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抗精神病药物与心源性猝死

Antipsychotic medications and sudden cardiac death.

作者信息

Harrison M Ojinga, Krishnan K Ranga

机构信息

Duke University Medical Center, Durham, North Carolina, USA.

出版信息

Psychopharmacol Bull. 2002 Summer;36(3):91-9.

Abstract

The objectives of this paper are to: 1) discuss practical aspects of antipsychotic induced QT prolongation, torsades de pointes (TdP) and sudden cardiac death, 2) discuss its possible mechanisms, 3) review data for each antipsychotic medication or class of medications and, 4) present recommendations from the literature. We performed computerized searches of the biomedical literature utilizing MEDLINE and PsycINFO computer databases (1966-2001), and by reviewing bibliographies to identify all pertinent case reports, case series, and formal studies using the following search terms: antipsychotics, sudden cardiac death, and QT prolongation. QT prolongation is a dynamic phenomena affected by various factors (mood, disease states, gender, medication, etc.). Sudden cardiac death attributable to antipsychotic medications seems to occurs in a step-wise fashion beginning with QT prolongation, leading to TdP, which can progress to cardiac arrest. Blocking the rapidly-acting potassium rectifier current appears be the primary mechanism of QT prolongation in drugs known to cause TdP and sudden cardiac death. All antipsychotic medications have been shown to cause QT prolongation, however, the degree to which this occurs and the risk of TdP varies. The risk of sudden cardiac death increases with higher doses of medications, use of phenothiazines or intravenous butyrophenones, and in patients with certain medical illnesses, especially cardiac disease. In order to prevent sudden death from antipsychotic medications, we recommend obtaining screening electrocardiograms in all at-risk patients, follow-up electrocardiograms after the initiation of medication, and using the lowest effective dose of medication. If QT prolongation occurs, the risks and benefits of therapy should be considered and medication adjustments made if warranted.

摘要

本文的目的是

1)讨论抗精神病药物引起QT间期延长、尖端扭转型室性心动过速(TdP)和心源性猝死的实际情况,2)讨论其可能的机制,3)回顾每种抗精神病药物或药物类别的数据,以及4)提出文献中的建议。我们利用MEDLINE和PsycINFO计算机数据库(1966 - 2001年)对生物医学文献进行了计算机检索,并通过查阅参考文献来识别所有相关的病例报告、病例系列以及使用以下检索词的正式研究:抗精神病药物、心源性猝死和QT间期延长。QT间期延长是一种受多种因素(情绪、疾病状态、性别、药物等)影响的动态现象。抗精神病药物所致的心源性猝死似乎呈逐步发展的态势,始于QT间期延长,进而导致TdP,TdP可进展为心脏骤停。阻断快速激活的钾整流电流似乎是已知可导致TdP和心源性猝死的药物中QT间期延长的主要机制。所有抗精神病药物均已被证明可引起QT间期延长,然而,其发生的程度以及TdP的风险各不相同。心源性猝死的风险随着药物剂量增加、使用吩噻嗪类药物或静脉注射丁酰苯类药物以及在患有某些疾病尤其是心脏病的患者中而增加。为预防抗精神病药物导致的猝死,我们建议对所有高危患者进行筛查心电图,在开始用药后进行随访心电图,并使用最低有效剂量的药物。如果发生QT间期延长,应考虑治疗的风险和益处,并在必要时调整用药。

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