4.3 Article

Pioglitazone induces regression and stabilization of coronary atherosclerotic plaques in patients with impaired glucose tolerance

Journal

DIABETIC MEDICINE
Volume 29, Issue 3, Pages 359-365

Publisher

WILEY-BLACKWELL
DOI: 10.1111/j.1464-5491.2011.03458.x

Keywords

adiponectin; coronary borderline lesions; impaired glucose tolerance; pioglitazone

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Aims To observe the effects of pioglitazone on coronary plaque area, plaque burden, serum high-sensitivity C-reactive protein, adiponectin and plasma endothelin-1 levels in patients with impaired glucose tolerance and coronary borderline lesions. Methods Thirty patients were randomly divided into two groups: a pioglitazone group and a control group. The latter was administered placebo in addition to standard therapy; the former pioglitazone 15 mg/d in addition to standard therapy. Before treatment and 6 months later, left ventricular ejection fraction, serum lipid profile, high-sensitivity C-reactive protein, adiponectin and plasma endothelin-1 levels were detected. Coronary plaque area and plaque burden were examined using intravascular ultrasound. Results No significant differences were found in left ventricular ejection fraction and serum lipid levels pre- and post-trial. Compared with the control group, 6 months treatment with pioglitazone significantly decreased coronary plaque burden (50.7 +/- 11.1 vs. 64.1 +/- 10.3%, P < 0.05), plaque area (6.22 +/- 2.03 vs. 8.31 +/- 4.29, P < 0.05), thin-cap fibroatheroma prevalence (11 vs. 22%, P < 0.05) and percentage of necrotic core area (16 +/- 8 vs. 31 +/- 7%, P < 0.05). Compared with the control group, serum high-sensitivity C-reactive protein and plasma endothelin-1 levels were significantly lower and adiponectin level significantly higher in patients in the pioglitazone group. Serum adiponectin level was negatively correlated with plasma endothelin-1 level and coronary plaque area (r = 0.739 and 0.431, respectively, both P < 0.05). Conclusions Pioglitazone may induce regression and stabilization of coronary atherosclerotic plaques. The mechanisms might involve inhibition of inflammation, increase in adiponectin level and improvement in endothelial function.

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