This mechanism resulted in downregulation of NO synthase, which leads to decreased endothelial cell survival.24 Thus, elevated EMP levels in AF may result from endothelial damage.18, 19, 20, 21 On the other hand, elevated EMP levels may contribute to endothelial dysfunction in AF.22, 23 in vitro study demonstrated that ET‐1 stimulates the release of EMP from human umbilical vein endothelial cells (HUVECs).25 Elevated ET‐1 levels have been reported in AF patients.26 Another possible mechanism of increased EMP levels in AF may result from ET‐1 stimulation. This evidence concerns the gene EDN1 and atrial fibrillation.