Atrial fibrillation in COVID-19: a review of possible mechanisms

Elijah Stone, Hosen Kiat, Craig S McLachlan

    Research output: Contribution to journalReview articlepeer-review

    19 Citations (Scopus)

    Abstract

    A relationship between COVID-19 infection and an increasing incidence of atrial fibrillation has been observed. However, the underlying pathophysiology as a precipitant to AF has not been reviewed. This paper will consider the possible pathological and immunological AF mechanisms as a result, of COVID-19 infection. We discuss the role myocardial microvascular pericytes expressing the ACE-2 receptor and their potential for an organ-specific cardiac involvement with COVID-19. Dysfunctional microvascular support by pericytes or endothelial cells may increase the propensity for AF via increased myocardial inflammation, fibrosis, increased tissue edema, and interstitial hydrostatic pressure. All of these factors can lead to electrical perturbances at the tissue and cellular level. We also consider the contribution of Angiotensin, pulmonary hypertension, and regulatory T cells as additional contributors to AF during COVID-19 infection. Finally, reference is given to two common drugs, corticosteroids and metformin, in COVID-19 and how they might influence AF incidence.

    Original languageEnglish
    Pages (from-to)11347-11354
    Number of pages8
    JournalFASEB Journal
    Volume34
    Issue number9
    DOIs
    Publication statusPublished - Sep 2020

    Keywords

    • Angiotensin-Converting Enzyme 2
    • Atrial Fibrillation/etiology
    • COVID-19
    • Coronavirus Infections/complications
    • Endothelial Cells/metabolism
    • Humans
    • Pandemics
    • Peptidyl-Dipeptidase A/metabolism
    • Pericytes/metabolism
    • Pneumonia, Viral/complications
    • Renin-Angiotensin System
    • heart
    • lung
    • atrial fibrillation
    • pathophysiology
    • immune system

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