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Body Iron Stores , Infection , and Risk of Acute Myocardial Infarction

Myocardial Infarction To the Editor: Tuomainen et al 1 have noted an association between increased iron stores, as measured by a reduced ratio of serum transferrin receptor concentration to serum ferritin concentration, and excess risk of acute myocardial infarction (AMI). It has been suggested that iron can catalyze toxic redox reactions, which may lead to an increased risk for coronary heart disease and AMI. Another mechanism by which iron might increase the risk of AMI involves a possible role for iron in facilitating some infections. Vertebrates have a hypoferremic response during infection that lowers the presence of iron as serum transferrin, temporarily storing the metal as ferritin. Intestinal absorption of iron also declines during infection. Bacterial mechanisms to obtain iron from a host include direct uptake of iron from the labile iron pool, siderophore-mediated iron uptake, and iron uptake by direct interaction with transferrin, lactoferrin, or hemecontaining proteins. Various mechanisms by which infectious processes might induce atherogenesis have been proposed, including cytopathic effects of infection on endothelial and smooth muscle cells, formation of circulating toxins or immune complexes that deposit on vessel walls, elicitation of an inflammatory response, induction of alterations of serum prostaglandin and lipid metabolism, or elicitation of a hypercoagulable state that increases the risk of thrombosis. Recent research has suggested that numerous organisms may be associated with an increased risk of AMI. These include Helicobacter pylori, Chlamydia pneumoniae, herpes simplex virus, and cytomegalovirus. 2