Myocardial hibernation in coronary artery disease.
Review
Overview
abstract
Coronary artery disease (CAD) is very prevalent in Western societies and is a leading cause of mortality and morbidity. Despite decreases in mortality rates from CAD over the past 30 years, ischemic heart failure remains an important problem because people with CAD are now living longer. Hibernating myocardium may be defined as reversible left ventricular dysfunction due to chronic CAD that shows improvement in function after revascularization. Many patients with ischemic cardiomyopathy have areas of hibernating myocardium, and thus can potentially show improvement in left ventricular regional and global function if they are revascularized. Whether hibernating myocardium represents an adaptive response to hypoperfusion in the face of chronic ischemia or whether it is a degenerative process is not entirely clear. Clearly, ultrastructural changes of de-differentiation are seen, and include loss of sarcomeres and the appearance of small mitochondria and glycogen accumulation. Although the mechanisms underlying the changes in morphology and depressed contractility, and the factors governing recovery of function are not clear, changes in adrenergic receptor density, cytokine upregulation, and the degree of fibrosis may all play a role. Identification of viability is commonly performed with dobutamine echocardiography or nuclear imaging. Because patients with extensive CAD and poor left ventricular systolic function are high-risk candidates for coronary bypass surgery, the preoperative identification of viability provides important prognostic information. Patients with viable myocardium who are treated with revascularization rather than medical therapy have better outcomes in terms of survival, left ventricular function, symptoms, and exercise capacity.
