© 2003 by BMJ Publishing Group & British Cardiac Society
EDITORIAL
Assessing perfusion and function in acute myocardial infarction: how and when?
Correspondence to:
Correspondence to:
Professor L Pierard, University Hospital, Department of Cardiology, B - 4000 Liege, Belgium
lpierard@chu.ulg.ac.be
Post-ischaemic myocardial perfusion is dynamic in nature, and microvascular damage may be reversible, even in an area of initial no reflow. The window for salvage of the myocardium may therefore be greater for some patients following acute myocardial infarction
Keywords: acute myocardial infarction; reperfusion; no reflow
| The first 150 words of the full text of this article appear below. |
Acute thrombotic coronary artery occlusion rapidly results in severe transmural ischaemia, contractile dysfunction, and a wavefront of myocardial injury and necrosis progressing from the endocardium to the epicardium. Myocardial cell injury is already present after 20–40 minutes of ischaemia. Microvascular damage develops slightly later, 60–90 minutes after occlusion.1
Immediate treatment usually restores patency of the occluded artery as a result of the infusion of a thrombolytic agent or preferably of direct percutaneous coronary intervention (PCI). Optimal angiographic recanalisation does not necessarily imply tissue reperfusion. Inadequate blood flow in the microcirculation despite recanalisation, termed "no reflow phenomenon", was first studied experimentally2 and was observed in the clinical setting by Ito and colleagues,3 using myocardial contrast echocardiography (MCE) with intracoronary injection of sonicated microbubbles.
No reflow or low reflow can be determined by several mechanisms. After thrombolysis, residual stenosis of the infarct related vessel is frequently severe and can be responsible for
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