Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Fibrinaloid Microclots and Atrial Fibrillation

Version 1 : Received: 26 January 2024 / Approved: 27 January 2024 / Online: 29 January 2024 (08:26:08 CET)

How to cite: Kell, D.B.; Lip, G.Y.; Pretorius, E. Fibrinaloid Microclots and Atrial Fibrillation. Preprints 2024, 2024011945. https://doi.org/10.20944/preprints202401.1945.v1 Kell, D.B.; Lip, G.Y.; Pretorius, E. Fibrinaloid Microclots and Atrial Fibrillation. Preprints 2024, 2024011945. https://doi.org/10.20944/preprints202401.1945.v1

Abstract

Atrial fibrillation (AF) is a comorbidity of a variety of other chronic, inflammatory diseases for which fibrinaloid microclots are a known accompaniment (and in some cases a cause, with a mechanistic basis). Clots are, of course, a well-known consequence of atrial fibrillation. We here ask the question as to whether the fibrinaloid microclots seen in plasma or serum may in fact also be a cause of (or contributor to) the development of AF. We consider known ‘risk factors’ for AF, and in particular exogenous stimuli such as infection and air pollution by particulates, both of which are known to cause AF. The external accompaniments of both bacterial (lipopolysaccharide and lipoteichoic acids) and viral (SARS-CoV-2 spike protein) infections are known to stimulate fibrinaloid microclots when added in vitro, and fibrinaloid microclots are cytotoxic by inducing hypoxia/reperfusion and other means. Strokes and thromboembolisms are also common consequences of AF. Consequently, taking a systems approach, we suggest that it is likely that microclots may well have an aetiological role in the development of AF. This has significant mechanistic and therapeutic implications.

Keywords

Atrial fibrillation; fibrinaloid; microclots; long Covid; inflammation; microthromboses

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

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