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QT间期延长可致潜在的致命性心律失常-尖端扭转型室性心动过速(TdP),已成为若干药物撤出市场的最重要原因之一。目前广泛使用的某些类别的抗感染药物(如大环内酯类、喹诺酮类、唑类、喷他脒、蛋白酶抑制剂、抗疟药和磺胺甲基异噁唑)可能诱发心律失常,但其临床重要性常被低估。尽管单一抗感染药物疗法诱发QT间期延长和TdP的风险很低,但不时有与其治疗相关的心律失常的临床报道。与其他药物之间的药动学和药效学相互作用可能会增加相关疗法出现心律失常的风险,这就要求临床医师既要熟悉具有潜在延长QT间期作用的抗感染药物,又必须具备有关药物相互作用的基本知识。此外,还应综合考虑与特定患者个体相关的QT间期延长及TdP的危险因素。本文综述了与抗感染药物治疗相关的QT间期延长及TdP,主要包括QT间期延长的机制、抗感染药物与其它药物之间的潜在相互作用以及在具体临床中的应对策略。
QT prolongation can lead to a potentially lethal arrhythmia - torsades de pointes (TdP), has become one of the most important reasons for the withdrawal of certain drugs from the market. Certain classes of anti-infectives (such as macrolides, quinolones, azoles, pentamidine, protease inhibitors, antimalarials and sulfamethoxazole) that are widely used today may induce arrhythmias, but Its clinical importance is often underestimated. Although single anti-infective drug therapy induces a low QT prolongation and a low risk of TdP, clinical reports of arrhythmias associated with its treatment have been available from time to time. Pharmacokinetic and pharmacodynamic interactions with other drugs may increase the risk of arrhythmia associated with therapy, which requires clinicians to be familiar with anti-infective drugs that have the potential to prolong the QT interval and must have relevant Basic knowledge of drug interactions. In addition, consideration should also be given to the QT prolongation associated with the individual patient and the risk factors for TdP. This article reviews the QT prolongation and TdP associated with antiretroviral therapy, including the mechanism of QT prolongation, the potential interactions between antiinfectives and other drugs, and the strategies for responding to them in specific clinical settings.