In a meta-analysis of predominantly case control studies, 14 of 17 papers supported the link between elevated homocysteine and an increase risk for vascular disease. Although these data appear impressive, there are several limitations to case control studies and the data from prospective studies are not convincing.
Because homocysteine levels increase after acute myo-cardial infarction and stroke, it makes case control studies less useful. The overabundance of hypothesized clarifi¬cations of homocysteine-induced cardiovascular disease reflects the lack of a proven unified mechanism of vascular injury.
Although homocysteine levels can be successfully reduced by folic acid administration, no benefit toward cardiovascular morbidity or mortality has been observed in randomized trials.
A. The Recent FACIT Trial; Lange et al.
A recent randomized clinical trial showed that folate therapy increases restenosis rates in intracoronary stent recipients. The folate therapy after coronary intervention (FACIT) trial enrolled 636 patients who underwent successful coronary stenting and were randomized to receive supplemental treatment with folate and vitamins B6 and B12. The trial investigated whether folate therapy, which is known to reduce high blood levels of homo-cysteine, can limit in-stent restenosis. After 6 months of follow up, folate therapy caused a significantly smaller minimum lumen diameter as well as higher restenosis and major adverse cardiac event rates; folate therapy should therefore be avoided following coronary stent implanta¬tion. Contrary to previous findings, the administration of folate, vitamin B6, and vitamin B12 after coronary stenting may increase the risk of in-stent restenosis and the need for target-vessel revascularization.

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