急性心肌梗死患者心肌顿抑发病机制探讨

心肌顿抑也称缺血后心肌功能障碍,为持续数小时、数天、甚至数周的心肌细胞可逆性损伤。可见于急性冠脉综合症早期再灌注、心脏移植、心脏瓣膜置换等心脏外科大手术术后,应激性心肌病、心脏骤停、心肺复苏、主动脉狭窄、高血压性心脏病、房颤转复。心肌梗死后发生心肌顿抑是导致心梗死亡、心衰再住院的重要病因,但目前其发病机制尚不明确。有关心肌顿抑的研究已经由器官细胞水平,深入到分子基因水平。具体而言,心肌顿抑的发病机制包括：缺血再灌注导致的心肌细胞直接损伤、心肌细胞兴奋收缩脱偶联、线粒体及内质网损伤、血管内皮细胞功能障碍及微循环痉挛、能量代谢障碍、氧自由基损伤、钙超载理论、炎性介质释放理论、心肌顿抑的基因组学机制等。目前,广为接受的是氧自由基理论和钙超载理论。前者认为心肌梗死时,心肌组织氧自由基产生增多,清除障碍,导致心肌细胞结构受伤和功能障碍;后者认为心肌梗死时,心肌细胞酸中毒,细胞膜通透性增加,钙内流增多,同时,钙库重吸收钙障碍,导致钙超载,引起心肌细胞破坏、肌钙蛋白溶解,导致心功能障碍。阐明心肌顿抑发病机制,指导心梗治疗,有助于完善救治策略,改善预后。

Mechanism of Myocardial Stunning Induced by Acute Myocardial Infarction

Myocardial stunning,also denominated as post-ischemic myocardial dysfunction,is a kind of irreversible myocardial damage which is widely found in patients with acute coronary syndrome,heart transplantation,cardiac valve replacement surgery,stressinduced cardiomyopathy,cardiac arrest,cardiopulmonary resuscitation,aortic stenosis,hypertensive cardiac disease and cardioversion of atrial fibrillation,et al.The mechanisms of myocardial stunning induced by acute myocardial infarction are not yet completely known.A large number of hypotheses have been proposed to illustrate the pathogenesis of myocardial stunning including of ischemia-reperfusion injury,of excitation-contraction uncoupling,of mitochondrial and endoplasmic reticulum dysfunction,theory of vascular endothelial cell dysfunction and microvascular spasm,theory of myocardial energy metabolism imbalance,of reactive oxygen species（ROS）,of calcium overload,theory of inflammatory mediators,and that of genomics.The ROS theory and the calcium overload theory are widely accepted.The former theory emphasizes the function of ROS in myocardial stunning,while the latter one outstands the role of calcium.To Clarify the pathogenesis of myocardial stunning c ontributes to improve the treatment strategy of myocardial infartion.