Insulin-Resistant CardiomyopathyClinical Evidence, Mechanisms, and Treatment Options
Ronald M. Witteles, MD* and
Michael B. Fowler, MB, FACC
Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California.
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Figure 2 Glucose and Insulin Versus Time After Oral Glucose Load
Glucose (top) and insulin (bottom) versus time after oral glucose load for nondiabetic patients with nonischemic cardiomyopathy (squares) versus matched healthy control subjects (diamonds). Note the baseline hyperinsulinemia and marked hyperglycemic/hyperinsulinemic responses to glucose loading in the heart failure population. Reproduced, with permission, from Witteles et al. (21).
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Figure 3 Myocardial Energy Metabolism in Response to Injury/Insulin Resistance
Relative size of font indicates relative metabolism of free fatty acids (FFA)/glucose. Acyl Co-A d = medium-chain acyl-coenzyme A dehydrogenase; CPT = carnitine palmitoyl transferase; GLUT = glucose transporter; PDH = pyruvate dehydrogenase; PPAR = peroxisome proliferator-activated receptor; UCP = uncoupling protein; 6PF-2-K = 6-phosphofructo-2-kinase.
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Figure 4 Insulin Resistance and Abnormal Glucose Metabolism in Nonischemic Heart Failure Patients
Myocardial perfusion (left) and glucose uptake (right) in a patient with idiopathic dilated cardiomyopathy and insulin resistance, as assessed by 13N-ammonia (NH3) and 18F-fluoro-2-deoxyglucose (FDG) positron emission tomographic imaging. Note the strong, consistent signal in the left ventricle for blood flow (solid arrow) compared with the weak, scattered signal for glucose uptake (dashed arrow), implying inefficient energy metabolism.
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