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机构地区:[1]北京大学人民医院,北京100044
出 处:《中国药物评价》2013年第5期278-281,共4页Chinese Journal of Drug Evaluation
基 金:国家自然科学基金;应用诱导多能干细胞建立体外PKP2和DSG2突变细胞模型探讨ARVC致病机制(81270166);首都医学发展科研基金;北京市青少年运动性心脏猝死预防筛查(2009~2031年)
摘 要:目的:药物导致的获得性长QT综合征是由药物引起的可逆性的QT间期延长的综合征,其主要机制是药物通过对IKr的阻断作用,导致动作电位3期快速复极延迟,表现为QT间期延长。在临床上,许多结构上无关的药物,包括抗精神病药物均可以导致QT间期的延长。药物导致的获得性长QT综合征容易导致尖端扭转性室性心动过速(TdP),临床上可以通过Tp-e和Tp-e/QT比值、巨大T-U波、QRS缓慢上升支和QT间期短期变异可以预测TdP的风险。治疗获得性长QT综合征,最根本的是识别和停用导致QT间期延长的药物并积极的纠正代谢异常,如低钾血症或低镁血症。大多数TdP的发作是短暂的,并可自行终止。然而,长时间发作会导致血流动力学紊乱,需要立即进行电复律。Drug induced acquired long QT syndrome is characterized with prolonged QT interval caused by drugs. The main mechanism of acquired long QT syndrome is the blockade of IKr by specific drugs, which causes a delay in phase 3 rapid repolarization of the action poten- tial, and QT interval prolongation. Many drugs including would lead to the prolongation of QT interval. Acquired long QT syndrome is char- acterized with high risk of TdP and some parameters such as Tpeak-Tend measurement and Tp-e/QT ratio, giant T-U waves, slow QRS up- stroke, and short-term variability of QT intervals tend to be useful clinical variables to predict risk of TdP. The cornerstone of the manage- ment of acquired LQTS includes the identification and discontinuation of any precipitating drug and the aggressive correction of any metabolic abnormalities, such as hypokalemia or hypomagnesemia. Most of the episodes of torsade de pointes are short-lived and can be automatically terminated. However, prolonged episodes result in hemodynamic compromise and require immediate cardioversion.
关 键 词:获得性长QT综合征 尖端扭转性室性心动过速(TdP) 药物诱导
分 类 号:R541.7[医药卫生—心血管疾病]
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