Key result
Inflammation is linked to AF initiation and its prothrombotic state via endothelial damage and platelet activation.
Why the study?
The review aimed to provide an update on the association of inflammation and AF, including the impact of inflammatory markers on clinical presentation and outcomes.
This review highlights the plausible mechanisms linking inflammation to the initiation, perpetuation, and prothrombotic complications of atrial fibrillation.
Supports inflammatory pathways in AF; leaves open whether targeting inflammation improves outcomes.
Atrial fibrillation (AF) is associated with increased risk for stroke and systemic embolism. There is plausible evidence linking inflammation to the initiation and perpetuation of AF and AF-related thrombosis. Various inflammatory markers (C-reactive protein, tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-8) have been associated with AF. Proposed mechanisms linking inflammation and the prothrombotic AF state include endothelial activation/damage, production of tissue factor from monocytes, increased platelet activation, and increased expression of fibrinogen. The present review aims to provide an update on the association of inflammation and AF, including the impact of inflammatory markers on clinical presentation and outcome of AF patients.
No takes yet. Share an insight, caveat, or question.
Guo et al. (2012) conducted a review in Atrial Fibrillation. Inflammation was evaluated. Inflammation is linked to the initiation and perpetuation of atrial fibrillation and its prothrombotic state through mechanisms like endothelial damage and increased platelet activation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: