Emergent Cardiovascular Risk Factor: Homocysteine

Cindy J. Warren, MSN, RN


Prog Cardiovasc Nurs. 2002;17(1) 

In This Article

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.[3] In the presence of circulating homocysteine, blood vessels lose their elasticity and ability to dilate,[2,3,10] causing intimal injury.[2] 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.[2] Reactive oxygen radicals accumulate in the intimal cells, releasing growth factors and promoting hyperplasia of these cells.[2] Fibrin is deposited within and over the surface of the plaques.[2] 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,[12] increases smooth muscle cell proliferation,[2,3] stimulates the oxidation of LDL,[2] 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.[2]


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