Premium
Atrial fibrillation in COVID‐19: A review of possible mechanisms
Author(s) -
Stone Elijah,
Kiat Hosen,
McLachlan Craig S.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202001613
Subject(s) - atrial fibrillation , medicine , fibrosis , pathophysiology , inflammation , cardiology , pathological , covid-19 , disease , infectious disease (medical specialty)
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.