Angiotensin and atherosclerotic vascular disease

Cardiovascular disease (CVD) is a global burden for both social and medical systems. In high-income countries, CVD are the leading cause of mortality and morbidity, being estimated on the basis of prevalence to become the major cause of death [1,2]. The occurrence of CVD at younger ages influences the socioeconomic balance despite therapeutic advances of both interventional therapeutic procedures and newly discovered drugs [3,4]. Atherosclerosis is a multifactorial process, in which genetic and environmental factors are involved [5]. Traditional cardiovascular risk factors such as smoking, hypertension, diabetes, obesity, and high cholesterol levels—although useful in population studies—fail to explain the variable nature of disease progression and interindividually different clinical presentations. Genetic polymorphisms of the enzymes responsible for endothelial cell function and for thrombotic factors may cause variability in clinical signs [6,7]. Genetic determinants of lipid metabolism, variations of coagulation factors, and fibrinogen lead to increased thrombogenicity. Coronary artery disease and hypertension have an increased risk of occurrence in patients with mutations of factors involved in renin–angiotensin pathway and certain variants of endothelial nitric oxide (NO) synthase [5,8].