Saffitz J E
Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Adv Exp Med Biol. 1997;430:291-301. doi: 10.1007/978-1-4615-5959-7_25.
Abnormal conduction is fundamental to the pathogenesis of both atrial fibrillation and ventricular tachycardia/fibrillation. Normal atrial and ventricular myocytes express different combinations of multiple gap junction channel proteins and are interconnected by gap junctions in markedly different spatial distributions. These observations suggest that the disparate anisotropic conduction properties of atrial and ventricular muscle are determined, in part, by both structural and molecular features of gap junctions. Alterations in gap junctional coupling likely contribute to conduction abnormalities underlying reentrant atrial or ventricular arrhythmias.
异常传导是心房颤动和室性心动过速/心室颤动发病机制的基础。正常的心房和心室肌细胞表达多种缝隙连接通道蛋白的不同组合，并通过缝隙连接以明显不同的空间分布相互连接。这些观察结果表明，心房和心室肌不同的各向异性传导特性部分是由缝隙连接的结构和分子特征决定的。缝隙连接偶联的改变可能导致折返性房性或室性心律失常的传导异常。
