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先天性长QT综合征患者尖端扭转型室性心动过速的心内膜致心律失常机制。

Endocardial arrhythmogenic mechanisms of torsades de pointes in patients with the congenital long QT syndrome.

作者信息

Chinushi Masaomi, Furushima Hiroshi, Hosaka Yukio, Komura Satoru, Sato Akinori, Iijima Kenichi, Aizawa Yoshifusa

机构信息

School of Health Science, Niigata University, Japan.

出版信息

Intern Med. 2011;50(16):1695-702. doi: 10.2169/internalmedicine.50.5114. Epub 2011 Aug 15.

DOI:10.2169/internalmedicine.50.5114
PMID:21841328
Abstract

We injected acetylcholine (Ach) into the coronary artery to ascertain whether coronary vasospasm contributed to the syncopal events or chest oppression suffered by 3 patients with long QT syndrome (LQTS). During the test, a quadripolar electrode catheter was placed in the right ventricle and the activation-recovery interval was reanalyzed from the stored data. Intracoronary Ach transiently prolonged the QT intervals in all 3 patients without inducing coronary vasospasm. The Ach-induced QT prolongation was associated with enhanced spatial and temporal dispersion of intra-ventricular repolarization. The electrophysiological abnormalities were consistent with the putative arrhythmogenic mechanisms identified in experimental studies of LQTS.

摘要

我们向冠状动脉内注射乙酰胆碱(Ach),以确定冠状动脉痉挛是否导致了3例长QT综合征(LQTS)患者出现的晕厥事件或胸部压迫感。在测试过程中,将四极电极导管置于右心室,并从存储的数据中重新分析激活-恢复间期。冠状动脉内注射Ach可使所有3例患者的QT间期短暂延长,且未诱发冠状动脉痉挛。Ach诱发的QT间期延长与心室内复极的空间和时间离散度增加有关。电生理异常与LQTS实验研究中确定的假定致心律失常机制一致。

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