AIMS: Amiodarone is one of the most efficient and safe antiarrhythmic drugs in the treatment of atrial fibrillation (AF). Although pro-arrhythmic effects of amiodarone therapy are rare, the aim of the present study was to identify clinical constellations which may lead to amiodarone-associated pro-arrhythmia. METHODS AND RESULTS: Sixty-three consecutive patients (pts) (49 males; 64+/-10.3 years; 35 with coronary heart disease, 17 with lone AF) were retrospectively included in this study. All received an oral (92.1%) or i.v. (7.9%) loading dose of amiodarone for the treatment of AF. Cardiac diseases, concomitant medical treatment, and incidence of pro-arrhythmic effects were analysed. Three pts (4.8% of the total population) developed a clinical relevant, polymorphic ventricular tachyarrhythmia, 3-48 h after initiation of amiodarone loading. Coronary heart disease was present in all of these pts, and in two of them left ventricular ejection fraction was severely reduced. The mean QTc in these pts was only slightly prolonged; mean heart rate was significantly decreased compared with the total study population (61.0+/-7.5 vs. 74.5+/-24.1 bpm; P < or = 0.05). In all pts with pro-arrhythmia, amiodarone (two pts i.v., one patient oral) was initiated during concomitant beta-blocker/digitalis therapy. Twenty-five per cent of the patients receiving this 'triple' therapy developed ventricular arrhythmia. CONCLUSION: The present study implies that initiation of amiodarone therapy in pts with structural heart disease and AF that are concomitantly treated with beta-blockers and digitalis may have an increased risk of amiodarone-associated pro-arrhythmia.
AIMS: Amiodarone is one of the most efficient and safe antiarrhythmic drugs in the treatment of atrial fibrillation (AF). Although pro-arrhythmic effects of amiodarone therapy are rare, the aim of the present study was to identify clinical constellations which may lead to amiodarone-associated pro-arrhythmia. METHODS AND RESULTS: Sixty-three consecutive patients (pts) (49 males; 64+/-10.3 years; 35 with coronary heart disease, 17 with lone AF) were retrospectively included in this study. All received an oral (92.1%) or i.v. (7.9%) loading dose of amiodarone for the treatment of AF. Cardiac diseases, concomitant medical treatment, and incidence of pro-arrhythmic effects were analysed. Three pts (4.8% of the total population) developed a clinical relevant, polymorphic ventricular tachyarrhythmia, 3-48 h after initiation of amiodarone loading. Coronary heart disease was present in all of these pts, and in two of them left ventricular ejection fraction was severely reduced. The mean QTc in these pts was only slightly prolonged; mean heart rate was significantly decreased compared with the total study population (61.0+/-7.5 vs. 74.5+/-24.1 bpm; P < or = 0.05). In all pts with pro-arrhythmia, amiodarone (two pts i.v., one patient oral) was initiated during concomitant beta-blocker/digitalis therapy. Twenty-five per cent of the patients receiving this 'triple' therapy developed ventricular arrhythmia. CONCLUSION: The present study implies that initiation of amiodarone therapy in pts with structural heart disease and AF that are concomitantly treated with beta-blockers and digitalis may have an increased risk of amiodarone-associated pro-arrhythmia.