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Sudden occlusion of a coronary artery initiates an expanding array of functional, metabolic and structural abnormalities, ultimately leading to myocyte necrosis, which extends from the subendocardial to the subepicardial layers of the perfusion bed—what Reimer called the ‘wavefront phenomenon’.1 In this setting, the myocardial area at risk (AAR) is defined as the myocardial tissue within the vascular territory that is distal to the culprit lesion of the infarct-related artery. If not timely reperfused, this area is at definite risk of ischaemic death. In humans, the portion of the AAR, that is irreversibly injured (ie, infarcted) ranges from 0% (aborted infarction) to as much as 88%.2 The proportion of the AAR that ultimately survives—that is, the salvaged myocardium—is dependent on multiple factors, including time to reperfusion, ischaemic preconditioning, collateral flow, distal embolisation, reperfusion injury and microvascular dysfunction. Since the extent of myocardial salvage is an important determinant of final infarct size, the quantitative assessment of myocardial salvage offers tremendous potential to aid in the development of novel therapeutic strategies targeted at reducing ischaemic/reperfusion injury in the setting of acute myocardial infarction (MI).
The extent of myocardial salvage is defined as the difference between the total AAR and final infarct size. Therefore, in recent years there has been a renewed interest in techniques used for the assessment of the myocardial AAR in patients with acute MI. However, in contrast to myocardial delayed enhancement MRI (MDE-MRI), which represents a robust and validated technique that allows for an accurate assessment and detailed characterisation of the infarcted regions,3 quantification of the AAR still remains challenging.
In animal studies, fluorescein staining and fluorescent microspheres are the reference standard for measuring the AAR.4–6 In humans, a commonly used technique is single-photon emission tomography, which requires …