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Fetuin-A is associated with calcified coronary artery disease

Mori, Katsuhitoa; Ikari, Yujic; Jono, Shuichia; Emoto, Masanoria; Shioi, Atsushib; Koyama, Hidenoria; Shoji, Tetsuoa; Ishimura, Eijia; Inaba, Masaakia; Hara, Kazuhiroc; Nishizawa, Yoshikia

doi: 10.1097/MCA.0b013e32832fe5d5
Diagnostic Method

Objective: Fetuin-A is a circulating glycoprotein that is involved in various stages of atherosclerosis. Despite the fact that emerging evidence suggests fetuin-A acts as a calcification inhibitor that protects against advanced calcified atherosclerosis in dialyzed patients, the role of fetuin-A in cardiovascular disease is still controversial. As diabetes and uremia make the role of fetuin-A in cardiovascular disease uncertain, we investigated the association between fetuin-A and calcified coronary artery disease in participants without diabetes and renal dysfunction.

Methods: Serum fetuin-A levels were measured in 92 participants who underwent coronary angiography. The number of diseased vessels and the presence of calcification were evaluated.

Results: Fetuin-A levels significantly decreased in patients with advanced three-vessel disease compared with those without stenosis (245.5±50.9, 289.0±71.8 μg/ml, respectively; P<0.05). Likewise, fetuin-A levels were significantly lower in patients with coronary artery calcification compared with those without coronary artery calcification (257.1±49.7, 288.0±63.1 μg/ml, respectively; P = 0.010). Multivariate logistic regression analysis revealed that fetuin-A levels inversely correlated with the presence of coronary artery calcification (odds ratio: 0.54; 95% confidence interval: 0.31–0.92; P = 0.025).

Conclusion: Serum fetuin-A levels inversely correlated with advanced calcified coronary artery disease.

Departments of aMetabolism, Endocrinology, and Molecular Medicine

bCardiovascular Medicine, Osaka City University Graduate School of Medicine, Osaka

cDivision of Cardiology, Mitsui Memorial Hospital, Tokyo, Japan

Correspondence to Dr Katsuhito Mori, MD, PhD, Department of Metabolism, Endocrinology, and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan

Tel: +81 6 6645 3806; fax: +81 6 6645 3808;

e-mail: ktmori@med.osaka-cu.ac.jp

Received 2 May 2009 Accepted 20 June 2009

© 2010 Lippincott Williams & Wilkins, Inc.