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Low Adiponectin Levels are Associated with Atherogenic Dyslipidemia and Lipid-Rich Plaque in Non-Diabetic Coronary Arteries

¹ Mid America Heart Institute, University of Missouri Kansas City, Kansas City, Missouri
²Washington University, Saint Louis, Missouri
³Atherotech, Inc, Birmingham, Alabama

smarso{at}saint-lukes.org

ABSTRACT

Objective: 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 anti-atherogenic 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 IVUS-. Plaque composition was categorized as fibrous, fibrofatty, necrotic core, or dense calcium and further classified as IVUS-derived (ID)-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 ID-pathological intimal thickening (r = –0.18, P = 0.01). With increasing quartiles of adiponectin, normalized volume of fibrofatty plaque decreased (P=0.03) which was driven by reductions in the non-diabetic cohort (Q1: 44.2 mm³; Q2: 28.2 mm³; Q3: 24.7 mm³; Q4: 23.4 mm³, P = 0.01). No similar association was present in diabetic patients. Low adiponectin levels were also associated with ID-pathological intimal thickening in non-diabetic (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, low HDL cholesterol), increased plaque volume, lipid-rich plaque, and ID-pathological intimal thickening in the total cohort which was driven by the non-diabetic population, suggesting an anti-atherogenic role in the early stages of lesion development.

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