Cardiac Hibernation. In ~40 % of patients with chronic cardiac ischaemia down-regulation of myocardial contractility has been observed, as a means of limiting the possibility of myocardial infarction, in a response commonly referred to as “myocardial hibernation” [16-17]. Diagnosis of myocardial hibernation is particularly important because it has been shown that upon the restoration of blood flow, these areas recover and contraction improves [18- 19], meaning that once identified this group of patients have an excellent prognosis. While the mechanisms underlying this phenomenon remain poorly understood despite having been described almost 30 years ago [20], the two most prominent theories suggest the existence of either “perfusion contraction matching” [21] or “repetitive stunning” [22], or possibly a combination of the two. Perfusion contraction matching has been described as a state of chronic hypoperfusion with reduced function in the absence of significant necrosis [23]. One may therefore expect these regions to be chronically hypoxic but viable. In the absence of a sufficient supply of oxygen, contractility is down-regulated in the affected region in order to preserve myocardial viability [18-19]. If this is the prevalent mechanism by which myocardium hibernates, then a hypoxia-specific imaging agent would potentially have some utility in its diagnosis. Myocardial stunning is the delayed recovery of contractility following a transient ischaemic episode. Calcium overload that results from the reperfusion of ischaemic tissue is thought to cause the production of reactive oxygen species (ROS), which may cause damage to cellular membranes, and the contractile apparatus of cardiomyocytes. Myocardial stunning is completely reversible but before normal contractility can resume a period of repair is required, during which time there will be a contractile deficit [22, 24]. In this context it may be likely that for much of the time hibernating myocardium is actually relatively well perfused, and therefore normoxic. The current gold standard technique for identifying hibernating myocardium is demonstration of elevated myocardial glucose uptake by 18F-fluorodeoxyglucose (18FDG) PET, coupled with demonstration of either normal or down-regulated flow (usually by perfusion imaging with 15NH3) – a “perfusion-metabolism mismatch”. If hibernating myocardium is predominantly normoxic and chronically stunned, then the lack of retention of a hypoxia imaging agent where hibernation has alread...
