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Arrhythmias and Coronary Slow Flow: A Potential Pathogenic Link.

Arrhythmias and Coronary Slow Flow: A Potential Pathogenic Link.

期刊: Journal of visualized experiments : JoVE 日期: 2026-05-29 PMID: 42296075 DOI: 10.3791/71474 浏览: 27
作者: Jinhong C, Zongyin W
C, J. & W, Z. (2026). Arrhythmias and Coronary Slow Flow: A Potential Pathogenic Link.. Journal of visualized experiments : JoVE. https://doi.org/10.3791/71474
C J, W Z. Arrhythmias and Coronary Slow Flow: A Potential Pathogenic Link.. Journal of visualized experiments : JoVE. 2026; doi: 10.3791/71474
C J, W Z. Arrhythmias and Coronary Slow Flow: A Potential Pathogenic Link.[J]. Journal of visualized experiments : JoVE. 2026. DOI: 10.3791/71474.
@article{c2026,
  author = {Jinhong C and Zongyin W},
  title = {Arrhythmias and Coronary Slow Flow: A Potential Pathogenic Link.},
  journal = {Journal of visualized experiments : JoVE},
  year = {2026},
  doi = {10.3791/71474},
  note = {PMID: 42296075},
}
TY  - JOUR
AU  - Jinhong C
AU  - Zongyin W
TI  - Arrhythmias and Coronary Slow Flow: A Potential Pathogenic Link.
T2  - Journal of visualized experiments : JoVE
PY  - 2026
DO  - 10.3791/71474
AN  - PMID:42296075
ER  - 

摘要

Coronary slow flow (CSF) is characterized by recurrent resting angina and delayed distal vessel filling, despite the absence of obstructive coronary artery disease on angiography. With the continuous advancement of coronary interventional techniques, cardiologists have increasingly recognized CSF as a distinct phenomenon, and its pathogenesis has become a major research focus. Arrhythmias, common cardiovascular conditions, often present with clinical manifestations similar to those of CSF. Moreover, both conditions share certain pathogenic factors and pathophysiological processes, including endothelial dysfunction, inflammation, autonomic imbalance, and microvascular abnormalities. A clearer understanding of these overlapping mechanisms may help clinicians manage patients with CSF more scientifically and comprehensively. The present review summarizes the proposed pathogenic mechanisms of CSF, including microvascular disorders, endothelial dysfunction, inflammation, arrhythmias, anatomical factors, early atherosclerosis, and genetic polymorphisms. It also discusses the possible association between CSF and arrhythmias, highlights current uncertainties regarding causality, and considers how these mechanisms may broaden future therapeutic perspectives for this disease.

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