[Cardiac effects of antipsychotics: mechanism of arrhythmias and sudden cardiac death].
[Cardiac effects of antipsychotics: mechanism of arrhythmias and sudden cardiac death].
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发表时间：
2004-03
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通讯作者：
V. Kecskeméti
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作者：
V. Kecskeméti
本文综述了抗精神病药物心脏副作用的实验和临床数据。某些抗精神病药物可能与QT间期延长相关，诱发室性心动过速、尖端扭转型室性心动过速、TdP和猝死。本文综述了该类药物的细胞作用、电生理机制以及对离子电流（主要是钾电流）影响的最新研究结果。大多数抗精神病药物与延迟整流钾通道的抑制有关。比较K+通道抑制和QT间期延长的效力与药物的治疗血浆水平，在奎替鲁、奥氮平和利培酮的情况下，抑制效力与治疗剂量之间的差异最大，而硫利达嗪显示出最小的差异。所有引起TdP的药物均延长QT间期并抑制K+整流通道，但这种关系并不精确。特定药剂、调节条件、因素（疾病、电解质紊乱、遗传损伤、药物相互作用）的一些额外的细胞效应使个体易受心律失常的影响。该文件强调药物相互作用引起的风险心律失常长期治疗精神病患者。
The review summarizes experimental and clinical data showing the cardiac side effects of antipsychotic drugs. Some antipsychotics may correlate with prolongation of QT interval, induce ventricular tachycardia, torsades de pointes, TdP, and sudden death. The author surveys the cellular actions of the drugs, the electrophysiological mechanisms and the recent data referring the drug's effects on ionic currents, mainly potassium currents. Most antipsychotics are associated with the inhibition of delayed rectifier K+ channels. Comparing the potency on K+ channel inhibition and the prolongation of the QT interval with the therapeutic plasma levels of the drugs, the difference between the inhibitory potency and the therapeutic dose is the highest in the case of quetiapine, olanzepine and risperidone, while thioridazine shows the smallest difference. All drugs that cause TdP prolong the QT interval and inhibit the K+ rectifier channel, but the relationship is not precise. Some additional cellular effects of particular agents, modulating conditions, factors (diseases, electrolytes disturbances, genetic damage, drug interactions) make the individual vulnerable to arrhythmia. The paper highlights drug interactions causing risk of arrhythmia during chronic treatment of psychiatric patients.