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The heart consumes more energy than any other organ in order to maintain its contractile performance.1 The healthy myocardium possesses the superb ability to utilize a wide variety of substrates including: free fatty acids, glucose, lactate, pyruvate, ketone bodies, and amino acids as energy sources, which makes it possible for it to function as a constant pump. In the healthy adult myocardium, free fatty acids are the major energy source; however, under certain conditions, such as the postprandial state when glucose is more available, the heart is capable of switching to a glucose-predominant substrate utilization pattern.2,3 During ischemia, when there is reduced oxygen available to the tissue, the heart must use anaerobic glycolysis for ATP and energy production. As such, glucose becomes the primary substrate for ischemic myocardium. 18F-fluorodeoxyglucose (FDG) is a glucose analog whose uptake parallels glucose and, therefore, can be used to reflect glucose utilization and the metabolic state of the myocardium. Viable myocardium that is ischemic or hibernating will take up glucose and thus FDG. Likewise normal myocardium (which is, of course, also viable) in the postprandial state will take up glucose and as such FDG.

As a metabolic viability test, cardiac PET imaging with FDG can assess the myocardium in either a fasting or a glucose-loaded state. A fasting protocol is preferred when one wants to suppress FDG uptake in normal tissue, as in the detection of inflammatory or infectious diseases, including: cardiac sarcoidosis, vasculitis, and infection of intravascular devices, pacemakers, and catheters. The fasting protocol is useful to suppress physiological myocardial FDG uptake, making it easier to distinguish between physiological and pathological FDG uptake (see Chapter 14 for discussion of preparation for FDG inflammation imaging).

In contrast, a glucose load protocol is selected for assessing myocardial viability in order to enhance FDG (glucose) uptake in the viable myocardium (both normal and ischemic/hibernating tissue). The most common protocol for glucose loading is with an oral load of 25–100 g. The glucose load induces a rapid increase in insulin secretion from β(beta)-cells of the pancreas, which enhances FDG uptake in the viable myocardium through the glucose transporter 4 (GLUT-4).4 However, oral glucose loading may not be as effective in patients with impaired glucose tolerance or diabetes because of the impaired response of the cells (including myocardial cells) to insulin stimulation as a result of insulin resistance, as well as a decrease in glucose transporter activity and reduction in transport rates owing to pretranslational suppression of GLUT-4 gene expression5 or their limited ability to produce endogenous insulin. Thus, the use of insulin along with close monitoring of blood glucose levels is used (routinely in some sites) to improve image quality in patients with diabetes or glucose intolerance.

In this chapter, we focus on FDG PET viability imaging with the glucose load protocol in patients with or without diabetes mellitus.


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