Key result
Myocardial hibernation involves metabolic adaptation and programmed cell death, and its diagnosis via imaging modalities is crucial for guiding revascularization in coronary artery disease.
This review summarizes the molecular mechanisms, diagnostic modalities, and clinical implications of myocardial hibernation, particularly regarding revascularization decisions in patients with coronary artery disease and reduced ejection fraction.
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May support imaging-guided revascularization in CAD with reduced EF; leaves open prospective validation of hibernation mechanisms.
Myocardial hibernation is a persistent inhibition of contractility of the viable myocardium of the left ventricle, resulting from its hypoperfusion. The most important manifestation of hibernation is the preservation of the viability of the myocardial tissue. This phenomenon is based on three main mechanisms: 1) myocardial metabolic adaptation, manifested by enhanced glucose uptake; 2) activation of the cardiomyocyte death gene program; 3) programmed cell death, i. e. autophagy and apoptosis of cardiomyocytes. Methods for diagnosing viable myocardium include dobutamine stress echocardiography, single photon emission computed tomography of the myocardium, positron emission tomography, magnetic resonance imaging and electromechanical mapping. In the clinical aspect, the presence and volume of viable myocardium are taken into account when addressing the issue of revascularization in patients with one- and two-vessel coronary artery disease without involvement of the anterior descending artery, as well as in patients with a significant decrease in the global myocardial contractile function, when surgery can lead to an increase in the left ventricular ejection fraction.
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Галагудза et al. (2019) conducted a review in Myocardial hibernation. Myocardial hibernation involves metabolic adaptation and programmed cell death, and its diagnosis via imaging modalities is crucial for guiding revascularization in coronary artery disease.
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