Extracellular vesicles (EVs) are defined as a heterogenic group of lipid bilayer vesicular structures with a size in the range of 30-4000 nm that are released by all types of cultured cells. EVs derived from platelets, mononuclears, endothelial cells, and adipose tissue cells significantly increase in several cardiovascular diseases, including in atrial fibrillation (AF). EVs are engaged in cell-to-cell cooperation, endothelium integrity, inflammation, and immune response and are a cargo for several active molecules, such as regulatory peptides, receptors, growth factors, hormones, and lipids. Being transductors of the intercellular communication, EVs regulate angiogenesis, neovascularization, coagulation, and maintain tissue reparation. There is a large amount of evidence regarding the fact that AF is associated with elevated levels of EVs derived from platelets and mononuclears and a decreased number of EVs produced by endothelial cells. Moreover, some invasive procedures that are generally performed for the treatment of AF, i.e., pulmonary vein isolation, were found to be triggers for elevated levels of platelet and mononuclear EVs and, in turn, mediated the transient activation of the coagulation cascade. The review depicts the role of EVs in thrombogenicity in connection with a risk of thromboembolic complications, including ischemic stroke and systemic thromboembolism, in patients with various forms of AF.
Keywords: atrial fibrillation; coagulation; extracellular vesicles; thromboembolic complications.