Ferrari R, Ceconi C, Curello S, Benigno M, La Canna G, Visioli O
Cattedra di Cardiologia, Universitá degli Studi di Brescia, Spedali Civili di Brescia, Italy.
J Cardiovasc Pharmacol. 1996;28 Suppl 1:S18-26. doi: 10.1097/00005344-199600003-00004.
Several potential manifestations and outcomes are associated with myocardial ischemia and reperfusion. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When ischemia is less severe or shorter in duration, recovery of contraction may occur instantaneously or more commonly, after considerable delay, which is the condition recognized as "stunned myocardium." Stunning is defined as a transient left ventricular dysfunction that persists after reperfusion despite the absence of irreversible damage and restoration of normal or near-normal coronary flow. Oxidative stress and alteration of calcium homeostasis during reperfusion are the probable causes of stunning. Clinically, stunning may occur after acute infarction, successful thrombolysis, unstable angina, angioplasty, resolution of coronary spasm, open-heart surgery, or transplantation. It can be treated with interventions aimed at prevention or reversal. When ischemia is prolonged but less severe, myocytes may remain viable but exhibit depressed contraction. Under these conditions, reperfusion restores normal contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed "hibernating myocardium." The intrinsic mechanisms of this condition are unknown. Clinically, it is very important to diagnose hibernation because reperfusion of the hibernating myocardium by angioplasty or heart surgery restores contraction, and this correlates with long-term survival. A number of methods are available to access the hibernating myocardium. These include cardiac imaging techniques that evaluate myocardial viability, such as positron emission tomography and thallium myocardial imaging, or methods that evaluate contractile reserve, such as low-dose dobutamine echocardiography. Interestingly, reperfusion of patients with end-stage ischemic cardiomyopathy and hibernating myocardium can be considered an alternative to transplantation.
心肌缺血和再灌注会引发多种潜在的表现和后果。当缺血严重且持续时间较长时，会发生不可逆损伤，收缩功能无法恢复。当缺血程度较轻或持续时间较短时，收缩功能可能会立即恢复，或者更常见的是，在相当长的延迟后恢复，这种情况被认为是“心肌顿抑”。心肌顿抑的定义是，尽管没有不可逆损伤且冠状动脉血流恢复正常或接近正常，但再灌注后仍持续存在的短暂左心室功能障碍。再灌注期间的氧化应激和钙稳态改变可能是心肌顿抑的原因。临床上，心肌顿抑可发生于急性心肌梗死、溶栓成功、不稳定型心绞痛、血管成形术、冠状动脉痉挛缓解、心脏直视手术或移植术后。可通过旨在预防或逆转的干预措施进行治疗。当缺血持续时间长但程度较轻时，心肌细胞可能仍存活，但收缩功能会受到抑制。在这些情况下，再灌注可恢复正常的收缩功能。这种导致可逆性慢性左心室功能障碍的缺血类型被称为“冬眠心肌”。这种情况的内在机制尚不清楚。临床上，诊断冬眠心肌非常重要，因为通过血管成形术或心脏手术对冬眠心肌进行再灌注可恢复收缩功能，这与长期生存率相关。有多种方法可用于评估冬眠心肌。这些方法包括评估心肌存活的心脏成像技术，如正电子发射断层扫描和铊心肌显像，或评估收缩储备的方法，如小剂量多巴酚丁胺超声心动图。有趣的是，对于终末期缺血性心肌病和冬眠心肌患者，再灌注可被视为移植的替代方案。
