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Adiponectin is associated with abnormal lipid profile and coronary microvascular dysfunction in patients with dilated cardiomyopathy without overt heart failure

Daniela GiannessiaCorresponding Author Informationemail address, Chiara Casellia, Silvia Del Rya, Maristella Maltintib, Silvia Pardinia, Stefano Turchia, Manuela Cabiatic, Tiziana Sampietroa, Nader Abrahamde, Antonio L'Abbatec, Danilo Negliaa

Received 29 September 2009; accepted 29 December 2009. published online 04 March 2010.
Corrected Proof

Abstract 

Reduced plasma adiponectin has been associated with abnormal lipid profile, reduced left ventricle (LV) function, and the extent of coronary atherosclerosis in coronary artery disease. The aim of this study was to assess these relationships in patients with dilated cardiomyopathy (DCM) without overt heart failure. Plasma adiponectin was measured in 55 DCM patients (age, 59 ± 12 years; male, 36; body mass index [BMI], 26.9 ± 0.49 kg/m2; LV ejection fraction, 39.8% ± 1.3%; New York Heart Association class I-II) and in 40 age- and BMI-matched healthy controls. In a subset of 25 patients, myocardial blood flow (MBF) was measured at rest and during intravenous dipyridamole (0.56 mg/kg in 4 minutes) by positron emission tomography and 13N-ammonia as a flow tracer. Adiponectin was 6.6 ± 0.34 μg/mL in controls and 10.9 ± 0.85 μg/mL in DCM patients (P < .001), where it was related inversely with BMI (P = .009) and directly with brain natriuretic peptide (P = .017), high-density lipoprotein (HDL) cholesterol (P = .002), and MBF dipyridamole (P = .020). Adiponectin lesser than median value in patients was associated with higher total to HDL cholesterol ratio (4.8 ± 0.24 vs 3.9 ± 0.18, P = .009) and lower MBF reserve (1.76 ± 0.16 vs 2.43 ± 0.19, P = .01). These results could suggest that down-regulation of the adiponectin levels and reduced HDL cholesterol have a key role in causing impaired coronary function and myocardial perfusion in DCM.

a Research National Council (CNR) Institute of Clinical Physiology-Laboratory of Cardiovascular Biochemistry, Pisa 56124, Italy

b Fondazione CNR-Regione Toscana Gabriele Monasterio, Pisa 56124, Italy

c Scuola Superiore S. Anna, Pisa 56124, Italy

d Department of Medicine, New York Medical College, Valhalla, NY 10595, USA

e Pharmacology, New York Medical College, Valhalla, NY 10595, USA

Corresponding Author InformationCorresponding author. CNR-IFC, 56100 Pisa, Italy. Tel.: +39 050 3152664; fax: +39 050 3152166.

PII: S0026-0495(10)00003-X

doi:10.1016/j.metabol.2009.12.030

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