Couderc Jean-Philippe, Kaab Stefan, Hinterseer Martin, McNitt Scott, Xia Xiaojuan, Fossa Anthony, Beckmann Britt M, Polonsky Slava, Zareba Wojciech
Heart Research Follow-Up Program, Cardiology Department, University of Rochester Medical Center, Rochester, NY 14642, USA.
J Clin Pharmacol. 2009 Jan;49(1):6-16. doi: 10.1177/0091270008325927. Epub 2008 Oct 28.
The authors investigated whether computerized parameters quantifying ventricular repolarization delay, heterogeneity, and instability characterize individuals who developed drug-induced Torsades de Pointes. Assessing an individual's propensity to Torsades de Pointes when exposed to a QT-prolonging drug is challenging because baseline QT prolongation has limited predictive value. Five-minute digital 12-lead electrocardiograms were acquired at baseline and after a sotalol challenge in 16 patients who had a history of Torsades de Pointes in the context of a QT-prolonging drug and 17 patients who did not have such history. Computerized measurements of QTc, T peak to T end intervals (TpTe), TpTe/QTc, and QT variability were implemented, and novel quantifiers of ventricular repolarization heterogeneity from the early (ERD) and late (LRD) part of the T wave were investigated. Compared with electrocardiograms of patients without a history of Torsades de Pointes, the baseline electrocardiograms of patients with a history of Torsades de Pointes had a longer QTc and an increased repolarization heterogeneity of the early part of the T wave (ERD30%: 44 +/- 13 vs 35 +/- 8 ms, P = .02). On sotalol, the electrocardiograms from individuals with Torsades de Pointes revealed a delay of the terminal part of the T wave that was not present in patients without Torsades de Pointes (TpTe: 27 +/- 40 vs -2 +/- 21 ms, P = .02; LRD70%: 20 +/- 29 vs 2 +/- 4 ms, P = .04). Results suggest that the electrocardiogram abnormalities characterizing patients with a history of Torsades de Pointes are (1) an increased repolarization heterogeneity at baseline and (2) a sotalol-induced prolongation of the terminal part of the T wave.
作者研究了量化心室复极延迟、异质性和不稳定性的计算机参数是否可用于表征发生药物性尖端扭转型室速的个体。评估个体在接触延长QT间期药物时发生尖端扭转型室速的倾向具有挑战性，因为基线QT延长的预测价值有限。对16例有因延长QT间期药物导致尖端扭转型室速病史的患者和17例无此类病史的患者，在基线时以及索他洛尔激发试验后采集了5分钟的数字化12导联心电图。实施了QTc、T峰至T末间期（TpTe）、TpTe/QTc和QT变异性的计算机测量，并研究了来自T波早期（ERD）和晚期（LRD）部分的心室复极异质性的新量化指标。与无尖端扭转型室速病史患者的心电图相比，有尖端扭转型室速病史患者的基线心电图QTc更长，T波早期部分的复极异质性增加（ERD30%：44±13 vs 35±8 ms，P = 0.02）。在索他洛尔作用下，有尖端扭转型室速患者的心电图显示T波终末部分延迟，而无尖端扭转型室速患者则无此现象（TpTe：27±40 vs -2±21 ms，P = 0.02；LRD70%：20±29 vs 2±4 ms，P = 0.04）。结果表明，有尖端扭转型室速病史患者的心电图异常表现为：（1）基线时复极异质性增加；（2）索他洛尔诱导的T波终末部分延长。
