Endothelial (Dys)Function in Lone Atrial Fibrillation

Atrial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia in adult population and confers significant thromboembolic risk. Endothelial dysfunction has been recognized as a possible contributor to thrombogenesis in AF. The arrhythmia has been associated with thrombogenic atrial endocardial lesions and evidence of increased circulating biomarkers of endothelial dysfunction (e.g. von Willebrand factor, soluble thrombomodulin, E-selectin, asymmetric dimethylarginine, circulating endothelial cells and microparticles), and impairment of endothelium-dependent vasodilatation in the peripheral and coronary circulation has been reported in AF patients. Increased levels of biomarkers of endothelial origin (e.g. von Willebrand factor, soluble thrombomodulin, E-selectin, asymmetric dimethylarginine) have been associated with adverse outcomes in AF patients. Importantly, endothelial dysfunction has been documented in AF patients without cardio-pulmonary comorbidities or risk factors (so-called ‘lone AF’), as well. In this review, we provide an overview of contemporary evidence for the alterations in endothelial function and endothelial injury in AF, with a focus on endothelial (dys)function in lone AF. Keywords: Lone atrial fibrillation, endothelial dysfunction, endothelial damage, endocardial dysfunction, von Willebrand factor, thrombomodulin, E-selectin, asymmetric dimethylarginine, circulating endothelial cells, progenitor endothelial cells, microparticles, endotheliumdependent vasodilatation, flow-mediated dilation.