Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 231

Hibernation is chronic impairment of the myocardial function that results from a severe, persistent coronary stenosis; the myocardium downregulates its function and its metabolism to survive and remains viable. Chronic ischemia may, however, lead to irreversible fibrosis. The myocardial segment has reduced nuclear uptake at rest and with stress, but unlike infarction, this nuclear uptake remains >50% at rest, metabolic uptake is preserved on PET imaging, and Q waves are absent.

Stunning is transient myocardial dysfunction occurring after a severe, transient episode of ischemia. Ischemia resolves and leaves a viable myocardium that will recover in time. This is the case of an acutely occluded MI artery that is opened with PCI or fibrinolytics, exertional ischemia that occurs at stress and resolves at rest, or ischemia induced by cardiac surgery or PCI. Some myocardium is necrotic already, some is stunned; only time will show. As opposed to hibernation, the artery is now open and there is no persistent ischemia. In the post-MI and post-cardiac surgery cases, temporary support with inotropes or IABP is sometimes needed until the myocardium recovers, provided there is no ongoing ischemia. Unlike hibernation, the artery is open and nuclear uptake is usually normal at rest. Repetitive stunning from a significant stenosis (exertional ischemia) can lead to persistent dysfunction and hibernation.

Recovery of function occurs 1–6 months after revascularization (faster with stunning, days to 1 month). See Chapter 4 for viability evaluation.

In a patient with active chest pain and severe CAD, the myocardial dysfunction is usually an actively ischemic dysfunction, rather than hibernation or stunning.

Ischemic preconditioning is the phenomenon whereby brief exposure to ischemia preconditions the heart and makes it more resilient to a later, prolonged and severe ischemia. In fact, ischemia stimulates protective myocyte receptors, such as adenosine receptors and G-protein receptors (protein kinase C). There are two windows of protection: the first starts within a few minutes of the brief ischemia and lasts a few hours; the second occurs at 24 hours and lasts 96 hours. This is partly why patients with pre-infarct angina suffer from smaller

infarcts and have better outcomes. Also, patients with severe pre-existing disease have already formed mature collaterals, which attenuate the infarct size.