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.

中文翻译：

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COVID-19 中的心房颤动：可能机制的回顾

已经观察到 COVID-19 感染与房颤发病率增加之间存在关系。然而，尚未审查作为 AF 诱发因素的潜在病理生理学。本文将考虑 COVID-19 感染可能导致的病理和免疫 AF 机制。我们讨论了表达 ACE-2 受体的心肌微血管周细胞的作用及其对 COVID-19 器官特异性心脏受累的潜力。由周细胞或内皮细胞提供的功能失调的微血管支持可能会通过增加心肌炎症、纤维化、增加组织水肿和间质静水压来增加 AF 的倾向。所有这些因素都会导致组织和细胞水平的电扰动。我们还考虑了血管紧张素、肺动脉高压、和调节性 T 细胞作为 COVID-19 感染期间 AF 的额外贡献者。最后，参考了 COVID-19 中的两种常见药物，皮质类固醇和二甲双胍，以及它们如何影响 AF 的发生率。