Völler H, Nixdorff U, Flachskampf F A
Klinik am See, Rüdersdorf.
Z Kardiol. 2000 Oct;89(10):921-31. doi: 10.1007/s003920070166.
Myocardial stunning (contractile dysfunction in the presence of normalized perfusion) and myocardial hibernation (contractile dysfunction matching reduced perfusion) have represented separate concepts of viable, but dyssynergic myocardium in the past. However, in vivo experimental and clinical work suggests that repetitive ischemia due to coronary artery disease may induce a gradual transition between stunned and hibernating myocardium. Myocardial hibernation itself can result from a spectrum of ischemic conditions ranging from impaired myocardial blood flow reserve to frank hypoperfusion. With increasing severity and duration of ischemia, degeneration of cardiac myocytes, accumulation of glycogen and cell death ensue. Additionally, there is an increase of extracellular matrix protein content leading to reparative fibrosis, which in turn limits functional recovery. In the light of these structural features, the available methods for detection of viable myocardium, in particular dobutamine echocardiography and nuclear imaging techniques, offer complementary rather than contradictory information. Dobutamine echo has satisfactory sensitivity, excellent specificity, and high diagnostic accuracy for the detection of viable dyssynergic myocardium. While in the past only its predictive accuracy for segmental recovery has been validated, newer data show an improved survival after revascularization if at least four viable dyssynergic left ventricular segments in a 16 segment model can be identified by dobutamine echocardiography. The complete (low and high dose) dobutamine protocol can elicit several types of contractile responses (sustained improvement in contraction or monophasic response, biphasic response, new wall motion abnormality) which should be interpreted in view of other clinical data including a previous infarction. The test protocol can be used safely at the end of the first week after myocardial infarction. If ischemia or viability is documented, revascularization should be performed promptly. A similar strategy should be followed in the setting of chronic coronary heart disease with left ventricular dysfunction. Since the structural changes of hibernating myocardium are progressive, time to revascularization is critical. On the other hand, responsible therapeutic planning requires proof of ischemia or viability before initiating a potentially hazardous revascularization procedure.
心肌顿抑（灌注正常情况下的收缩功能障碍）和心肌冬眠（收缩功能障碍与灌注减少相匹配）在过去曾代表存活但不协调心肌的不同概念。然而，体内实验和临床研究表明，冠状动脉疾病导致的反复缺血可能会使顿抑心肌和冬眠心肌之间逐渐转变。心肌冬眠本身可由一系列缺血情况引起，从心肌血流储备受损到明显的灌注不足。随着缺血严重程度和持续时间的增加，心肌细胞会发生变性、糖原积累并导致细胞死亡。此外，细胞外基质蛋白含量增加会导致修复性纤维化，进而限制功能恢复。鉴于这些结构特征，现有的检测存活心肌的方法，尤其是多巴酚丁胺超声心动图和核成像技术，提供的是互补而非矛盾的信息。多巴酚丁胺超声心动图对检测存活的不协调心肌具有令人满意的敏感性和出色的特异性，诊断准确性高。虽然过去仅验证了其对节段恢复的预测准确性，但新数据表明，如果通过多巴酚丁胺超声心动图在16节段模型中能识别出至少4个存活的不协调左心室节段，血管重建术后生存率会有所提高。完整的（低剂量和高剂量）多巴酚丁胺方案可引发几种类型的收缩反应（收缩持续改善或单相反应、双相反应、新的壁运动异常），应结合包括既往梗死在内的其他临床数据进行解读。该检测方案可在心肌梗死后第一周结束时安全使用。如果记录到缺血或存活情况，应立即进行血管重建。在伴有左心室功能障碍的慢性冠心病患者中也应遵循类似策略。由于冬眠心肌的结构变化是渐进性的，血管重建的时机至关重要。另一方面，负责任的治疗规划需要在启动潜在危险的血管重建手术前证明存在缺血或存活情况。
