title: Monophasic action potentials in patients with torsades de pointes.
abstract: The initiating mechanism of torsades de pointes is still unclear, although it is believed to be related to repolarization abnormalities such as QT prolongation and abnormal U wave. Recording monophasic action potentials in vivo can provide useful information about ventricular repolarization. To investigate the mechanism of torsades de pointes, monophasic action potentials were recorded by the contact electrode method in 20 patients. The patients were classified into three groups (Group 1; 4 patients at the acute phase of torsades de pointes, Group 2; 6 patients at the improved phase of torsades de pointes, Group 3; 10 patients with bradyarrhythmias without torsades de pointes). Action potential duration 90% (duration from monophasic action potential upstroke to 90% repolarization), repolarization time (duration from QRS onset to 90% repolarization), and effective refractory period were measured at several right ventricular endocardial sites during spontaneous rhythm and right ventricular pacing at several pacing cycle lengths. Humps during the repolarization phase were observed in all of the patients in Group 1 and in 1 patient in Group 3 during spontaneous rhythm. Action potential duration 90% and repolarization time in Group 1 were significantly longer than those in Groups 2 and 3. The dispersion of action potential duration 90% and repolarization time in Group 1 were also greater than those in Groups 2 and 3. With rapid ventricular pacing, the hump observed in Group 1 either disappeared completely or the amplitude of the hump decreased, and the dispersion of the action potential duration 90% and repolarization time was also reduced. A significant correlation was observed between action potential duration 90% and effective refractory period. (r = 0.78, p < 0.001). In conclusion, these results suggest that the hump and the dispersion of repolarization play a key role in the genesis of torsades de pointes. Pacing therapy may be useful in correcting these abnormalities.
authors.affiliation: First Department of Internal Medicine, Kobe University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Miwa
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Yokoyama
mesh_terms: D000200:Action Potentials; D000328:Adult; D000368:Aged; D001919:Bradycardia / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D004699:Endocardium / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012032:Refractory Period, Electrophysiological; D016171:Torsades de Pointes / Q000503:physiopathology*