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收缩重构是心房颤动(简称房颤)时心房重构的重要组成部分,收缩重构可导致血流淤滞,增加血栓形成、栓塞及脑卒中的风险,甚至在转复后出现新发血栓。房颤收缩重构的可能机制包括胞浆内Ca2+超载及L-Ca2+电流(Ical)下调、心房组织微细结构破坏及去分化改变、房颤时心房肌收缩相关蛋白重构等。房颤终止后心房重构可发生逆转,包括电生理重构、组织重构、收缩重构等方面。房颤转复后的逆重构现象从另一侧面验证了“房颤诱发房颤”的观点。
Shrinkage remodeling is an important component of atrial remodeling during atrial fibrillation (abbreviated as atrial fibrillation). Shrinkage remodeling can lead to blood stasis, increased risk of thrombosis, embolism, and stroke, and even new thrombus formation upon reversion. Possible mechanisms of atrial fibrillation and remodeling include cytoplasmic Ca2 + overload and L-Ca2 + current (Ical) down, atrial tissue destruction and dedifferentiation, atrial fibrillation-related protein remodeling and atrial fibrillation. Atrial remodeling after termination of atrial fibrillation can be reversed, including electrophysiological reconstruction, tissue remodeling, contraction and reconstruction. The inverse remodeling phenomenon after AF has verified the view of “AF-induced AF” from the other side.