Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3723_Библиотеки_им_академика_М_И_Перельмана

In the context of chronic ischemia, myocar­dium can undergo metabolic and functional changes referred to as “hibernation”—in con­trast to stunning, hibernating myocardium is a persistent state of impaired functionality associ­ated with reduced resting ow. While the initial hypothesis behind hibernating myocardium was that chronic ischemia would lead to a self­protective decrease in function and metabolic changes to match supply, a review of the evi­dence suggests that hibernation is more likely to be associated with repeat episodes of ischemia and stunning, as well as an impairment of myo­cardial ow reserve rather than reduced blood ow per se [92, 93]. A clinically important aspect of hibernating myocardium is that it often shows an improvement in function after revasculariza­tion; however, the recovery of function can be prolonged and occur over weeks to months fol­lowing therapy. A metabolic hallmark of hiber­nating myocardium is preserved or even increased glucose metabolism compared to other reference areas in the heart [94]. This preserved use of glucose is associated with an increase in intracellular glycogen accumulation within hibernating myocardium and increased expres­sion of GLUT4 [95, 96]. Although the reason for the shift in glucose metabolism by hibernating myocardium remains unclear, this may reect a protective adaptive mechanism to ensure ade­quate supply of substrate for anaerobic metabo­lism during repeat episodes of ischemia. Conversely, FFA metabolism with a relatively higher oxygen requirement would seem to be