Association of plasma visfatin levels with inflammation, atherosclerosis and acute coronary syndromes (ACS) in humans.

Clin Endocrinol (Oxf)

Department of Cardiology, Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.

Published: August 2009

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Article Abstract

Objectives: Visfatin is a new cytokine that act as an insulin analogue on the insulin receptor and may link obesity and insulin resistance. It was recently shown that visfatin plays a role in plaque destabilization. However, the role of visfatin in atherosclerosis remains to be elucidated. We sought to assess whether plasma visfatin level is independently associated with inflammation, atherosclerosis and acute coronary syndromes (ACS).

Design And Patients: Two hundred and fifty-three patients undergoing coronary angiography were divided into three subgroups: chronic coronary artery disease (CAD) (n = 102), ACS (n = 100) and control patients (n = 51). The plasma samples were thawed and analysed for circulating visfatin, monocyte chemoattractant protein 1 (MCP-1), interleukin-6 (IL-6), high sensitivity C-reactive protein (hs-CRP). The association of visfatin with risk factors, inflammation, atherosclerosis, and ACS was determined.

Results: Plasma visfatin levels were significantly higher in chronic CAD and ACS compared with control patients. Multiple regression analysis demonstrated that plasma visfatin levels correlated with inflammatory factors and were associated with chronic CAD (odds ratio [OR][95% confidence interval], for second, third and fourth quartiles were 1.74 [0.96-2.69], 1.54 [0.85-2.28] and 1.84 [0.98-2.87], respectively) and ACS (ORs for second, third and fourth quartiles were 2.56 [1.57-3.34], 4.61 [1.94-10.96] and 6.52 [2.34-18.12], respectively) following adjustment for established risk factors and other inflammatory factors.

Conclusions: Plasma visfatin levels are significantly associated with CAD, particularly ACS, independent of well-known CAD risk factors.

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http://dx.doi.org/10.1111/j.1365-2265.2008.03453.xDOI Listing

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