Thorac Cardiovasc Surg 2011; 59(4): 201-206
DOI: 10.1055/s-0030-1250211
Original Cardiovascular

© Georg Thieme Verlag KG Stuttgart · New York

Adiponectin – Its Potential to Predict and Prevent Coronary Artery Disease

C. A. Skrabal1 , J. Czaja1 , K. Honz1 , R. Emini1 , A. Hannekum1 , R. Friedl2
  • 1Department of Cardiac Surgery, University of Ulm, Ulm, Germany
  • 2Department of Cardiac Surgery, University Clinic of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany
Further Information

Publication History

received April 12, 2010

Publication Date:
17 March 2011 (online)

Abstract

Background: Recent evidence suggests that epicardial adipose tissue may contribute locally to the pathogenesis of coronary artery disease (CAD). We investigated how local and systemic adiponectin, an adipokine with anti-inflammatory and insulin sensitizing properties, is related to the presence of CAD and cardiovascular risk factors. Methods: Serum and adipose tissue samples from subcutaneous and pericoronary depots were collected from sixty consecutive patients with CAD who required coronary artery bypass grafting or patients without CAD who underwent cardiac surgery for aortic valve replacement. Western blot, ELISA and PCR were used to detect and determine the adiponectin concentrations and expression in the samples. Results: Adiponectin concentrations in the serum and pericoronary fat of patients without CAD were significantly higher than in patients with CAD (p < 0.01). However, the expression of adiponectin mRNA did not differ in any instances. Male gender, BMI > 30 and type 2 diabetes were significantly correlated to decreased serum adiponectin (p < 0.03). Conclusion: Pericoronary fat specifically secretes metabolically active adiponectin. Its local and systemic concentrations are inversely correlated to the presence of coronary artery disease, indicating its anti-atherogenic effects. As for patients with CAD, adiponectin might be a promising marker for intra-individual monitoring of cardiovascular risk factors and thus a course of secondary prevention. Further evaluation is necessary to elucidate whether a novel therapeutic option could be derived against the onset and progression of CAD.

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Dr. Christian A. Skrabal, MD, PhD

Department of Cardiac Surgery
University of Ulm

Steinhoevelstrasse 9

89075 Ulm

Germany

Phone: +49 7 31 50 05 44 03

Fax: +49 7 31 50 05 43 02

Email: cskrabal@fastmail.fm

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