This study seeks to investigate changes in
iron homeostasis and carotid arteries in women at risk of
atherosclerosis, addressing a relatively unexplored hypothesis explaining why women have a 5-10 year lag in initial atherosclerotic events. Recent evidence points to
hepcidin, the key regulator of macrophage
iron uptake and release, as a potential mediator of risk. Furthermore,
iron catalyzes the generation of
free radicals that oxidize
cholesterol stimulating
atheroma formation. Magnetic resonance imaging (MRI) is ideally suited to study
iron because of
iron's local effects on magnetic susceptibility that can be quantified using a relaxation parameter called T2* ('T2-star'), as well as the ability to noninvasively characterize and quantify
atherosclerotic plaque with MRI. This work outlines the rationale and study design to provide critical evidence related to the
iron hypothesis, such that novel diagnostics and
therapeutics to attenuate risk may be derived from a better understanding of
iron's role in
atherosclerosis.