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Endothelial function in individuals with coronary artery disease with and without type 2 diabetes mellitus

Gissette Reyes-Soffera, Steve Holleranb, Marco R. Di Tullioc, Shunichi Hommac, Bernadette Boden-Albalad, Rajasekhar Ramakrishnanb, Mitchell S. Elkindd, Ralph L. Saccod, Henry N. GinsbergaCorresponding Author Informationemail address

Received 8 April 2009; accepted 21 December 2009. published online 27 January 2010.
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Abstract 

The goal of this study was to determine if individuals with coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM) had greater endothelial dysfunction (ED) than individuals with only CAD. Flow-mediated dilation (FMD), calculated as percentage increase in brachial artery diameter in response to postischemic blood flow, was measured after an overnight fast in 2 cohorts. The first cohort included 76 participants in the Northern Manhattan Study with CAD; 25 also had T2DM. The second cohort was composed of 27 individuals with both T2DM and CAD who were participants in a study of postprandial lipemia. Combined, we analyzed 103 patients with CAD: 52 with T2DM (T2DM+) and 51 without T2DM (T2DM−). The 52 CAD T2DM+ subjects had a mean FMD of 3.9% ± 3.2%, whereas the 51 CAD T2DM− subjects had a greater mean FMD of 5.5% ± 4.0% (P < .03). An investigation of various confounders known to affect FMD identified age and body mass index as the only significant covariates in a multiple regression model. Adjusting for age and body mass index, we found that FMD remained lower in T2DM+ subjects compared with T2DM− subjects (difference, −1.99%; P < .03). In patients with CAD, the concomitant presence of T2DM is independently associated with greater ED, as measured by FMD. This finding may be relevant to the greater early and late morbidity and mortality observed in patients with both CAD and T2DM.

a Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA

b Department of Pediatrics, Columbia University Medical Center, New York, NY 10032, USA

c Department of Cardiology, Columbia University Medical Center, New York, NY 10032, USA

d Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA

Corresponding Author InformationCorresponding author. Tel.: +1 212 305 9562; fax: +1 212 305 3213.

PII: S0026-0495(09)00535-6

doi:10.1016/j.metabol.2009.12.023

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