Editor-in-Chief: Dimitri P. Mikhailidis Academic Head, Department of Clinical Biochemistry Royal Free Hospital Campus University College London Medical School University College London (UCL) Pond Street London, NW3 2QG UK
Affiliation: Haemostasis, Thrombosis and Vascular Biology Unit, University of Birmingham Centre for Cardiovascular Science, City Hospital, Birmingham, B18 7QH, United Kingdom.
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.