911-37 Quinidine or Sotalol-induced Changes in QT-Dispersion During Pharmacological Conversion Therapy of Atrial Fibrillation: Link to Proarrhythmia as Assessed in a Prospective, andomized Trial

Abstract

QT dispersion (QTD;QT max -QT min ) 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; 1000 mg/day) or sotalol (S;320 mg/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. 22/25 Q-treated pts converted to SR compared to 17/25 S pts (p = ns). There were 4 cases of proarrhythmia (torsade de pointes in 3 pts, monomorphic VT in 1 pt) in the Q- but none in the S-pts. Whereas ventricular depolarization (QRS) was not affected by either drug, Q and S caused a comparable increase in QTmax. QTD, however, increased only in the Q group whereas no significant changes were observed in S pts. QTD increased by > 50% in all 3 pts with Q-associated torsade de pointes. QRS (msec) QTmax (msec) QTD (msec) control drug control drug control drug Q 86 ± 17 90 ± 17 363 ± 38 4 ± 39 # 34 ± 9 43 ± 14 * S 89 ± 21 89 ± 18 367 ± 40 425 ± 58 # 36 ± 18 40 ± 17 * p < 0.05 # p < 0.01 In pts with AF, precordial QTD increases significantly during Q- but not during S-therapy desp te a comparable increase in QT max .This finding may reflect a greater propensity for the development of proarrhythmia associated with Q therapy. Determination of QTD may help to increase the safety of pharmacological therapy in this patient population.