The Recovery of Hibernating Hearts Lies on a Spectrum: from Bears in Nature to Patients with Coronary Artery Disease

Abstract

Clinicians often use the term "hibernating myocardium" in reference to patients with ischemic heart disease and decreased function within viable myocardial regions. Because the term is a descriptor of nature's process of torpor, we provide a comparison of the adaptations observed in both conditions. In nature, hearts from hibernating animals undergo a shift in substrate preference in favor of fatty acids, while preserving glucose uptake and glycogen. Expression of electron transport chain proteins in mitochondria is decreased while antioxidant proteins including uncoupling protein-2 are increased. Similarly, hibernating hearts from patients have a comparable metabolic signature, with increased glucose uptake and glycogen accumulation and decreased oxygen consumption. In contrast to nature however, patients with hibernating hearts are at increased risk for arrhythmias, and contractility does not fully recover following revascularization. Clearly, additional interventions need to be advanced in patients with coronary artery disease and hibernating myocardium to prevent refractory heart failure.

Uncoupling Protein 2 in Cardiovascular Health and Disease

“…Myocardial ischemic injury is a major clinical problem leading to cardiac dysfunction, in which the oxidative stress and damage play a key role. Accumulating evidences indicate that the expression level of UCP2 is upregulated in the ischemic myocardium, probably in response to the increased oxidative stress during hypoxia either with or without reperfusion ( McFalls et al, 2006 ; Cabrera et al, 2012 ; Safari et al, 2014a ; Colbert et al, 2015 ). UCP2 protein expression increases in the ischemic left ventricles early after acute myocardial I/R injury, but it is unchanged in the non-ischemic right ventricles of rats.…”

The vasculature: a therapeutic target in heart failure?

“…In this sense, recovering microvasculature function might be of especial interest for patients that present a stunned or hibernating myocardium. 76 …”

Identifying and Managing Hibernating Myocardium: What’s New and What Remains Unknown?

“…A fall in beta-adrenergic density likely modulates the reduced contractile reserve to limit myocardial oxygen demand to match perfusion reserve [ 22 , 23 ]. Fascinatingly, the metabolic signature of hibernating hearts in patients appears comparable to those observed in bears during seasonal hibernation [ 24 ], where cardiac index falls to a mean of 0.63 l/min/kg [ 25 ]. This supports the presumption that hibernation is an innate adaptive process of mammalian myocardium that is activated to deleterious effect in ischaemic heart failure.…”