Key result
Atrial fibrillation in COVID-19 is driven by multiple mechanisms including reduced ACE2 availability, cytokine storm, electrolyte imbalances, and autonomic nervous system dysfunction.
This review summarizes the multifaceted pathophysiological mechanisms by which acute COVID-19 infection may trigger atrial fibrillation, highlighting targets for future research and management.
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AF in acute COVID-19 warrants clinical vigilance; leaves open mechanistic pathways for targeted research.
Atrial fibrillation (AF) is the most frequent form of cardiac arrhythmia in COVID-19 infected patients. The occurrence of AF paroxysms is often associated with the acute period of infection in time. At the same time, the pathophysiological mechanisms of the occurrence of AF associated with COVID-19 remain insufficiently studied. The review considers the available literature data on the influence of factors such as reduced availability of angiotensin-converting enzyme 2 re- ceptors, interaction of the virus with the cluster of differentiation 147 and sialic acid, increased inflammatory signaling, “cytokine storm”, direct viral damage to the endothelium, electrolyte and acid-alkaline balance in the acute phase of severe illness and increased sympathetic activity.
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Moseichuk et al. (2023) conducted a review in COVID-19 and Atrial Fibrillation. COVID-19 was evaluated. Atrial fibrillation in COVID-19 is driven by multiple mechanisms including reduced ACE2 availability, cytokine storm, electrolyte imbalances, and autonomic nervous system dysfunction.
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