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Sodium Channel Blockade as an Antiarrhythmic Mechanism

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Antiarrhythmic Drugs
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Abstract

Despite the increasing use of implantable devices and ablative procedures, drugs remain the mainstay of therapy for cardiac arrhythmias. The local anesthetic-class drugs are the most widely prescribed antiarrhythmic agents. They exert their antiarrhythmic effect by blockade of the inward sodium current [1]. The adverse impact of drug treatment on survival of patients in Cardiac Arrhythmia Suppression Trial and in patients with atrial fibrillation have forced serious reconsideration of the indications for and selections of drugs [2, 3]. The trial results have also provided a strong impetus for the study of the basic mechanisms of action of these drugs. Such studies may relate basic mechanisms of action to proarrhythmic potential and ultimately lead to safer, more effective treatment. This paper reviews the normal function of the sodium channel, the mechanism(s) of its blockade by drugs and the implication of the blocking mechanisms to the clinical use of these drugs.

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Grant, A.O. (1995). Sodium Channel Blockade as an Antiarrhythmic Mechanism. In: Breithardt, G., Borggrefe, M., Camm, A.J., Shenasa, M., Haverkamp, W., Hindricks, G. (eds) Antiarrhythmic Drugs. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85624-2_1

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