been foreseen or, at least, thoroughly analyzed. As an example, when Task Force Working Group on Arrhythmias European Society Cardiology called attention to fact CAST mortality curve for patients treated with encainide or flecainide was very different from expected case traditional proarrhythmia, it also suggested negative interaction might occurred between electrophysiological actions those Na+ channel blockers and episodes transient myocardial ischemia associated increases sympathetic activity [1]. That suggestion later confirmed by experimental observation has potential actually favor onset life-threatening arrhythmias acute is accompanied activation [2] (Fig. 1).