Inflammation, endothelial dysfunction, and platelet activation contribute to the prothrombotic
pro-inflammatory state associated with AF. Inflammatory biomarkers, such as C-reactive protein
and interleukin 6, promote the production of tissue factor (TF) and von Willebrand factor (vWF) and
aggravate endothelial dysfunction leading to increased coagulation and depressed fibrinolytic activity.
The interaction of vWF and glycoprotein Ib (vWF-GPIb) receptor activates 'thrombo-inflammatory'
pathways promoting thromboembolism. Moreover, platelet activation driven by plateletleukocyte/
monocyte interaction attribute to AF-related thrombosis. Biochemical pathways such as CD40-CD40 ligand and
P-selectin-P-selectin glycoprotein ligand 1 are considered important mediators of platelet-leukocyte interactions in the setting
of AF. Further studies are required to address the clinical implications of inflammatory biomarkers in the prediction
of AF-related thromboembolism. Indeed, inflammatory pathways could be also considered as therapeutic targets in an effort
to reduce the clinical consequences of thromboembolism and improve outcomes in AF.
Keywords: Atrial fibrillation, stroke, inflammation, Virchow's triad, endothelial dysfunction, platelet activation.
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