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.