title: Atrial fibrillation: what are the effects of drug therapy on the effectiveness and complications of electrical cardioversion?
abstract: Atrial fibrillation is the most common cardiac rhythm disorder associated with hospitalization. Two therapeutic options have been available: antiarrhythmic drug therapy, and external or internal electrical cardioversion. Electrical cardioversion of atrial fibrillation remains one of the most widely used and effective treatments for the restoration of normal sinus rhythm. However, many patients continue to receive an antiarrhythmic drug before and after cardioversion in an attempt either to cardiovert the arrhythmia chemically or to maintain sinus rhythm after successful cardioversion. Because some pharmacological agents can affect the cardioversion procedure for atrial fibrillation or flutter, and because many patients with such arrhythmias may require electrical cardioversion when they are taking antiarrhythmic drugs, the question of a possible effect of drug therapy on the efficacy and safety of electrical cardioversion of atrial fibrillation arises. Early reports of direct current cardioversion provoking potentially lethal ventricular arrhythmias raised suspicions of an arrhythmogenic role for digoxin antiarrhythmic therapy, and it is customary to withhold these drugs for 24 to 48 h before cardioversion is attempted. However, this complication is likely to arise only in patients who are close to, or actually manifesting, signs of drug toxicity. On the other hand, treatment with therapeutic concentrations of antiarrhythmic drugs before cardioversion may in some cases be associated with a significant reduction in the number of shocks and decreased energy required to restore sinus rhythm, a lower incidence of postshock arrhythmias and a reduced risk of early recurrence of atrial fibrillation.
authors.affiliation: Seconda Università degli Studi di Napoli, Facoltà di Medicina e Chirurgia, Istituto Medico Chirurgico di Cardiologia, Napoli, Italy.
authors.forename: B
authors.initials: B
authors.lastname: Sarubbi
authors.forename: V
authors.initials: V
authors.lastname: Ducceschi
authors.forename: A
authors.initials: A
authors.lastname: D'Andrea
authors.forename: B
authors.initials: B
authors.lastname: Liccardo
authors.forename: L
authors.initials: L
authors.lastname: Santangelo
authors.forename: A
authors.initials: A
authors.lastname: Iacono
mesh_terms: D000638:Amiodarone / Q000009:adverse effects / Q000494:pharmacology; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology* / Q000506:poisoning; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000628:therapy*; D003131:Combined Modality Therapy; D004077:Digoxin / Q000494:pharmacology / Q000506:poisoning; D004554:Electric Countershock / Q000009:adverse effects; D005424:Flecainide / Q000009:adverse effects / Q000494:pharmacology; D006801:Humans; D011342:Procainamide / Q000009:adverse effects / Q000494:pharmacology; D011802:Quinidine / Q000009:adverse effects / Q000494:pharmacology; D014700:Verapamil / Q000009:adverse effects / Q000494:pharmacology
chemical_list: D000889:Anti-Arrhythmia Agents; D004077:Digoxin; D014700:Verapamil; D011802:Quinidine; D005424:Flecainide; D011342:Procainamide; D000638:Amiodarone