This was a double-blind, randomized, placebo-controlled, multicenter trial which enrolled 193 post-CABG patients with
type 2 diabetes.
Atherosclerosis changes in one SVG were assessed with intravascular ultrasound at baseline and at 12 months. Serial cardiometabolic assessments were performed. At baseline, both groups had mean HbA(1C)<7%,
LDL-cholesterol (
LDL-C)<2.3 mmol/l,
HDL-cholesterol (HDL-C)>1.0 mmol/l and blood pressure<130/75 mmHg. After 12 months, plaque volume in SVG had increased (median [interquartile range]) by 7.7 mm(3) (-17.2 to 37.9) in the placebo group and decreased by 0.3mm(3) (-19.1 to 22.3) in the
rosiglitazone group (P=0.22). Compared to placebo,
rosiglitazone treated patients had a higher (mean + or - SD)
body weight (89 + or - 15 kg vs. 84 + or - 15 kg, P=0.02) at the end of the study, mostly related to an increment in subcutaneous adipose tissue.
Rosiglitazone treated patients also displayed further improvements in
glycemic control compared to placebo (HbA(1C): 6.4 + or - 0.7% vs. 7.0 + or - 0.9%, P<0.001) as well as in several cardiometabolic parameters such as
lipids (HDL-C: 1.16 + or - 0.28 mmol/l vs. 1.06 + or - 0.23 mmol/l, P=0.003), inflammatory profile (
C-reactive protein: 0.92 mg/l [0.51-1.56] vs. 1.37 mg/l [0.79-3.08], P=0.02), and
adiponectin levels (11.1 microg/ml [8.19-17.9] vs. 4.65 microg/ml [3.27-7.15], P<0.001). There was no significant difference in the incidence of serious adverse cardiovascular events. However, more patients in the
rosiglitazone group had peripheral oedema (33% vs. 18%, P=0.0019).
CONCLUSION: After a 12-month follow-up, we found no evidence for a statistically significant effect of
rosiglitazone on SVG
atherosclerosis whereas significant effects on
glycemic control and on the cardiometabolic risk profile appeared to be modulated in part by changes in subcutaneous adiposity.