Abstract 2859: Baseline Values and Drug-induced Changes of the Ventricular Repolarization Morphology in the Electrocardiograms of Patients with a History of Drug-induced Torsades de Pointes.
Background: Assessing propensity to torsades de pointes (TdP) when exposed to QT-prolonging drug is challenging because baseline QT-prolongation has limited predictive value for identifying risk of TdP. The aim of this study was to determine whether computer-based repolarization morphology parameters could identify individuals who developed drug-induced TdP.
Method: Five-minute standard digital 12-lead ECGs were acquired at baseline and after a controlled sotalol challenge (2 mg/kg BW, i.v.) in 34 cardiac patients of whom 17 had a history of TdP (+TdPs) in the context of a QT prolonging drug and 17 had no history of TdP (-TdPs).Computerized ECG parameters including QT, TpTe (T peak to T end interval) and a morphological measure of the duration of the early part of the repolarization interval (ERD) were implemented. All parameters were corrected for the effect of heart rate (HR).
Results: There were 9 females among the + TdP patients and 12 females in the -TdP group (p = 0.8). The drugs triggering TdPs were: antidepressant, antibiotics, antiarrhythmic and anti-migraine. They included sotalol, amiodarone, bisacodyl, erythromycin, imipramime, cipramil and sumatriptan. The table⇓ below shows the comparison of baseline values and the on-sotalol changes of the repolarization parameters after HR correction. The analysis revealed a longer QT interval duration at baseline in patient +TdPs. This prolongation was only present in the early part of the T-wave (ERD, p = 0.02). On sotalol, the patients with a history of TdPs have longer QT prolongation associated with a significant increased late part of the repolarization (TpTe, p = 0.01).
Conclusion: Our results revealed that specific repolarization features are present at baseline and on sotalol challenge in patients with and without history of TdPs. These parameters could complement the role of the QT prolongation as a proarrhythmic surrogate marker.