Open AccessUse-dependent prolongation of ventricular tachycardia cycle length by type I antiarrhythmic drugs in humans.
Author(s) -
Gregory A. Kidwell,
Arnold J. Greenspon,
R. M. Greenberg,
KENT J. VOLOSIN
Publication year - 1993
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.87.1.118
Subject(s) - flecainide , procainamide , medicine , lidocaine , prolongation , sodium channel , sodium channel blocker , cardiology , antiarrhythmic agent , ventricular tachycardia , anesthesia , drug , anti arrhythmia agents , tachycardia , pharmacology , sodium , heart disease , chemistry , organic chemistry , atrial fibrillation
Type I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug.
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