Is homocysteine an iron-dependent cardiovascular risk factor?

Recent studies of endothelial function suggest that adverse vascular effects of homocysteine are iron-dependent. Iron sucrose worsens and iron chelation eliminates homocysteine-associated decreases in flow-mediated dialation. There may be no vasculopathic effect of homocysteine without available reactive iron. Iron-dependent amplification of the vascular effects of homocysteine may be one of several mechanisms by which stored iron increases cardiac risk.