Dumaine Robert, Antzelevitch Charles
Masonic Medical Research Laboratory, Utica, New York 13501, USA.
Curr Opin Cardiol. 2002 Jan;17(1):36-42. doi: 10.1097/00001573-200201000-00006.
Recent studies of the molecular basis of the long QT syndrome (LQTS) have advanced our understanding of the mechanisms responsible for the abnormal prolongation of ventricular repolarization and revealed associations between LQTS and other primary electrical diseases of the heart such as Brugada syndrome. The role of DNA single nucleotide polymorphisms in acquired LQTS and differences between the Romano-Ward and Jervell-Lange-Nielsen forms of congenital LQTS are gradually coming into focus. In this brief review, our goal is to summarize the molecular mechanisms proposed to underlie the susceptibility to arrhythmias in LQTS and discuss the direction of current and future research.
近期关于长QT综合征（LQTS）分子基础的研究，加深了我们对心室复极异常延长机制的理解，并揭示了LQTS与其他原发性心脏电疾病（如Brugada综合征）之间的关联。DNA单核苷酸多态性在获得性LQTS中的作用以及先天性LQTS的Romano-Ward型和Jervell-Lange-Nielsen型之间的差异正逐渐受到关注。在这篇简短的综述中，我们的目标是总结提出的作为LQTS心律失常易感性基础的分子机制，并讨论当前及未来研究的方向。
