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Therapy and clinical trials.

For almost a quarter of a century, it has been speculated that body iron stores may be related to atherosclerosis. Although still unproven, this hypothesis may not be as ‘rusty’ as some might think [1,2 ]. Iron, of course, is a pro-oxidant co-factor associated with increased production of the hydroxyl radical in cardiovascular tissues. A deleterious effect of iron overload is a possible explanation for the long-standing epidemiologic observations that women in the pre-menopausal years are protected from atherosclerosis as compared to men and that with hysterectomy, but without oophorectomy, women develop an increased coronary heart disease (CHD) risk. Moreover, in those with a genetic disorder of iron metabolism, heritable hemochromatosis, endothelial dysfunction was seen only in untreated male heritable hemochromatosis patients with excessive iron overload, whereas females patients with heritable hemochromatosis had no difference in endothelial dysfunction when compared with controls, irrespective of treatment with phlebotomy [3]. Indeed, in untreated women with heritable hemochromatosis there is an almost balanced iron status, which could be explained, in part, by an additional iron loss due to menstruation. Unfortunately, there are inconsistent results in epidemiologic observations on the effects of blood transfusion on CHD.