title: Coronary microvascular reperfusion injury and no-reflow in acute myocardial infarction.
abstract: OBJECTIVE
  To review (1) the mechanisms of coronary microvascular reperfusion injury, particularly in the relationships between microvascular endothelium dysfunction, microstructure damage, microemboli and no-reflow phenomena; (2) the no-reflow presentation and management at ischemia-reperfusion to suggest future direction for no-reflow therapy in acute myocardial infarction.
  
  
  METHODS
  Original articles and reviews published between 1997 and 2007 and focusing on the no-reflow phenomenon in MEDLINE and PubMed. The search terms used were "no-reflow", "microvascular injury", "acute myocardial infarction" and "reperfusion injury". All papers identified were English-language, full text papers. In addition, the reference lists of identified relevant articles were also searched.
  
  
  CONCLUSIONS
  The no-reflow phenomenon is characterised by damage to microvascular function and microstructure at ischaemia-reperfusion. Microemboli contribute to no-reflow. Clinical myocardial contrast echocardiography (MCE), scintigraphic and magnetic resonance imaging (MRI) have shown evidence of microvascular damage, eg, perfusion defects are closely related to lack of contractile recovery and irreversible myocyte damage. Clinical agents and devices targeting microvascular injury (especially protection of endothelium and reduction of microemboli) after acute myocardial infarction may be key points to improve no-reflow.
authors: Department of Cardiology, Cardiovascular Institute & Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. kangsheng2008@163.com
authors: Sheng
authors: S
authors: Kang
authors: Yuejin
authors: Y
authors: Yang
mesh_terms: D003326:Coronary Circulation; D004452:Echocardiography; D006801:Humans; D008279:Magnetic Resonance Imaging; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*