As in any area of medicine, especially one that has more than its share of controversy, it is important to define terms if one is to have any hope of making sense of the problem. Although the pathophysiology of myocardial hibernation and stunning remains controversial, the following points are clear. Both entities share in common impaired contractile function of the left ventricle. Classically, stunning was thought to differ from hibernation since the former was characterized by relatively normal myocardial blood flow and myocardial oxygen consumption out of proportion to the decreased contractile function of the myocardium involved.1,2,3,4 In contrast, hibernation classically was thought to involve a matched reduction in myocardial blood flow, contractile function, and oxygen consumption.1,2,3,4 In patients with ischemic heart disease and in animal models,5,6 PET studies have demonstrated that both patterns of myocardial blood flow and impairment contractile function may exist, sometimes even in the same subject.7 It also appears to be true that chronic stunning often precedes hibernation.8,9 It has also been suggested that hibernation may occur in the absence of prior stunning.1,6,10 Further, the underlying histopathology is also somewhat controversial but has been characterized by glycogen accumulation, myocyte dedifferentiation, increased interstitial fibrosis, and in some but not all series, evidence of myocyte loss by apoptosis.1,11,12,13,15 A detailed review of the data relevant to this controversy is beyond the scope of this chapter. What is important for the purposes of this review is that both states, however arrived at, are characterized by dysfunctional myocardium, and both have the potential to improve with myocardial revascularization. Thus, there is a need to distinguish viable myocardium (i.e., hibernating or stunned) from nonviable myocardium, which is largely composed of scar tissue.

Myocardial viability, in turn, has been defined in one of two ways. The first employs what may be termed a cellular definition. This approach rests on the notion that accumulation of various radiotracers (e.g., Thallium, technetium-99m-sestamibi, rubidium-82) requires cellular concentrating mechanisms such as the sodium-potassium ATPase pump (Thallium, rubidium-82) or the electrochemical gradient of intact mitochondria (Tc-99m-sestamibi), and since these pumps require energy to function, a cell that can accumulate the tracer of interest must be viable.16,17 An alternate and perhaps more widely accepted definition holds that viable myocardium is best characterized by return or improvement of contractile function following coronary revascularization.18,19,20 The argument in support of this definition runs to the effect that what is important to the individual is whether or not myocardium with impaired contractility is functionally improved when it is revascularized. A surrogate end point such as tracer accumulation, although it is a marker for an energy-requiring metabolic process, has a lesser oxygen consumption requirement (only about 20% of basal MVO₂) than that of contraction, which ultimately is what the patient lives or dies by. The argument against this definition is the often subjective nature of contractile function assessment, typically by echocardiography, though gated MRI has also been used, and the fact that myocardial tethering, interstitial fibrosis, and cellular dedifferentiation all may occur, so that even if the segment(s) in question are successfully revascularized, contractile function still may not be restored depending on when contractile function is reevaluated. Nonetheless, the improvement of contractile function of the left ventricle following coronary revascularization remains the most widely accepted definition of myocardial “viability,” and those tests that best predict this outcome are thought to be the best for viability assessment.