Abstract 11351: Hepcidin, an Iron Regulatory Hormone, is Associated with Degree of Subclinical Atherosclerosis in Perimenopause
Background: Hepcidin is a central regulator of iron homeostasis, has been reported to increase with inflammation, and inhibits macrophage iron release. As monthly iron loss ceases with menopause, we sought to explore interactions among hepcidin and other atherosclerotic serologies in relation to subclinical atherosclerosis in a cohort of perimenopausal women. Our driving hypothesis is that hepcidin modifies atherosclerosis risk in the transition to menopause.
Methods and Results: 117 perimenopausal women age 49.8±3.8 years with ≥1 atherosclerosis risk factor were prospectively enrolled to participate in a longitudinal study of iron and atherosclerosis. Plasma hepcidin-25 was measured by enzyme immunoassay, and subjects underwent noncontrast carotid artery MRI on a 3T scanner using a custom-built 8-element carotid coil. Vessel wall volume was calculated over a standardized region of the carotid artery from a volumetric dark blood T1-weighted TSE acquisition. In this obese cohort (BMI 32±9 kg/m2) with preserved renal function (estimated GFR 86±16 mL/min/m2), hepcidin levels were similar in women with Framingham-derived cardiovascular disease risk score (CVDrisk) <6% compared to those with CVDrisk≥20% (45.4±10.6 vs. 43.3±20.5 ng/mL, p=0.65), as was high-sensitivity c-reactive protein (4.92±2.05 vs. 5.69±2.23, p=0.44). Hepcidin levels correlated with serum ferritin (R=0.53, p<0.01) but not with serum iron. After adjustment for CVDrisk score, hepcidin level showed a modest inverse relationship with vessel wall volume (R=0.30, p=0.01; Figure).
Conclusions: Hepcidin may have a protective effect against subclinical arterial wall thickening. Serial assessment of hepcidin and vascular disease in the transition to menopause is warranted to better understand how changes in iron homeostasis may contribute to increased post-menopausal atherosclerosis risk.
- © 2011 by American Heart Association, Inc.