ELECTROCARDIOGRAPHIC AND CLINICAL PREDICTORS OF TORSADES-DE-POINTES INDUCED BY ALMOKALANT INFUSION IN PATIENTS WITH CHRONIC ATRIAL-FIBRILLATION OR FLUTTER - A PROSPECTIVE-STUDY

The aim of this study was to identify predictors of torsades de pointe s (TdP) in patients with atrial fibrillation (AF) or flutter exposed t o the Class III antiarrhythmic drug almokalant. TdP can be caused by d rugs that prolong myocardial repolarization. One hundred patients rece ived almokalant infusion during AF (infusion 1) and 62 of the patients during sinus rhythm (SR) on the following day (infusion 2). Thirty-tw o patients converted to SR. Six patients developed TdP. During AF, T w ave alternans was more common prior to infusion (baseline) in patients developing TdP 150% vs 4%, P < 0.01). After 30 minutes of infusion 1, the TdP patients exhibited a longer QT interval (493 +/- 114 vs 443 /- 54 ms [mean +/- SD], P ( 0.01), a larger precordial QT dispersion ( 50 +/- 74 vs 27 +/- 26 ms, P < 0.05), and a lower T wave amplitude (0. 12 +/- 0.21 vs 0.24 +/- 0.16 mV, P < 0.01). After 30 minutes of infusi on 2, they exhibited a longer QT interval (672 +/- 26 vs 489 +/- 74 ms , P < 0.001), a larger QT dispersion in precordial (82 +/- 7 vs 54 +/- 52 ms, P < 0.01) and extremity leads (163 +/- 0 vs 40 +/- 34 ms, P < 0.001), and T wave alternans was more common (100% vs 0%, P < 0.001). Risk factors for development of TdP were at baseline: female gender, v entricular extrasystoles, and treatment with diuretics; and, after 30 minutes of infusion: sequential bilateral bundle branch block, ventric ular extrasystoles in bigeminy, and a biphasic T wave. Patients develo ping TdP exhibited early during almokalant infusion a pronounced QT pr olongation, increased QT dispersion, and marked morphological T wave c hanges.