title: Facilitating electrical cardioversion of persistant atrial fibrillation by antiarrhythmic drugs: update on clinical trial results.
abstract: Results from clinical trials suggest that antiarrhythmic drugs (AD) can facilitate electrical cardioversion (EC) for persistent atrial fibrillation (AF) (duration >48 hours, no spontaneous termination) by suppression of immediate reinitiation of AF following the procedure. Class IC agents may increase the atrial defibrillation threshold (DFT) by significantly reducing the availability of Na+-channel for depolarization. In contrast, class III agents may decrease the atrial DFT by markedly prolonging atrial refractoriness. Among all AD, ibutilide and amoidarone have been shown to be most effective in enhancing the acute outcome of EC. In patients who are over 65 years of age at high risks of stroke (e.g., atherosclerotic cardiovascular disease, diabetes, hypertension, previous thromboembolism, etc.), the rhythm control strategy offers no survival advantage over the rate control strategy and frequently subjects patients to serious adverse effects of AD therapy. It can not be overemphasized that adequate anticoagulation (INR 2.0-3.0) with warfarin is needed regardless of whichever strategy is chosen unless there are contraindications. On the other hand, in patients who are under 65 years of age without structural heart disease or other risk factors of stroke, rhythm control can be the treatment of choice. Specifically, if a patient has failed EC alone or if the patient has characteristics (e.g., duration of AF >6 months, left atrium >50 mm, etc.) that EC could fail, AD may be given before the procedure to facilitate EC. In the subgroup of patients who are symptomatic with hypertrophic cardiomyopathy and severe diastolic dysfunction requiring maintenance of sinus rhythm to have sufficient ventricular function for optimization of cardiac output, an aggressive approach for rhythm control with amiodarone along with adequate anticoagulation with warfarin should be encouraged.
authors.affiliation: Division of Cardiovascular Medicine, Department of Medicine, Stanford University, School of Medicine, Stanford, CA, USA. rsung@cvmed.stanford.edu
authors.forename: Ruey J
authors.initials: RJ
authors.lastname: Sung
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000628:therapy*; D004554:Electric Countershock; D006801:Humans; D011405:Propafenone / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D013015:Sotalol / Q000627:therapeutic use; D016896:Treatment Outcome; D014700:Verapamil / Q000627:therapeutic use
chemical_list: D000889:Anti-Arrhythmia Agents; D011405:Propafenone; D013015:Sotalol; D014700:Verapamil