Myocardial Infarction (MI) is irreversible necrosis of heart muscle secondary to prolonged ischemia. Atherosclerosis of the coronary arteries commonly causes MI and angina pectoris .Free oxygen radicals act directly on the endothelial cells and has a close interaction with lipid peroxidation, causing a modification of LDL and facilitating LDL deposition, with the consequent formation of atherosclerotic plaques. Free radical production is catalyzed and accelerated in the presence of iron. Such molecules are highly reactive. Superoxide anions produced by oxidative stress and reducing agents have been found to be capable of mobilizing iron from ferritin. Lipid hydroperoxides decompose in the presence of iron to form cytotoxic aldehydes, such as Malondialdehyde. This potential toxicity of reactive oxygen species is counteracted by cytoprotective enzymes such as Glutathione peroxidase which limit the damage caused by such species. The present study is an humble effort to evaluate the role of ferritin as an oxidant and to test whether excess body iron stores as estimated by serum ferritin concentration is associated with increase in risk of Myocardial Infarction.