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作 者:阙冬冬[1] 宋旭东[1] QUE Dongdong;SONG Xudong(Department of Cardiovascular,Zhujiang Hospital of Southern Medical University,Guangzhou Guangdong 510280,China)
机构地区:[1]南方医科大学珠江医院(第二临床医学院)心血管内科,广东广州510280
出 处:《实用心电学杂志》2021年第6期404-407,共4页Journal of Practical Electrocardiology
基 金:广东省自然科学基金资助项目(2021A1515012568)。
摘 要:房颤的发病机制非常复杂,与心房的重构(包括电学重构、解剖重构和自主神经系统重构)密切相关。房颤可诱导离子通道蛋白表达和(或)功能异常,进而反馈性地促进心房功能性折返基质的形成,发生电学重构;循环往复的电学重构造成心房基质的改变,失活的心房肌细胞被纤维组织替代,心房逐渐纤维化,出现解剖重构;与此同时,心房广泛的纤维化进一步阻碍电冲动的传导,反过来加重电学重构;自主神经系统重构可通过正向反馈环机制促进房颤的维持和复发。早期治疗心房重构可延迟甚至预防房颤的发生和发展。The mechanism of atrial fibrillation(AF)is complicated and closely related to atrial remodeling including electrical,anatomical and automatic nervous system remodeling.Abnormal ion channel protein expression and(or)function could be induced by AF,which further promotes the formation of functional atrial reentry substrate as a feedback and ultimately causes electrical remodeling.Circulating electrical remodeling results in changing atrial substrates;inactivated atrial myocytes are replaced by fibrous tissue,which contributes to the gradual formation of atrial fibrosis and anatomical remodeling.Meanwhile,extensive atrial fibrosis further impedes electric impulse conduction and aggravates electrical remodeling in reverse.Automatic nervous system remodeling promotes the maintenance and recurrence of AF via the mechanism of positive feedback loop.The occurrence and development of AF might be delayed or even prevented by the anti-atrial-remodeling therapy in an early phase.
关 键 词:电学重构 解剖重构 房颤 心房重构 自主神经系统
分 类 号:R541.75[医药卫生—心血管疾病]
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