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The risk of myocardial infarction is increased in diabetes (1), and the outcome is poor with these patients. It has been suggested that one reason might be abnormal myocardial substrate [...], Rosiglitazone therapy improves insulin sensitivity and glucose uptake in patients with uncomplicated type 2 diabetes. In coronary artery disease (CAD), glucose is an important source of energy and preserved myocardial glucose uptake is essential for the viability of jeopardized myocardium. The aim was to test whether rosiglitazone changes myocardial metabolism in type 2 diabetic patients with CAD. We studied 54 patients (38 men and 16 women) with type 2 diabetes (Hb[A.sub.1c] 7.2 + 0.9%) and CAD. Myocardial glucose uptake was measured with [[sup.18]F]fluoro-2-deoxy-D-glucose positron emission tomography in ischemic (evaluated by single-photon emission tomography and coronary angiography) and nonischemic regions during euglycemic-hyperinsulinemic clamp before and after a 16-week intervention period with rosiglitazone (n = 27) or placebo (n = 27). Rosiglitazone significantly improved glycemic control (P < 0.0001) and whole-body insulin sensitivity (P < 0.0001). Rosiglitazone increased myocardial glucose uptake from 20.6 ± 11.8 to 25.5 ± 12.4 µmol x 100 [g.sup.-1] x [min.sup.-1] (P = 0.038 vs. baseline, P = 0.023 vs. placebo) in ischemic regions and from 21.7 ± 12.1 to 28.0 ± 12.7 µmol x 100 [g.sup.-1] x [min.sup.-1] (P = 0.014 vs. baseline, P = 0.003 vs. placebo) in nonischemic regions. The increase in myocardial glucose uptake was partly explained by the suppression of free fatty acid levels during clamp. Rosiglitazone therapy significantly increased insulin sensitivity and improved myocardial glucose uptake in type 2 diabetic patients with CAD. These results suggest that rosiglitazone therapy may facilitate myocardial glucose storage and utilization in these patients. Diabetes 54: 2787-2794, 2005