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Fibrinaloid Microclots and Atrial Fibrillation.
Douglas B Kell1,2,3, Gregory Y H Lip4,5, Etheresia Pretorius1,3
1Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Crown St, Liverpool L69 7ZB, UK.
Biomedicines
|April 27, 2024
Summary
Fibrinaloid microclots, often found with inflammatory diseases, may contribute to the development of atrial fibrillation (AF). This research suggests microclots could play a causal role in AF, impacting treatment strategies.
Area of Science:
- Cardiology
- Pathology
- Systems Biology
Background:
- Atrial fibrillation (AF) is frequently associated with chronic inflammatory conditions.
- Fibrinaloid microclots are known to accompany these inflammatory diseases and are a consequence of AF.
- The potential causal role of microclots in AF development remains underexplored.
Purpose of the Study:
- To investigate whether fibrinaloid microclots contribute to the etiology of atrial fibrillation.
- To explore the link between known AF risk factors and microclot formation.
- To consider the implications of microclots as a potential cause of AF.
Main Methods:
- Review of existing literature on AF, inflammatory diseases, and microclots.
- Analysis of the role of exogenous stimuli (infection, air pollution) in AF and microclot formation.
- Examination of in vitro data on microclot stimulation by infectious agents (e.g., SARS-CoV-2 spike protein).
Main Results:
- Infections and air pollution, known AF triggers, stimulate fibrinaloid microclots in vitro.
- Fibrinaloid microclots exhibit cytotoxicity, potentially through hypoxia/reperfusion.
- Evidence suggests a plausible etiological role for microclots in AF development.
Conclusions:
- Microclots may be a causative factor or contributor to atrial fibrillation development.
- This hypothesis has significant implications for understanding AF mechanisms.
- Potential for novel therapeutic strategies targeting microclots in AF.
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