Leukocyte count and vascular function in Type 2 diabetic subjects with treated hypertension

R.J. Woodman, Gerald Watts, Ian Puddey, Valerie Burke, Trevor Mori, Jonathan Hodgson, Lawrence Beilin

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31 Citations (Scopus)

Abstract

Background: Traditional cardiovascular risk factors may only partially explain abnormal vascular function in Type 2 diabetic patients. This Study examined the associations between vascular function and markers of inflammation in Type 2 diabetic subjects with treated hypertension. Methods: Flow-mediated dilatation (FMD) and glyceryl-trinitrate mediated dilatation (GTNMD) of the brachial artery were used to assess endothelium-dependent and -independent function, respectively, in 29 hypertensive Type 2 diabetic Subjects (HbA1c <9%), and 17 healthy control subjects. Plasma C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and leukocyte count were used as markers of inflammation. Soluble L-selectin, P-selectin, and von Willebrand factor (vWf) were measured to assess leukocyte, platelet and endothelial cell activation, respectively. Results: Compared with controls, diabetic subjects had impaired FMD (3.9+/-3.0 vs. 5.5 +/-2.4%, P = 0.07) and GTNMD (11.4+/-4.8%, vs. 15.4+/-7.1%, P = 0.04). They also had higher levels of CRP (2.7+/-2.6 vs. 1.4+/-1.1 mg/l, P = 0.03), fibrinogen (3.4+/-0.7 vs. 2.7+/-0.3 g/ 1, P <0.001) and TNF-alpha (20.9 +/- 13.4 vs. 2.5 +/- 1.7 pg/l, P <0.001). In diabetic subjects, after adjustment for age and gender, leukocyte Count was an independent predictor of FMD (P = 0.02), accounting for 17% of total variance. Similarly, leukocyte count (P <0.001) accounted for 23% and IL-6 (P = 0.03) for 12% of the variance in GTNMD. vWf was correlated with leukocyte count (r = 0.38 P = 0.04), FMD (r = -0.35, P = 0.06) and GTNMD (r = -0.47, P - 0.009), whilst P-selectin correlated with fibrinogen (r = 0.58, P = 0.001). Conclusion: These cross-sectional observations are consistent with the hypothesis that reduced FMD and GTNMD in Type 2 diabetes is at least in part secondary to increased inflammation, with associated endothelial and platelet activation. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
Original languageEnglish
Pages (from-to)175-181
JournalAtherosclerosis
Volume163
DOIs
Publication statusPublished - 2002

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