Targeting microvascular injury, specifically protecting the endothelium and reducing microemboli, may be key to improving no-reflow in acute myocardial infarction.
May guide microvascular-targeted trials in AMI no-reflow; leaves open confirmation of clinical benefit.
PURPOSE: 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. SOURCES: 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.
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Kang et al. (2007) studied this question.
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