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This study compared the efficacy and safety of sotalol and quinidine for conversion and prevention of recurrent atrial fibrillation.

To improve the clinical value of ambulatory Holter electrocardiographic (ECG) monitoring as a tool of antiarrhythmic therapy control, a new statistical model was developed. In a patient group at increased risk of sudden cardiac death, the spontaneous variability of ventricular arrhythmias was assessed, with simultaneous consideration of single ventricular premature complexes, couplets and salvos. The study included 100 patients who suffered from coronary heart disease or idiopathic dilated cardiomyopathy and for whom >30 ventricular premature complexes/h and couplets had been demonstrated on the last Holter ECG before the study. Between 3 and 12 Holter recordings were made for each patient in a drug-free state; the mean follow-up period was 260 days (maximum 1,403). The mean hourly values of the ectopic events (EE) were assessed separately for ventricular premature complexes, couplets and salvos. The spontaneous variability (SY) was calculated for single ventricular premature complexes, couplets and salvos as SV = log (EEday 2+ 0.01/EEday 1+ 0.01) and linked in one, two and three dimensions.

QT dispersion (QTD;QTmax-QTmin) is considered to reflect inhomogeneous ventricular recovery. In pts with atrial fibrillation (AF), however, the effects of antiarrhythmic drugs on QTD have not been systematically evaluated particularly with respect to their association with drug-induced proarrhythmia. Thus, QTD was assessed in a prospective, randomized trial including 50 pts with AF receiving quinidine (Q; 1000mg/day) or sotalol (S;320mg/day) in an attempt to restore sinus rhythm (SRI. Precordial QTD was measured by means of a digitizer-based software before and during drug therapy.