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.
Bibliographical noteFunding Information:
The work was supported in part by grants from The Veterans Affairs Merit Review and The Lillehei Foundation (High-Risk High Reward).
Dr. Garcia is a recipient of a career development award (1IK2CX000699-01) from the VA Office of Research and Development.
© 2015, Springer Science+Business Media New York (outside the USA).
- Coronary artery disease
- Heart failure
- Hibernating myocardium
- Uncoupling protein