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Homocysteine
Book chapter

Homocysteine

Sanjana Dayal and Steven R Lentz
Atherosclerosis, pp.53-62
John Wiley & Sons, Inc
03/27/2015
DOI: 10.1002/9781118828533.ch5

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Abstract

The evolution of homocysteine as a cardiovascular risk factor dates to the 1960s, when adverse vascular events were first reported in patients with excessive levels of urinary homocysteine, a condition termed “homocystinuria.” In 1969, autopsy findings from two children suffering from homocystinuria led to the hypothesis that homocysteine may directly cause arteriosclerosis and thrombosis. Subsequently, a series of retrospective and prospective association studies implicated hyperhomocysteinemia as an independent risk factor for cardiovascular disease. Several clinical trials thereafter examined the potential benefit of homocysteine‐lowering therapy in preventing vascular events in subjects with hyperhomocysteinemia. The most beneficial effects of homocysteine‐lowering therapy have been observed in patients with severe hyperhomocysteinemia due to inborn genetic defects in homocysteine metabolic enzymes. In contrast, homocysteine‐lowering therapy has not been proven to provide protection from secondary vascular events in patients with moderate hyperhomocysteinemia, with the possible exception of certain subgroups of patients − such as those with ischemic stroke. The general failure of the homocysteine‐lowering intervention trials has created controversy regarding the role of homocysteine as a treatable cardiovascular risk factor. In this chapter, we review the current status of homocysteine as a risk factor, including knowledge gained from patients with mutations in enzymes involved in homocysteine metabolism as well as seminal studies in animal models of hyperhomocysteinemia.
 homocysteine hyperhomocysteinemia arteriosclerosis thrombosis homocystinuria

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