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Low Adiponectin Levels Are Associated With Atherogenic Dyslipidemia and Lipid-Rich Plaque in Nondiabetic Coronary Arteries

  1. Steven P. Marso, MD1,
  2. Sameer K. Mehta, MD1,
  3. Andrew Frutkin, MD1,
  4. John A. House, MS1,
  5. Justin R. McCrary, MD2 and
  6. Krishnaji R. Kulkarni, PHD3
  1. 1Mid America Heart Institute, University of Missouri Kansas City, Kansas City, Missouri
  2. 2Washington University, St. Louis, Missouri
  3. 3Atherotech, Birmingham, Alabama
  1. Address correspondence and reprint requests to Steven P. Marso, MD, Clinical Scholar, Mid America Heart Institute, Associate Professor of Medicine, University of Missouri Kansas City, 4401 Wornall Rd., Kansas City, MO 64111. E-mail: smarso{at}saint-lukes.org

Abstract

OBJECTIVE—The purpose of this study was to determine whether an association exists between adiponectin and plaque composition in human coronary arteries.

RESEARCH DESIGN AND METHODS—Adiponectin is an adipocyte-derived protein with antiatherogenic and insulin-sensitizing properties. To date, the relationship between adiponectin and plaque composition is unknown. Fasting blood samples were collected from 185 patients undergoing coronary angiography and intravascular ultrasound (IVUS). Plaque composition was categorized as fibrous, fibrofatty, necrotic core, or dense calcium and further classified as IVUS-derived adaptive or pathological intimal thickening, fibroatheroma, fibrocalcific, or thin cap fibroatheroma.

RESULTS—Adiponectin correlated with normalized plaque volume (r = −0.16, P = 0.025) and atheroma lipid content as measured by normalized fibrofatty volume (r = −0.19, P = 0.009). Low adiponectin levels were associated with IVUS-derived pathological intimal thickening (r = −0.18, P = 0.01). With increasing quartiles (Q) of adiponectin, the normalized volume of fibrofatty plaque decreased (P = 0.03), which was driven by reductions in the nondiabetic cohort (Q1 44.2 mm3; Q2 28.2 mm3; Q3 24.7 mm3; and Q4 23.4 mm3; P = 0.01). No similar association was present in diabetic patients. Low adiponectin levels were also associated with IVUS-derived pathological intimal thickening in nondiabetic (r = −0.20, P = 0.03) but not diabetic patients.

CONCLUSIONS—Low adiponectin levels are associated with atherogenic lipoproteins (elevated triglycerides, small dense LDL cholesterol, and low HDL cholesterol), increased plaque volume, lipid-rich plaque, and IVUS-derived pathological intimal thickening in the total cohort that was driven by the nondiabetic population, suggesting an antiatherogenic role in the early stages of lesion development.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 5 February 2008. DOI: 10.2337/dc07-2024. Clinical trial reg. no. NCT00428961, clinicaltrials.gov.

    S.P.M. is a consultant for and has received research grants from Volcano Corp. K.R.K. receives royalties from the University of Alabama at Birmingham.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted January 26, 2008.
    • Received October 18, 2007.
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This Article

  1. Diabetes Care May 2008 vol. 31 no. 5 989-994
  1. All Versions of this Article:
    1. dc07-2024v1
    2. 31/5/989 most recent
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