[Atherothrombosis in patients with type 2 diabetes mellitus: an overview of pathophysiology]

Type 2 diabetes mellitus is a well known condition characterized by a functional and metabolic milieu that promotes the development of the atherosclerotic process and its macrovascular complications (e.g., acute myocardial infarction, stroke, peripheral arterial disease). In diabetic patients, several negative alterations lead to the progression of the atherosclerotic disease. These alterations involve the coagulation cascade, the endothelial function, platelet and monocyte adhesiveness, macrophage function, and fibrinolysis: all these processes are adversely affected by hyperglycemia and insulin resistance. In diabetic patients, the fluid and the cellular phases are modified to generate a prothrombotic phenotype. In this review we will discuss about the main pathophysiological mechanisms involved in diabetic atherotrombosis in order to look beyond the usual "hydraulic-rheologic" picture of macrovascular diabetic disease, and to better understand the importance of the adverse interactions that occur between the endothelial wall and the circulating cells.