| pubmed-article:10505494 | pubmed:abstractText | Antiarrhythmic drugs remain the mainstay of treatment of atrial fibrillation, but their potential proarrhythmic effects hamper their optimal use. Drug-induced tachyarrhythmias (ventricular tachycardia or atrial tachyarrhythmias with rapid ventricular response) are life-threatening and often cause syncope. Because these events tend to cluster shortly after drug initiation, it is common practice to routinely hospitalize patients for drug initiation under continuous electrocardiographic surveillance. The low incidence of serious proarrhythmia makes the cost-effectiveness of this practice controversial. Torsades de pointes, in particular, can be predicted by the presence of one or more of the following risk factors: female gender, structural heart disease, prolonged baseline QT interval, bradycardia, hypokalemia, previous proarrhythmic responses, and higher drug plasma levels. Proarrhythmia induced by class IC agents is seen almost exclusively in patients with structural heart disease and ventricular dysfunction. A variety of monitoring devices permit electrocardiographic monitoring of patients in the outpatient setting. Efficient clinical pathways for the safe initiation of antiarrhythmic drugs in patients with atrial fibrillation do not require universal hospital admission. In patients without structural heart disease, outpatient initiation of most antiarrhythmic drugs appears safe. In patients with significant structural heart disease, class IC drugs are contraindicated, and most other drugs should be initiated in the hospital under continuous monitoring. The incidence of severe proarrhythmia is very low when loading doses of amiodarone of 600 mg/d or less are given to outpatients with structural heart disease. | lld:pubmed |
