Mechanisms of Action of Antiarrhythmic Drugs in Atrial Fibrillation

  • Alexander Burashnikov
  • Charles Antzelevitch


The principal goal of antiarrhythmic therapy in the management of atrial fibrillation (AF) is to prolong the effective refractory period (ERP), which makes rapid activation of the atria impossible. Currently available antiarrhythmic drugs (AADs) prolong ERP by (1) prolonging the atrial action potential as in the case of delayed rectified potassium channel current (IKr) blockers such as d-sotalol, dofetilide, or ibutilide; (2) reducing excitability, thus promoting post-repolarization refractoriness (PRR), as in the case of sodium channel current (INa) blockers such as flecainide and propafenone, or (3) via both mechanism as in the case of multiple ion channels blockers such as amiodarone, dronedarone, ranolazine and vernakalant. The role of conduction slowing in anti-AF actions of INa blockers remains poorly understood. The present chapter describes our current understanding of anti-AF mechanisms of action of AADs.


Atrial fibrillation Antiarrhythmic drugs Effective refractory period Action potential Reentry Triggered activity 



Supported by grants from the National Institutes of Health HL 47678 (CA), NYSTEM # C026424 (CA), the American Heart Association, New York State Affiliate (AB), and the Masons of New York State and Florida.


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© Springer-Verlag London 2013

Authors and Affiliations

  1. 1.Experimental CardiologyMasonic Medical Research LaboratoryUticaUSA
  2. 2.Gordon K. Moe ScholarMasonic Medical Research LaboratoryUticaUSA

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