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

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.