Assessing Myocardial Ischemia and Viability: Is It Still a Relevant Question?

Left ventricular (LV) function is a well-established and powerful predictor of poor outcome, especially when associated with the clinical syndrome of heart failure(1). Among patients with severe LV dysfunction, those with coronary artery disease (CAD) have the worse long-term outcome (2,3). A critical and relatively common clinical problem is the distinction between ischemic and non-ischemic cardiomyopathy, especially because of the limitations of coronary angiography (4). The etiology of heart failure has important implications for risk stratification (2, 3), and also impacts management decisions especially the possible need for revascularization, and the selection of pharmacologic therapies(5). However, the determination of heart failure etiology in an individual patient may be difficult even if obstructive CAD is present on angiography(4). Indeed, patients with HF and no angiographic CAD may have typical angina or regional wall motion abnormalities on noninvasive imaging, while patients with angiographically obstructive CAD may have no symptoms of angina or history of myocardial infarction (MI). Thus, the appropriate classification for any given patient is not always clear, and it often requires the complementary information of coronary angiography and non-invasive imaging. The study by Aramayo and colleagues (6) in this issue of the journal provides important information about the potential complementary role of Positron Emission Tomography (PET) imaging for characterization of the extent of ischemia/viability in a relatively small cohort of patients (n=27) with severe LV dysfunction (mean LVEF: 29%) and angiographically demonstrated CAD. The study sought to describe the relationship between the degree of angiographic stenosis, myocardial blood flow, and the pattern of myocardial viability as defined by PET perfusion and metabolic imaging, which included the use of radiolabeled glucose (FDG). They described four different myocardial patterns of viability in these patients: 1) normal perfusion and glucose uptake, 2) concordant reduction in perfusion and glucose uptake reflecting non-viable myocardium (so-called PET match), 3) reduced perfusion with preserved glucose uptake reflecting hiber-