Vatner S F, Heyndrickx G R
New England Regional Primate Research Center, Southborough, Massachusetts 01772-9102, USA.
Basic Res Cardiol. 1995 Jul-Aug;90(4):253-6. doi: 10.1007/BF00797892.
The prolonged depression of myocardial function following episodes of myocardial ischemia now known as myocardial stunning, appears ubiquitous in both the experimental and clinical settings. With recent therapies designed to ameliorate ischemic myocardium, e.g., coronary artery bypass, coronary thrombolysis, coronary angioplasty, the inexorable progression from ischemia to necrosis has been averted more successfully and frequently, which permits appearance of myocardial stunning to become clearer. Myocardial stunning occurs in the presence of a multitude of inciting stimuli to myocardial ischemia, including a fixed stenosis, relief from stenosis or even in the presence of reduced coronary reserve, without a coronary stenosis. It will be potentially most interesting to determine if myocardial stunning also belies the hibernating myocardium and is, in fact, its actual mechanism.
心肌缺血发作后出现的心肌功能长期抑制,即现在所知的心肌顿抑,在实验和临床环境中似乎都普遍存在。随着近期旨在改善缺血心肌的治疗方法,如冠状动脉搭桥术、冠状动脉溶栓、冠状动脉血管成形术的应用,缺血到坏死这一不可阻挡的进程已更成功、更频繁地得以避免,这使得心肌顿抑的表现变得更加明显。心肌顿抑发生在多种诱发心肌缺血的刺激因素存在的情况下,包括固定性狭窄、狭窄解除,甚至在冠状动脉储备减少但无冠状动脉狭窄的情况下。确定心肌顿抑是否也掩盖了冬眠心肌,以及实际上是否是其真正机制,可能会非常有趣。