Atrial Fibrillation in Inherited Channelopathies

Al-Azaam, Baha'a; Darbar, Dawood

doi:10.1016/j.ccep.2020.10.004

Cited by 7 publications

(1 citation statement)

References 61 publications

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“…Cardiac amyloidoses [424,425] are of especial interest here. The multifaceted clinical complexity of patients with AF has led to the current overall holistic or integrated care management approach to AF care [426,427], as is recommended in Specifically, if microclots themselves lead to AF (as do other particulates, see above), one mechanism is their known membrane activities that would more or less directly cause channelopathies, which are themselves known to be causative in AF, especially when inherited [403][404][405][406][407]. In a similar vein, therapeutic options for physicians to consider might include ramped-up versions of anticoagulation/anti-platelet drugs such as the 'triple treatment' [408], while there is also a clear role for fibrinolytic enzymes [89,128]; some of these, such as nattokinase and serrapeptase, are readily available.…”

Section: Final Discussion and Conclusion And A Forward Lookmentioning

confidence: 99%

Fibrinaloid Microclots and Atrial Fibrillation

Kell,

Lip,

Pretorius

2024

Biomedicines

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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 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, as with other amyloid proteins, can be cytotoxic, both by inducing hypoxia/reperfusion and by other means. Strokes and thromboembolisms are also common consequences of AF. Consequently, taking a systems approach, we review the considerable evidence in detail, which leads us to 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.

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