Proarrhythmia in patients treated for atrial fibrillation or flutter.

OBJECTIVE

To review data on the type, mechanism, and prevalence of the proarrhythmic effect of drugs used to treat atrial fibrillation or flutter.

DATA SOURCES

English-language literature from the early 1960s to the present was identified by manual search of the literature; relevant articles were reviewed. Pertinent earlier studies were identified from references in the articles reviewed and were included when relevant.

STUDY SELECTION

All studies, controlled and uncontrolled, as well as individual case reports that contained data convincingly linking atrial antiarrhythmic therapy to a proarrhythmic side effect were included.

DATA EXTRACTION

Key data were extracted from each article in studies in which a causal relationship between the use of a drug and a proarrhythmic response appeared likely.

DATA SYNTHESIS

Antiarrhythmic therapy aimed at stabilizing the atrium may have adverse effects on the ventricle including torsade de pointes and, less commonly, sustained ventricular tachycardia. Different antiarrhythmic agents appear to have differing potentials for this proarrhythmic response, which is most common with class 1A agents. Other proarrhythmic responses to atrial antiarrhythmic agents include the acceleration of the ventricular response either by enhancing atrioventricular nodal or bypass tract conduction or by converting atrial fibrillation to flutter with 1:1 conduction. Calcium-channel blocking agents and, less commonly, digoxin may perpetuate the duration of paroxysmal atrial fibrillation, and virtually all agents can cause sinus node dysfunction or atrioventricular block.

CONCLUSIONS

Although drug therapy for atrial fibrillation or flutter is generally well tolerated, the potential exists for uncommon but serious proarrhythmic effects. Knowledge of the risk factors and symptoms of these adverse reactions will help to further reduce this risk.