IntroductionThe link between oxidative stress, endothelial dysfunctionand cardiovascular diseases (CVDs) has been well established[1]. Clinical studies have shown that there is increased produc-tion of reactive oxygen species in CVD patients as demonstratedby clinical studies [2]. The increase in reactive oxygen speciesinduces oxidative stress, which then initiates atherosclerosis
at the endothelium. Endothelial dysfunction is the first stepin artherosclerosis and a major signal of cardiovascular com-plications [3]. Lee et al. [4] reported that oxidative stress isnot only linked to endothelial dysfunction, but to all the pro-cesses involved in atherogenesis up to myocardial infarctions.Furthermore, hypercholesterolemia has been shown to induceoxidative stress [5] thereby causing tissue damage [6]. Low-ering cholesterol levels has been shown to reduce the risk ofmyocardial infarctions and also increased endothelium depend-ent vasodilation [7]. A vasoconstrictor that has been linked tocardiovascular complications is angiotensin II, which is pro-duced by the renin–angiotensin system and has also been linkedto increased oxidative stress [8].Therefore, the therapeutic targets for the management ofcardiovascular complications include angiotensin-I converting