A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine.
A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine.
复制标题
DOI：
10.1097/fjc.0b013e3181a1b9e7
复制
发表时间：
2009-10
影响因子：
3
通讯作者：
Maier LS
中科院分区：
文献类型：
--
作者：
Maier LS
峰值钠电流是心肌兴奋性和传导的基础，但峰值后的晚期钠电流有助于维持和延长动作电位平台，也有助于细胞内钠负荷，进而增加细胞内钙离子，从而影响心律失常和舒张期功能。晚期钠电流在遗传性和获得性心脏病中都有病理上的增加，使其成为治疗心律失常、心力衰竭和心绞痛的有吸引力的靶点。本综述综述了晚期钠电流阻断的临床意义的基础。
The peak sodium current underlies excitability and conduction in heart muscle, but a late sodium current flowing after the peak contributes to maintaining and prolonging the action potential plateau, and also to intracellular sodium loading, that in turn increases intracellular calcium with consequent effects on arrhythmia and diastolic function. Late sodium current is pathologically increased in both genetic and acquired heart disease, making it an attractive target for therapy to treat arrhythmia, heart failure, and angina. This review provides an overview of the underlying bases for the clinical implications of late sodium current block.