摘要
冠状动脉扩张症是一种非阻塞性、缺血性冠状动脉疾病,临床表现为胸闷、心悸和心绞痛,甚至出现心肌梗死。尽管冠状动脉扩张的病理机制仍不完全清楚,但近几年的研究发现,各种致病因素作用下慢性进展的强烈的血管壁炎性反应导致的血管壁结构破坏和重构在其发病中起重要作用;C反应蛋白、基质金属蛋白酶、白细胞介素、细胞黏附分子等多种炎性物质参与了此炎性反应过程。
Coronary artery ectasia( CAE )is a non-obstructive coronary artery disease with myocardial ischemia and can lead to chest tightness,angina and even myocardial infarction. Although the pathological mechanism of CAE remains unclear,studies in recent years have showed the destruction and reconstruction of vessel wall caused by a strong and chronically progressive inflammatory response play an important role in the pathogenesis. C-reactive protein,matrix metalloproteinases, interleukin, cell adhesion molecules and other inflammatory sub- stances are involved in the course of this inflammatory response.
出处
《医学综述》
2009年第21期3204-3206,共3页
Medical Recapitulate
关键词
冠状动脉扩张症
发病机制
炎性标志物
Coronary artery ectasia
Pathogenesis
Inflammatory markers