综述

心房颤动合并冠状动脉慢血流的机制研究进展

  • 柴宇燕 ,
  • 康启帆 ,
  • 白雪莲 ,
  • 李志梅 ,
  • 魏玮 ,
  • 凌天佑
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  • 1.张掖市第二人民医院心内科,甘肃 张掖 734000
    2.上海交通大学医学院附属瑞金医院心内科,上海 200025
作者贡献/Authors’ Contributions柴宇燕负责撰写初稿与修改;康启帆负责文献检索;白雪莲负责文献整理;李志梅负责编辑;魏玮负责项目管理;凌天佑负审阅及研究实施。
凌天佑 E-mail:lty0919@hotmail.com

收稿日期: 2026-03-16

  修回日期: 2026-04-28

  录用日期: 2026-07-02

  网络出版日期: 2026-08-19

基金资助

上海交通大学教育发展基金项目(TQ-0133-00-0062)

版权

版权所有 © 2026 内科理论与实践编辑部

Research progress on the mechanisms of atrial fibrillation complicated with coronary slow flow

  • CHAI Yuyan ,
  • KANG Qifan ,
  • BAI Xuelian ,
  • LI Zhimei ,
  • WEI Wei ,
  • LING Tianyou
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  • 1. Department of Cardiology, Zhangye Second People's Hospital, Zhangye 734000, China
    2. Department of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

Received date: 2026-03-16

  Revised date: 2026-04-28

  Accepted date: 2026-07-02

  Online published: 2026-08-19

Copyright

Copyright © 2026 Journal of Internal Medicine Concepts & Practice. All rights reserved.

摘要

冠状动脉慢血流(coronary slow flow,CSF)指冠状动脉造影未见明显狭窄病变,但远端血流灌注延迟的特殊临床现象,与动脉粥样硬化、炎症反应、内皮功能障碍密切相关。心房颤动(atrial fibrillation,AF)是常见心律失常,与CSF存在一定临床关联,AF患者中CSF发生率明显高于窦性心律人群。本文从流行病学、血流动力学及病理生理学3个层面梳理AF与CSF的关联,认为微循环调节障碍是连接二者的重要病理环节,主要表现为微血管内皮功能损伤与血液流变学异常,并阐述宏观血流动力学紊乱如何通过生物力学信号逐渐演变为微循环结构性重塑。明确内皮功能障碍与血液流变学异常在AF合并CSF中的相互作用,为临床早期干预提供理论依据。

本文引用格式

柴宇燕 , 康启帆 , 白雪莲 , 李志梅 , 魏玮 , 凌天佑 . 心房颤动合并冠状动脉慢血流的机制研究进展[J]. 内科理论与实践, 2026 , 21(03) : 270 -276 . DOI: 10.16138/j.1673-6087.2026.03.14

Abstract

Coronary slow flow (CSF) refers to a distinct clinical phenomenon in which coronary angiography reveals no obvious stenotic lesions, yet distal blood flow perfusion is delayed. It is closely associated with atherosclerosis, inflammatory responses, and endothelial dysfunction. Atrial fibrillation (AF), a common cardiac arrhythmia, exhibits a certain clinical correlation with CSF: the incidence of CSF is notably higher in patients with AF than in those with sinus rhythm. This article reviews the associations between AF and CSF at 3 levels — epidemiological, hemodynamic, and pathophysiological — and identifies microcirculatory dysregulation as an essential pathological link connecting the two conditions, primarily manifested as microvascular endothelial dysfunction and hemorheological abnormalities. It also elaborates on how macroscopic hemodynamic disturbances gradually evolve into structural microcirculatory remodeling through biomechanical signals. By clarifying the interaction between endothelial dysfunction and hemorheological abnormalities in AF complicated with CSF, this review aims to provide a theoretical basis for early clinical intervention.

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