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Clinical Chemistry 52: 853-859, 2006. First published March 23, 2006; 10.1373/clinchem.2005.060509
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Right arrow Lipids, Lipoproteins, and Cardiovascular Risk Factors
(Clinical Chemistry. 2006;52:853-859.)
© 2006 American Association for Clinical Chemistry, Inc.


Lipids, Lipoproteins, and Cardiovascular Risk Factors

Relationship of Adiponectin with Markers of Systemic Inflammation, Atherogenic Dyslipidemia, and Heart Failure in Patients with Coronary Heart Disease

Maximilian von Eynatten1,a, Andreas Hamann1, Dorothee Twardella2, Peter P. Nawroth1, Hermann Brenner2 and Dietrich Rothenbacher2

1 Department of Medicine I (Endocrinology and Metabolism), Ruprecht-Karls-University of Heidelberg, Heidelberg, Germany.
2 Department of Epidemiology, German Centre for Research on Ageing, Heidelberg, Germany.

aAddress correspondence to this author at: Department of Medicine I (Endocrinology and Metabolism), University of Heidelberg, INF 410, D-69120 Heidelberg, Germany. Fax 49-6221-56-4233; e-mail maximilian.eynatten{at}med.uni-heidelberg.de.

Background: Adiponectin, an adipocyte-derived hormone, appears to be a modulator of lipid metabolism and systemic inflammation and is present in particularly low concentrations in patients with coronary heart disease (CHD). However, the clinical importance of adiponectin in individuals at markedly high risk for future cardiovascular morbidity and mortality has not been fully elucidated. We examined the associations between serum adiponectin and several biomarkers related to cardiovascular disease and heart failure in a large high-risk population comprising patients with prevalent CHD.

Methods: We measured fasting adiponectin, interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and markers of lipoprotein metabolism in 1174 patients with CHD.

Results: After adjustment for age and sex, adiponectin was associated with HDL-cholesterol (HDL-C; r = 0.25; P <0.0001), NT-proBNP (r = 0.17; P <0.0001), and plasma triglyceride (r = –0.21; P <0.0001) concentrations. There was, however, no statistically significant association between adiponectin and markers of systemic inflammation. In partial correlation analyses further adjusted for body mass index, alcohol intake, smoking status, presence of diabetes and/or hypertension, lipid-lowering drug therapy, and fasting plasma glucose, adiponectin remained significantly associated with HDL-C (r = 0.21; P <0.0001), NT-proBNP (r = 0.15; P <0.0001), and plasma triglycerides (r = –0.16; P <0.0001).

Conclusions: Serum adiponectin is associated with the presence of atherogenic dyslipidemia and with NT-proBNP concentration but not with markers of systemic inflammation in patients with manifest CHD. Thus, atherogenic dyslipidemia may link adiponectin with the progression of atherosclerosis. Moreover, serum adiponectin may be related to BNP in patients with CHD.




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