The importance of 18F-FDG cardiac PET/CT for the assessment of myocardial viability in ischaemic heart disease.

The worldwide increase in coronary artery disease and its associated metabolic diseases is a major cause of human morbidity and mortality [1] and, as such, advancing cardiovascular disease remains a significant burden on the healthcare systems in western countries. The focus has been on the impact of advances in medical therapy and interventional cardiology on lowered mortality rates,but these came with more widespread availability of noninvasive methods allowing early diagnosis and effective risk stratification [2]. The concept of myocardial viability emerged from the postoperative clinical observations in the first decades of aorto-coronary bypass grafting. Then it was generally thought that left ventricular dysfunction in ischaemic heart disease was irreversible, since no persistent myocardial ischaemic state would have been possible in abnormal resting myocardium [3]. However, in the early 1980s Rahimtoola [3], in line with previous observations [4, 5], extensively described the improvement of left ventricular contractility after surgical revascularisation in patients with left ventricular dysfunction and ischaemic heart disease. Following these observations, many efforts have been made to understand the pathophysiological processes underlying this recovery phenomenon, as well as the diagnostic tools to achieve an accurate evaluation of the recovery potential in the clinical setting. Nowadays, the term myocardial viability in territories presenting altered contractility, beyond the concept of myocardial ischaemia, encompasses two phenomena: myocardial stunning and myocardial hibernation [6]. Myocardial stunning is characterised by persistent myocardial contractile dysfunction resulting from transient episodes of hypoperfusion. Its duration depends on the severity and the duration of the ischaemic episode [7]. This state can potentially of fully recover after restoration of blood supply, as long as no irreversible damage (necrosis) has occurred. In the case of prolongued or chronic ischaemia, ischaemic myocardial cells undergo adaptive changes, leading to a shift from fatty acid metabolism to glucose utilisation, as well as to downregulation of the contractile function in order to reduce the demand for oxygen and metabolic substrates [8, 9]. These changes are believed to induce the state of “hibernating myocardium”, a clinical condition characterised by contractile dysfunction with abnormal resting myocardial blood flow, and with a potential for full recovery after blood flow restoration [10, 11]. Repetitive episodes of myocardial stunning may also cause structural changes within the cardiomyocytes [9, 11], which tend to become irreversible over time. The correct identification of viable myocardium has a strong rationale, in that the myocardium may potentially regain its function after revascularisation in the setting of myocardial hibernation or stunning. It is therefore clear that diagnostic tools able to provide an early and precise diagnosis as well as prognostic information are highly warranted. Owing to the tendency to progress toward irreversible structural changes within the myocytes, viability imaging plays a pivotal role both in identifying patients at increased risk of coronary artery disease progression and in driving the choice of appropriate therapeutic measures. In fact, restoration of contractile function can be achieved by referring the patient earlier to invasive coronary revascularisation in the case of viable myocardium [12, 13]. Among the available techniques able to identify a viable myocardium, positron emission tomography / computed tomography (PET/CT) with fluorine 18-fluorodeoxyglucose (18FFDG), in combination with myocardial perfusion imaging, constitutes a cornerstone of myocardial viability assessment in nuclear cardiology [14]. The identification of myocardial viability relies on the metabolic shift towards gluCorrespondence: Federico Caobelli, MD, FEBNM, Clinic of Radiology and Nuclear Medicine, University Hospital Basel and University of Basel, Petersgraben 4, CH-4031 Basel, federico.caobelli[at]usb.ch