Current diagnostic techniques of assessing myocardial viability in patients with hibernating and stunned myocardium. Myocardial stunning and hibernation: the physiology behind the colloquialisms. Hibernation and stunning of the myocardium. The relationship between regional blood flow and contractile function in normal, ischemic, and reperfused myocardium. Postextrasystolic potentiation of ischemic myocardium by atrial stimulation. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. Clinical overview of management of chronic ischemic heart disease. A perspective on the three large multicenter randomized clinical trials of coronary bypass surgery for chronic stable angina. Coronary bypass surgery for chronic angina – 1981. Evolving therapies for myocardial ischemia/reperfusion injury. Early effects on local myocardial function and the extent of myocardial necrosis. In patients with chronic coronary syndrome and contractile dysfunction, improvement in contractile function after revascularization provides evidence for the existence of myocardial hibernation. With limited coronary flow reserve, repetitive myocardial stunning induced by stress-related myocardial ischaemia transitions to a situation of matched reductions in contractile function and blood flow. Short-term myocardial hibernation is characterized by matched moderate reductions in blood flow and contractile function, metabolic recovery and maintenance of myocardial viability. Myocardial stunning occurs in patients after percutaneous coronary interventions or exercise-induced myocardial ischaemia, but is not haemodynamically compromising. Myocardial stunning reflects genuine reperfusion injury as a consequence of increased formation of reactive oxygen species and reduced calcium responsiveness. Myocardial stunning is the reversible, but only slowly recovering, contractile dysfunction that follows brief periods of myocardial ischaemia. Therefore, this Review summarizes the current knowledge of the pathophysiology of these characteristic reperfusion phenomena and highlights their clinical implications. A better understanding of the pathophysiology of myocardial stunning and hibernation is important for a more precise indication of revascularization and its consequences. Several trials in the past two decades have challenged the superiority of revascularization over medical therapy for symptomatic relief and prognosis in patients with chronic coronary syndromes. Myocardial hibernation is clinically identified with the use of imaging techniques, and the myocardium recovers after revascularization. Myocardial stunning is observed clinically and must be recognized but is rarely haemodynamically compromising and does not require treatment. Chronic myocardial hibernation is characterized by severe morphological alterations and altered expression of metabolic and pro-survival proteins. ![]() Short-term myocardial hibernation is an adaptation of contractile function to the reduced blood flow such that energy and substrate metabolism recover during the ongoing ischaemia. ![]() ![]() Hibernating myocardium is characterized by reduced regional contractile function and blood flow, which both recover after reperfusion or revascularization. ![]() Reperfusion precipitates a burst of reactive oxygen species formation and alterations in excitation–contraction coupling, which interact and cause the contractile dysfunction. Stunned myocardium is characterized by a disproportionately long-lasting, yet fully reversible, contractile dysfunction that follows brief bouts of myocardial ischaemia. Unlike acute myocardial infarction with reperfusion, in which infarct size is the end point reflecting irreversible injury, myocardial stunning and hibernation result from reversible myocardial ischaemia–reperfusion injury, and contractile dysfunction is the obvious end point.
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