Pathophysiology of Acute or Short-Term Hibernation
Myocardial hibernation refers to a clinical state of chronic regional contractile dysfunction characterized by a reduced regional myocardial blood flow, either persistently at rest1-2 or repetitively during stress 3, that can be partially or completely restored to normal upon coronary revascularization. In hibernation, the observed reduction in function reflects preservation of viability rather than the occurrence of necrosis. Stress echocardiography using low-dose dobutamine infusion is at present the preferred initial approach for the selection of patients with hibernating or viable myocardium who would benefit from coronary revascularization 4. Additional techniques to assess viability include fluorine-18(18F) fluorodeoxyglucose positron emission tomography (FDG-PET), technetium- 99m (99mTc) sestamibi single photon emission tomography (SPECT), or thallium-201 (201TI) rest-redistribution SPECT imaging. Although the concept of chronic adaptive reduction of contractile function in response to reduction in myocardial blood flow is straightforward and simple, the mechanisms responsible for the development and maintenance of hibernation are unclear at present. This is mainly due to a large distance between the available experimental models of (acute or short-term) hibernation and the clinical scenario of (chronic or long-term) hibernation. In this chapter an experimental model of short-term hibernation will be discussed that is based on the observation that the majority of patients with hibernating myocardium has a history of an acute ischemic insult (either in the form of a transmural myocardial infarction or prolonged ischemic pain) followed by hypoperfusion5.
KeywordsMyocardial Blood Flow Ischemic Precondition Regional Myocardial Blood Flow Isolate Rabbit Heart Myocardial Hibernation
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