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肺静脉肌袖内肌纤维走形紊乱,厚度不均及肌纤维的不连贯性都促进了心律失常的发生,而增龄使局部发生的淀粉样变和瘢痕化加剧了此效应。肺静脉肌袖遍布缝隙连接蛋白,其中Cx43的表达浓度较高,Cx40的表达较弱;而随着年龄的增加缝隙连接蛋白发生三维重排,导致肺静脉内传导速度和各向异性增加,从而成为心房颤动的解剖学基质;心房颤动促进肺静脉内缝隙连接蛋白的重构,而其重构又促进了心房颤动的维持。
Pulmonary venous muscle myocutaneous muscle fibers take shape disorder, uneven thickness and muscle fiber inconsistencies have contributed to the arrhythmia, and aging to make local occurrence of amyloidosis and scarring exacerbated this effect. The pulmonary sleeves around the connective tissue of the connectives, including Cx43 expression of higher concentration, Cx40 expression is weaker; and with age increases the three-dimensional rearrangement of connexin, leading to increased pulmonary venous conduction velocity and anisotropy, which became the atrium Fibrillation of the anatomic matrix; atrial fibrillation promotes the remodeling of connexin in pulmonary veins, which in turn facilitates the maintenance of atrial fibrillation.