Previous studies show a correlation between cardiac complications and hereditary hemochromatosis. Tissue iron deposition could be harmful, because Fe can react with H2O2 to form OH- radicals and Fe2+ can react with O2 to form reactive oxygen species. Free radicals react with cell membranes and cell organelles and could lead to the development of atherosclerosis by initiating lipid peroxidation. Hereditary hemochromatosis provides an opportunity for studying the effects of iron on cardiovascular disease. Some studies have shown that individuals who carried HFE mutations may be at greater risk of developing coronary heart disease than those without the mutations. In contrast, a large number of studies have reported no association between HFE mutations and coronary heart disease. We studied the relation between HFE mutations and acute myocardial infarction in two sets of subjects. The first one was composed of 200 patients (114 males and 86 females) who suffered myocardial infarction. The second one was composed of 200 healthy controls (103 males and 97 females). All patients were genotyped for HFE mutation. DNA typing was performed for C282Y, H63D and S65C HFE alleles. There were no significant differences in frequencies of the different HFE alleles between acute myocardial infarction patients and controls. Thus, our study, performed in two samples of genetically homogeneous patients and controls, does not support the suggestion that HFE mutations may be associated with acute myocardial infarction in susceptible individuals.