Deleterious Effects of High Homocysteine
Homocysteine, in elevated amounts, is toxic to endothelial cells.[2,7,11] The toxicity is associated with hydrogen peroxide formation, in the presence of copper ions.[2,3] Copper concentrations have been reported to be lower in patients with coronary artery disease than in other subjects, although the association of homocysteine with copper remains unclear. In the presence of circulating homocysteine, blood vessels lose their elasticity and ability to dilate,[2,3,10] causing intimal injury. Especially in areas of high pressure and turbulent blood flow, calcium, cholesterol, and collagen adhere to sites of intimal injury to form fibrous atherosclerotic plaques. Reactive oxygen radicals accumulate in the intimal cells, releasing growth factors and promoting hyperplasia of these cells. Fibrin is deposited within and over the surface of the plaques. In animal models, in vitro studies, and human investigations, elevated homocysteine also affects a number of other factors important to the atherosclerotic process. It promotes platelet aggregation,[2,3,12] impairs endogenous tissue-type plasminogen activator activity, increases smooth muscle cell proliferation,[2,3] stimulates the oxidation of LDL, increases the binding of lipoprotein(a) (Lp[a]) to fibrin,[11,12] inhibits natural anticoagulants, such as antithrombin III and factor C,[2,12] and stimulates clotting factors V, X, and XII.[3,11,12] Homocysteine increases the likelihood of atherosclerotic aneurysms, thrombus formation, and the progression of narrowing arteries.
Prog Cardiovasc Nurs. 2002;17(1) © 2002 Le Jacq Communications, Inc.
© 2007 Prog Cardiovasc Nurs
Cite this: Emergent Cardiovascular Risk Factor: Homocysteine - Medscape - Jan 01, 2002.