Oxidant stress plays an important role in the pathogenesis of atherosclerosis. 
In the late 1980s, biological studies demonstrated that oxygen-free radicals 
oxidize low-density lipoprotein-cholesterol, resulting in the creation of foam 
cells and inciting the cascade of biological events that ultimately result in 
the formation of atherosclerosis. In vitro studies showed the ability of 
antioxidant vitamins to scavenge free radicals and block the oxidation of 
low-density lipoprotein. This data was supported in vivo by early observational 
studies suggesting the benefit of antioxidants, particularly vitamin E, in the 
prevention of coronary artery disease. On the basis of these studies, the use of 
antioxidant supplements by the general population increased substantially and 
became a multibillion dollar industry. Despite strong biological evidence and 
promising observational data, more rigorous scientific evaluation did not 
support a causational relationship between vitamin supplements and lowering 
coronary artery disease risk. Several prospective, double-blind, 
placebo-controlled trials showed no benefit and possibly harmful effects. 
Therapies such as angiotensin-converting enzyme inhibitors, angiotensin receptor 
blockers, and statins, which are known to have benefit in preventing and 
treating atherosclerosis by reducing blood pressure and cholesterol, also have a 
"pleiotropic" effect in reducing the formation of reactive oxygen species (ROS). 
Advances in molecular biology and the study of ROS led to a better understanding 
of the mechanisms that govern their production and role in atherogenesis. This 
progress identified unforeseen pathways by which these drugs favorably alter the 
balance in ROS production, and have raised possibilities for future targeted 
therapies in the prevention of atherosclerosis.