Hypertension give rise to vascular endothelial injury through shear stress, triggering coagulation and fibrinolysis systems.30 Activated platelets recruited monocytes to the walls of blood vessels and then evolved into macrophages, promoting the atherosclerosis.31 When active atherosclerotic plaques rupture, circulating platelets are exposed to subcutaneous collagen, fibronectin, and von Willebrand factor, stimulating platelet activation and eventually thrombosis.32 Platelet activation is also affected by tHcy. This evidence concerns the gene VWF and hypertensive disorder.