ABSTRACT
The recognition of hypercholesterolemia, tobacco use, hypertension, family history, and diabetes mellitus as risk factors for cardiovascular disease has contributed to the significant decline in cardiovascular morbidity and mortality. The cardiovascular hallmark of this disease is premature atherothrombosis of the peripheral, coronary, and cerebral vasculature. The clinician must confront three factors when interpreting a laboratory value for homocysteine concentration: the methodologic variability of homocysteine concentration analysis, the biological variability of homocysteine concentration in the subject, and the estimation of patient risk. The patient’s clinical situation also affects the measured homocysteine concentration. Plasma homocysteine concentration is dependent on the interplay between genetics, nutritional intake, disease states, and environmental factors. A number of in vivo studies have analyzed the relationship between homocysteine levels and endothelial dysfunction in healthy volunteers and in patients with cardiovascular disease. The normal endothelium regulates local vascular tone and growth, thrombosis and thrombolysis, leukocyte adhesion, and platelet aggregation.
