Canty J M, Fallavollita J A
Department of Veterans Affairs Western New York Health Care System and the Department of Medicine, University at Buffalo, School of Medicine and Biomedical Sciences, NY 14214, USA.
J Nucl Cardiol. 2000 Sep-Oct;7(5):509-27. doi: 10.1067/mnc.2000.109683.
Identification of myocardial viability is of increasing clinical importance in managing patients with coronary artery disease and advanced left ventricular dysfunction. Although viable chronically dysfunctional myocardium is always the result of repetitive episodes of reversible ischemia, there may be multiple mechanisms responsible for the contractile dysfunction. Many patients have contractile dysfunction with normal resting perfusion, as determined by imaging, that is related to chronic myocardial stunning. Viability studies are generally unnecessary because normal resting perfusion would preclude significant fibrosis. The clinical problem arises in evaluating patients with depressed resting flow that can be due to hibernating myocardium or nontransmural infarction. In this circumstance viability studies are required to assess the likelihood of functional recovery after revascularization. Although hibernating myocardium was originally posited to develop in response to prolonged episodes of myocardial ischemia (experimentally termed "short-term hibernation"), subsequent studies have shown that this tenuous balance can only be maintained for a period of several hours before resulting in some degree of subendocardial infarction. More recent experimental studies have demonstrated that there is a progression from chronic stunning with normal flow to hibernating myocardium with reduced resting flow. This presumably arises from repetitive episodes of spontaneous ischemia that increase in frequency as the physiologic significance of a coronary stenosis progresses. Thus in this new paradigm reduced flow is a result, rather than the cause, of the contractile dysfunction. This review summarizes basic and clinical pathophysiologic studies supporting the claim that chronic stunning and hibernation are distinct entities that may represent opposite ends of a continuum of mechanisms in viable chronically dysfunctional myocardium.
在冠心病和晚期左心室功能障碍患者的管理中，确定心肌存活性具有越来越重要的临床意义。虽然存活的慢性功能障碍心肌总是可逆性缺血反复发作的结果，但可能有多种机制导致收缩功能障碍。许多患者经影像学检查显示静息灌注正常，但存在收缩功能障碍，这与慢性心肌顿抑有关。由于正常的静息灌注可排除显著纤维化，一般无需进行心肌存活性研究。评估静息血流降低的患者时会出现临床问题，这种情况可能是由于心肌冬眠或非透壁性梗死所致。在这种情况下，需要进行心肌存活性研究以评估血运重建后功能恢复的可能性。虽然最初认为心肌冬眠是对长时间心肌缺血发作（实验中称为“短期冬眠”）的反应，但随后的研究表明，这种脆弱的平衡只能维持几个小时，之后就会导致某种程度的心内膜下梗死。最近的实验研究表明，存在从血流正常的慢性顿抑到静息血流降低的心肌冬眠的进展过程。这可能是由于自发性缺血反复发作，随着冠状动脉狭窄生理意义的进展，发作频率增加。因此，在这种新的模式中，血流降低是收缩功能障碍的结果而非原因。本综述总结了基础和临床病理生理学研究，支持慢性顿抑和冬眠是不同实体的观点，它们可能代表存活的慢性功能障碍心肌连续机制的两端。
