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

Oleh:

Marso, Steven P. ; Mehta, Sameer K. ; Frutkin, Andrew ; House, John A.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 31 no. 05 (May 2008), page 989-994.
Topik: Adiponectin; Dyslipidemia

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2008.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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.

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