The objective of this article is to review the role of
vitamin E in
cardiovascular disease. We begin by describing the general characteristics and metabolism of
vitamin E and the pathogenesis of
atherosclerosis as it relates to oxidation. We also discuss key in vitro studies, animal studies, observational studies, and clinical trials regarding the potentially cardioprotective effect of
vitamin E. Lastly, we outline the current recommendations regarding
vitamin E in the prevention and treatment of
cardiovascular disease as stated by the American Heart Association.
Vitamin E is a fat-soluble
antioxidant vitamin and
alpha-tocopherol is its most naturally abundant and active form. Oxidation is a key step in
atherogenesis.
Oxidized low-density lipoprotein stimulates endothelial cells to produce inflammatory markers, is involved in foam cell formation, has cytotoxic effects on endothelial cells, inhibits the motility of tissue macrophages, and inhibits
nitric oxide-induced vasodilatation.
Vitamin E has been shown to increase oxidative resistance in vitro and prevent
atherosclerotic plaque formation in mouse models. Consumption of foods rich in
vitamin E has been associated with lower risk of
coronary heart disease in middle-aged to older men and women. Clinical studies at large have not demonstrated a benefit of
vitamin E in the primary and
secondary prevention of
cardiovascular disease.
Vitamin E supplementation might be associated with an increase in total mortality,
heart failure, and
hemorrhagic stroke. The American Heart Association does not support the use of
vitamin E supplements to prevent
cardiovascular disease, but does recommend the consumption of foods abundant in
antioxidant vitamins and other nutrients.