Insulin resistance (IR) is recognized to be of critical importance in a variety of metabolic diseases and coronary artery disease (CAD). Impaired skeletal muscle glucose utilization (SMGU) plays an important role in the pathogenesis of IR, whereas it is controversial whether myocardial IR is similar in this respect. Methods: Twenty-two studies of myocardial IR and skeletal muscle IR using positron emission tomography (PET) and/or whole body IR were reviewed. Heart and skeletal muscle IR were measured with PET and¹⁸F-FDG under hyperinsulinemic euglycemic insulin clamp technique. Whole body IR was also determined at the time of PET under hyperinsulinemic euglycemic insulin clamp technique. Results: One study reported that heart and skeletal muscle IR is present in untreated type 2 diabetes mellitus (T2DM), hypertension and CAD (as reflected in a myocardial glucose utiliation rate (MGU) in T2DM vs control [p < 0.01], and an SMGU in T2DM vs control [p < 0.01]). A significant negative relationship between MGU and FFA (r = -0.665, p < 0.01) and a significant positive relationship between MGU and whole body IR (r = 0.855, p < 0.01) was also observed in T2DM. Significantly reduced MGU and SMGU and a positive correlation between them (r = 0.78, P < 0.0001) were noted in the normal myocardial segments of patients with CAD. Another study showed that heart and skeletal muscle IR was present in T2DM both with CAD (MGU):, p < 0.01; SMGU: p < 0.01) or without CAD (MGU: p < 0.01; SMGU: p = 0.06). A significant positive relationship between the whole body glucose disposal rate and MGU (r = 0.60, p < 0.01) as well as SMGU (r = 0.76, p < 0.01) was also reported. Much more severe myocardial IR in T2DM and hypertriglyceridemia (p < 0.05) due to increased plasma free fatty acids, FFA (r = -0.60, p < 0.01) and plasma triglycerides levels (r =-0.74, p < 0.001) was reported. A significant negative relationship between MGU and plasma triglycerides (r = -0.74, p < 0.001) was also noted. However, other studies reported that MGU was increased in essential hypertension despite the fact that SMGU and whole body IR were present. Furthermore, it has also been reported that MGU in hypertensive T2DM without medication for diabetes was similar to controls (p = ns) despite the presence of skeletal muscle IR (p < 0.01) and whole body IR. Myocardial IR was not detected in non-diabetic non-hypertensive hypertriglyceridemia (Myocardial¹⁸F-FDG Uptake (MFU) in hypertriglyc-eridemics was (p = ns) despite findings of reduced skeletal muscle¹⁸F-FDG uptake (SMFU in hyper-triglyceridemia (p < 0.01) and whole body IR (GDR) in hypertriglyceridemia (p < 0.01). Myocardial IR was not detected under very high dose insulin clamping (about 10 times higher than the usual dose) with MGU in T2DM vs control p = ns, while whole body IR in T2DM was still present, (p < 0.02) and skeletal muscle (p < 0.01). Preserved MGU under chronic use of sul-fonylurea drugs in T2DM has been reported (T2DM with SU vs control, p = ns). Moreover, myocardial IR was not seen in hypertensive T2DM despite the existence of skeletal muscle and whole body IR. Myocardial IR in T2DM with CAD could be improved by thiazolidinediones (MGU before rosiglitazone, vs after rosiglitazone p < 0.05) and in mixed combined hyperlipidemia with CAD before-vs-after pioglitazone (p < 0.01). This suggests that myocardial IR in T2DM and CAD paralleled an improvement of skeletal muscle and whole body IR. However, troglitazone failed to improve myocardial IR in T2DM without CAD within 12 weeks therapy (MGU before therapy vs after, p = ns). Nonetheless, it did improve myocardial IR in T2DM without CAD after 12 months’ therapy (before therapy vs after 12 months, p < 0.05). Conclusion: The myocardium possesses mechanisms to resist IR different from those in the rest of the body. Therefore, myocardial IR does not always parallel skeletal muscle and whole body IR.