|coronary artery disease
|left anterior descending
|positron emission tomography
|right coronary artery
Heart failure is a common cardiac diagnosis and the prevalence is increasing, with a prediction of more than 8 million affected adults in the United States by 2030.1 Despite recent improvement in survival, prognosis remains poor with a 5-year mortality of 50% following diagnosis.2 The most frequent etiology continues to be coronary artery disease (CAD) in the developed countries.3 Evidence supports the idea that viability imaging to guide revascularization therapy may be the best strategy for patients with multiple comorbidities and severe left ventricular (LV) dysfunction.4–12 Several studies have demonstrated that revascularization in appropriate patients with CAD improves outcomes in these high-risk patients.6 Viable but dysfunctional myocardium caused by abnormal coronary flow may restore its function with normalization of coronary blood flow. In this chapter, we review the approach to the interpretation of viability scans acquired with 18F-fluorodeoxyglucose (18FDG) and positron emission tomography (PET) and reporting with recommendations for clinical management. This topic has been reviewed in the recent PET imaging guidelines cosponsored by the American Society of Nuclear Cardiology and the Society of Nuclear Medicine and Molecular Imaging.13
VIABLE, STUNNED, AND HIBERNATING MYOCARDIUM
Viable, stunned, and hibernating myocardium are important concepts that need to be understood for appropriate interpretation of PET viability scans. Viable versus nonviable dysfunctional myocardium is a simple binary classification that refers to dysfunctional myocardium that may recover (viable or stunned/hibernating) or not (nonviable or scar) with revascularization.
Dysfunctional viable myocardium may have a spectrum of different levels of metabolism and flow caused by repeated transient or persistent ischemia.14 Stunned myocardium may occur after ischemia and is characterized by normal rest flow and transiently impaired contractility caused by previous ischemia.15–17 Microscopically, stunned myocardium has minimal structural injury but complex metabolic changes.18–20 The severity of impaired metabolism will depend on the number, extent, and duration of the ischemic episodes.21 Stunned myocardium may completely recover normal function or progress to a hibernation (still viable) or irreversible fibrosis (nonviable). Hibernating myocardium is dysfunctional myocardium with reduced rest flow and function that occurs after chronic repeated episodes of reduced blood supply.21 By definition, hibernating myocardium is considered viable and has the capacity to recover function if adequate revascularization is performed in a timely fashion.22,23 Glucose metabolism is preserved or even enhanced in hibernating myocardium because of preferential use of glucose by ischemic myocardium.24–31 18FDG is a glucose analogue taken up by the myocyte-like glucose using sarcolemmal transporters and phosphorylated by hexokinase to 18FDG-phosphate.32 18FDG-phosphate is "trapped" in the myocyte because it ...