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Ischemic left ventricular (LV) dysfunction due to coronary artery disease (CAD) is steadily increasing as a consequence of the aging of the population and of improved survival of patients with acute coronary syndromes and currently represents the first cause of heart failure (1). Mechanisms of LV dysfunction in CAD patients are complex and have been elucidated in recent years. A landmark understanding was that ischemic LV dysfunction may be sustained by repetitive ischemia, myocardial stunning, and hibernation and, therefore, completely or partially reversible in a substantial number of patients who undergo revascularization (2,3). From this evidence emerged the concept of viability or viable myocardium—that is, the distinction between reversible and irreversible dysfunction due to myocardial necrosis—that became part of the diagnostic workup of patients with ischemic LV dysfunction. Accordingly, several imaging approaches looking at myocardial viability were developed with the aim of selecting patients in whom recovery of LV function (mostly defined as increase of ejection fraction [EF] at rest) and improvement of prognosis would outweigh the risk of surgical revascularization. From these studies, it was also evident that most patients with ischemic LV dysfunction show evidence of viable myocardium as identified by viability testing (4,5). Most studies for which the aim was to identify viable myocardium were designed having as the endpoint the shortterm increase of regional or global LV function at rest after revascularization, both of which were assumed to represent the surrogate endpoint for clinical benefits—that is, survival and qualityof-life improvement. The evidence from these studies clearly indicated that methods that explore the integrity of cell membrane or metabolic activity, such as nuclear techniques, are more sensitive for predicting recovery of LV function than those that explore the contractile reserve of dysfunctional myocardium (6–8). Additionally, it was also demonstrated that revascularization of viable myocardium influences recovery of LV remodeling independently of changes in EF (9), pointing to additional mechanisms of clinical benefits.

Looking for Myocardial Viability After a STICH Trial: Not Enough to Close the Door