Antiarrhythmic agents in facilitating electrical cardioversion of atrial fibrillation and promoting maintenance of sinus rhythm.
Atrial fibrillation (AF) is a prevalent arrhythmia associated with significant morbidity and mortality. Electrical cardioversion of AF is a potentially definitive treatment, but as little as 67% of patients may be successfully cardioverted and, after normal sinus rhythm (NSR) is achieved, AF often recurs. Class IA, IC, and III antiarrhytmic agents are used for both facilitation of electrical cardioversion and subsequent maintenance of NSR. The mechanisms of these agents may be related to suppressing automaticity, prolonging the wavelength of reentrant wavelets, and preventing electrical remodeling. The possibility of proarrhythmia and other adverse effects complicates use of these drugs, and no large trials have been completed to elucidate definite indications. Several factors may predict failure with electrical cardioversion alone (duration of AF, atrial size, age, underlying disease, and factors that affect transthoracic impedance), calling for empiric pharmacotherapy to facilitate cardioversion. For this purpose, class IA agents hold some promise, evidence for class IC agents is conflicting, and class III agents are the most effective. Adverse effects are rare given the short course before cardioversion, but ibutilide, the most efficacious in this regard, may be proarrhythmic after only a single dose. In promoting maintenance of sinus rhythm, antiarrhythmics across the different classes have similar efficacies: NSR may be maintained in approximately 40-65% of patients compared to approximately 30-35% with placebo at 1 year. Amiodarone is distinct in its success, with approximately 60-80% of patients remaining in NSR. For all of these agents, long-term therapy may lead to proarrhythmia or other substantial adverse effects. Finally, a serial antiarrhythmic strategy may be effective, with maintenance of NSR and minimal adverse effects ultimately achieved by trial and error.
Marcus
G M
GM
Department of Internal Medicine, Stanford University Hospital, Stanford, CA 94305, USA. greg.marcus@stanford.edu
Sung
R J
RJ
D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D003131:Combined Modality Therapy; D004554:Electric Countershock; D006801:Humans; D055502:Secondary Prevention
D000889:Anti-Arrhythmia Agents