Abstract

See related article, pages 730–736. The paradigm that homocysteine is associated with atherosclerotic disease has been discussed since the 1960s. Since then, large observational studies and meta-analyses showed a strong relationship between homocysteine and cardiovascular risk. However, several recent trials using homocysteine-lowering therapies for secondary prevention failed to show beneficial effects in patients with prior stroke or known coronary artery disease.1–3 These trials showed no advantage of either folic acid and/or vitamin B complex therapy on “hard” end points such as mortality or cardiovascular events. Thus, the “homocysteine hypothesis” for atherothrombotic disease became controversial. Kaul et al4 stated in a recent review that it remains unclear whether a causal relationship exists between homocysteine and cardiovascular risk, or if homocysteine is related to other confounding risk factors or is a marker of existing disease burden. This discussion is now continued and refuelled with a new study published in this issue of Stroke . Hodis and coworkers present a work that assesses homocysteine-lowering therapy as primary prevention in patients without preexisting cardiovascular disease. The goal was to show a reducing effect of a high-dose combination of B-vitamins on progression of carotid intima media thickness …

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