Plasma Homocysteine and Vascular Disease

Abstract

Vascular disease is the leading cause of death and disability in the Western World: atherosclerosis is responsible for the majority of deaths in virtually all westernized societies; pulmonary embolism, a complication of deep venous thrombosis, is the leading cause of morbidity and mortality, resulting in approximately 50,000 deaths per year in the United States; approximately 1.5 million acute myocardial infarcts occur each year, each infarction bearing a 30% mortality rate; and strokes represent the third leading cause of death in developed countries (1). While the adverse effects of hypertension, hypercholesterolemia, diabetes, and smoking on the vascular system have received widespread publicity, another important risk factor for vascular disease--less well-known outside the medical community but recently gaining increasing attention in the literature is an elevated plasma level of the amino acid homocysteine. Bolstered by findings of an association between hyperhomocysteinemia and a variety of vascular disorders, theories implicating homocysteine in the pathogenesis of these disorders have inspired researchers to explore novel approaches in the prevention and treatment of vascular disease. With the biochemistry of homocysteine metabolism already well understood, vitamin supplementation has emerged as a promising strategy for reduction of plasma homocysteine levels, with consequent arrest or reversal of the postulated pathogenic mechanisms involved in homocysteine-associated disorders of the vasculature, and, thus, potential prevention and treatment of vascular disease in hyperhomocysteinemic patients.