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Homocysteine lowering interventions for peripheral arterial disease and bypass graftsHansrani M, Stansby GP SummaryHomocysteine lowering interventions for peripheral arterial disease and bypass graftsHomocysteine is an amino acid, found in proteins. High levels of homocysteine in the blood has been associated with hardening or blocking of arteries (atherosclerosis) and are a risk factor for the progression of peripheral arterial disease. Blood levels of homocysteine can be normalised by taking vitamin B (folic acid, vitamins B12 and B6 or pyridoxine) supplements and betaine. People with peripheral arterial disease have poor blood flow in their legs caused by atherosclerosis. Symptoms include a limited ability to exercise or walk without developing cramping pains in the legs. There is growing evidence that even people without symptoms have a two to three times greater cardiovascular risk than the general population. Although people can be treated surgically (such as a bypass graft) or radiologically (angioplasty) to remove blood clots and improve arterial circulation there is an appreciable risk of failure within 12 months, mainly because the arteries narrow and close up again (restenosis). High levels of homocysteine (hyperhomocysteinaemia) may contribute to restenosis. The review authors made a thorough search of the medical literatures looking for randomised controlled trials using any therapy for the set purpose of lowering plasma homocysteine levels compared with no active treatment. They did not find any completed trials. There is currently a trial underway in the USA, called the Homocysteine and Progression of Atherosclerosis Study (HPAS), where patients are randomised to treatment with 4 mg/day folic acid versus non-active placebo, with a follow up period of five years.
This is a Cochrane review abstract and plain language summary, prepared and maintained by The Cochrane Collaboration, currently published in The Cochrane Database of Systematic Reviews 2010 Issue 1, Copyright © 2010 The Cochrane Collaboration. Published by John Wiley and Sons, Ltd.. The full text of the review is available in The Cochrane Library (ISSN 1464-780X).
This version first published online:
July 22. 2002 AbstractBackgroundElevated plasma levels of the amino acid homocysteine (hyperhomocysteinaemia) are associated with hardening or blocking of the arteries (atherosclerosis) In addition, there is a poorer prognosis, both in the progression of the disease and outcome after therapy. Treatment to lower homocysteine levels has been shown to be both effective and cheap in healthy volunteers. However, the impact of reducing homocysteine levels on the progression of atherosclerosis and patency of vessels after treatment for atherosclerosis is still unknown and forms the basis for this review. ObjectivesTo assess the effects of plasma homocysteine-lowering therapy on the clinical progression of disease in patients with peripheral arterial disease (PAD) and hyperhomocysteinaemia, including, as a subset, those who have undergone surgical or radiological intervention. Search strategyThe authors (MH,GS) searched the Cochrane Peripheral Vascular Diseases Group trials register (last searched October 2006), the Cochrane Central Register of Controlled Trials in The Cochrane Library, Issue 4, 2006, MEDLINE, EMBASE and reference lists of relevant articles. Selection criteriaRandomised trials of the treatment of hyperhomocysteinaemia in patients with peripheral arterial disease, before and after surgical or radiological intervention versus no treatment for hyperhomocysteinaemia. Data collection and analysisTwo authors (MH,GS) independently assessed trial quality and extracted data. Information on adverse events was collected from the trials. Main resultsThere are currently no randomised trials available for analysis. Authors' conclusionsWell constructed trials assessing the impact of the treatment of hyperhomocysteinaemia in patients with peripheral arterial disease are urgently required. |