Vitamin E, a modifier of platelet function: Rationale and use in cardiovascular and cerebrovascular disease

Abstract

Vitamin E has emerged as a major factor in the prevention and inhibition of cardiovascular disease. The inhibition of platelet function, especially adhesion, which is an important event in the development and propagation of cardiovascular disease, plays a crucial role in the beneficial effect that vitamin E exerts on such diseases. Although it is best known for its antioxidant activity, vitamin E interferes with platelet adhesion via a mechanism that is independent of this action. Vitamin E-induced inhibition of protein kinase C leads to decreased platelet pseudopodia formation upon stimulation by agonists, a process that is instrumental in reducing platelet adhesion. In conjunction with potent inhibitors of platelet aggregation, vitamin E has become a widely applied treatment regimen for this group of diseases. Increased bleeding, especially when vitamin E is combined with a potent platelet aggregation inhibitor, has to be considered a side effect of its mechanism of action, but should not detract from the potential benefits for the majority of patients who take this vitamin.