Tisdale J E, Rasty S, Padhi I D, Sharma N D, Rosman H
College of Pharmacy and Allied Health Professions, Wayne State University, Detroit, MI 48202, USA.
J Clin Pharmacol. 2001 Dec;41(12):1310-8. doi: 10.1177/00912700122012896.
The objective of this study was to determine the effect of intravenous haloperidol on QT interval dispersion in critically ill patients and to compare increases in QT interval dispersion and QTc intervals in patients who developed haloperidol-induced Torsades de Pointes versus those in patients who did not. This was a case-controlled study of 30 critically ill patients who received intravenous haloperidol for delusional agitation. Cases were patients (n = 6) who developed Torsades de Pointes during haloperidol therapy. Controls were patients (n = 24) who did not experience haloperidol-induced Torsades dePointes. QTc intervals were measured and QT interval dispersion was calculated. Haloperidol prolonged QTc interval compared to pretreatment values in Torsades de Pointes patients (606 +/- 61 ms vs. 501 +/- 44 ms, p = 0.007) by a greater magnitude than in patients who did not experience Torsades de Pointes (507 +/- 60 ms vs. 466 +/- 44, p = 0.01). Twelve-lead analysis revealed that QT interval dispersion increased in patients who experienced Torsades de Pointes (from 63 +/- 11 to 95 +/- 22 ms, p = 0.03) but not in those who did not (62 +/- 18 vs. 60 +/- 26 ms, p = 0.66). Analysis of precordial leads only showed no significant haloperidol-associated increases in QTinterval dispersion in eithergroup. The odds of developing haloperidol-induced Torsades de Pointes were highest in patients with QTc interval > 521 ms during haloperidol therapy(odds ratio = 12.1). It was concluded that intravenous haloperidol prolongs QTc intervals in critically ill patients. The degree of prolongation is greater in patients who experience Torsades de Pointes. QT interval dispersion may be increased in patients who develop haloperidol-induced Torsades de Pointes compared with those who do not. However, these effects are dependent on the method of measurement (12 leads vs. precordial leads). In addition, the odds of haloperidol-induced Torsades de Pointes are higherin patients with QTc intervalprolongation compared with increased QT interval dispersion. Therefore, QTc interval determination remains preferable to QT interval dispersion as a means assessment of risk for haloperidol-induced Torsades de Pointes.
本研究的目的是确定静脉注射氟哌啶醇对重症患者QT间期离散度的影响，并比较发生氟哌啶醇诱导的尖端扭转型室速的患者与未发生该情况的患者在QT间期离散度和QTc间期增加方面的差异。这是一项病例对照研究，纳入了30例因妄想性躁动而接受静脉注射氟哌啶醇的重症患者。病例组为在氟哌啶醇治疗期间发生尖端扭转型室速的患者（n = 6）。对照组为未发生氟哌啶醇诱导的尖端扭转型室速的患者（n = 24）。测量QTc间期并计算QT间期离散度。与治疗前相比，尖端扭转型室速患者的氟哌啶醇使QTc间期延长（606±61 ms对501±44 ms，p = 0.007），延长幅度大于未发生尖端扭转型室速的患者（507±60 ms对466±44，p = 0.01）。12导联分析显示，发生尖端扭转型室速的患者QT间期离散度增加（从63±11 ms增至95±22 ms，p = 0.03），而未发生该情况的患者则未增加（62±18 ms对60±26 ms，p = 0.66）。仅对胸前导联进行分析时，两组中均未显示氟哌啶醇相关的QT间期离散度有显著增加。在氟哌啶醇治疗期间QTc间期>521 ms的患者发生氟哌啶醇诱导的尖端扭转型室速的几率最高（优势比 = 12.1）。研究得出结论，静脉注射氟哌啶醇会延长重症患者的QTc间期。发生尖端扭转型室速的患者延长程度更大。与未发生者相比，发生氟哌啶醇诱导的尖端扭转型室速的患者QT间期离散度可能增加。然而，这些影响取决于测量方法（12导联与胸前导联）。此外，与QT间期离散度增加相比，QTc间期延长的患者发生氟哌啶醇诱导的尖端扭转型室速的几率更高。因此，作为评估氟哌啶醇诱导的尖端扭转型室速风险的手段，测定QTc间期仍优于QT间期离散度。
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