Iron is an essential element for normal cellular function and general healt
h. However, iron may play a pathologic role in certain cardiac conditions i
ncluding reperfusion injury, hemochromatosis, beta-thalassemia and coronary
atherosclerosis. II also may play a role in injury due to anthracycline ca
rdiotoxicity. Removal of iron via phlebotomy for hemochromatosis and chelat
ion therapy for beta-thalassemia are proven treatments. Cell culture, and i
solated organ and animal studies suggest that depleting iron stores may pre
vent reperfusion injury, restenosis and even atherogenesis. This article wi
ll review mechanisms by which iron overload states and normal iron stores c
ontribute to cardiovascular pathophysiology and the accumulating evidence t
hat iron chelation may prevent restenosis and atherogenesis.