Signs or symptoms of macrovascular disease are frequently found even prior to the development of noninsulin-dependent diabetes mellitus (NIDDM) [1]. This suggests that coronary heart disease (CHD) and NIDDM share a pathophysiologic feature, which predisposes to both diseases. Classic risk factors such as serum cholesterol, age, gender, hypertension and smoking explain only a fraction of the 2±4-fold increase in cardiovascular mortality in patients with NIDDM [1,2]. Insulin resistance, usually measured by quantitating the rate of insulin-stimulated glucose uptake, qualifies as the underlying pathophysiologic abnormality for both CHD and NIDDM, since it predicts, independent of other risk factors, both disorders [3,4].The mechanisms linking insulin resistance to CHD are unclear but could involve lipid abnormalities such as an increase in the concentration of atherogenic small dense LDL particles, which accompanies insu- Diabetologia (1998) Summary Skeletal muscle insulin resistance and coronary heart disease (CHD) often precede non-insulin-dependent diabetes mellitus (NIDDM). A recent study showed the myocardium of patients with CHD to be insulin resistant, independent of blood flow. We determined whether myocardial insulin resistance is a feature of NIDDM patients with no CHD. Skeletal muscle and myocardial glucose uptake were determined in 10 patients with NIDDM and 9 ageand weight-matched normal men of similar age and body mass index men using [18 F]-2-fluoro-2-deoxy-dglucose and positron emission tomography under normoglycaemic hyperinsulinaemic conditions. Whole body glucose uptake, as determined by the euglycaemic clamp technique, was significantly lower in the patients with NIDDM (35 ± 3 mmol/kg body weight´min) than the normal subjects (45 ± 3 mmol/ kg body weight´min, p < 0.02). Insulin-stimulated femoral muscle glucose uptake was significantly lower in the patients with NIDDM (71 ± 6 mmol/kg muscle´min) than in the normal subjects (96 ± 5 mmol/ kg muscle´min, p < 0.01). Whole body glucose uptake was correlated with femoral muscle glucose uptake in the entire group (r = 0.76, p < 0.001), in patients with NIDDM and in normal subjects. Rates of insulin-stimulated myocardial glucose uptake were comparable between the patients with NIDDM (814 ± 76 mmol/kg muscle´min) and the normal subjects (731 ± 63 mmol/kg muscle´min, p > 0.4). Whole body or femoral muscle, and myocardial glucose uptake were not correlated in all subjects, patients with NIDDM or normal subjects. We conclude that insulin resistance of the myocardium is not a feature of uncomplicated NIDDM. [Diabetologia (1998) 41: 555-559] Keywords Myocardium, insulin resistance, non-insulin-dependent diabetes mellitus, positron emission tomography.

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 (HbA 1c 7.2 ؉ 0.9%) and CAD. Myocardial glucose uptake was measured with [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 mol ⅐ 100 g ؊1 ⅐ min ؊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 mol ⅐ 100 g ؊1 ⅐ min ؊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

Myocardial oxygen consumption per unit weight is increased in hypertensive patients without LVH but is normal in those with LVH. The normalization of oxygen consumption via hypertrophy occurs at the expense of efficiency, which may predispose hypertensive patients with LVH to heart failure.

Exercise training improves exercise tolerance and LV function. This is accompanied by a decrease in biventricular oxidative metabolism and enhanced forward work efficiency. Therefore, exercise training elicits an energetically favorable improvement in myocardial function and exercise tolerance in patients with DCM.