High plasma concentrations of the amino acid homocysteine have been associated with atherothrombotic disease, first in individuals with inborn errors of homocysteine metabolism, who have very high plasma homocysteine concentrations, and later also in the general population. In general, the cardiovascular risk associated with hyperhomo-cysteinemia is significant, but modest and probably differs between populations. High homocysteine concentrations are thought to impair endothelial function, increase oxida-tive stress, impair methylation reactions, and alter protein structure. Although some studies have shown improvement of vascular surrogate end points, homocysteine-lowering treatment has not yet been associated with a significant reduction of cardiovascular events. Studies that have examined the relationship between plasma homocysteine and arterial stiffness parameters have shown heterogenous results.
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