Article Text

Download PDFPDF

Assessing perfusion and function in acute myocardial infarction: how and when?
Free
  1. L A Pierard
  1. Correspondence to:
    Professor L Pierard, University Hospital, Department of Cardiology, B - 4000 Liege, Belgium
    lpierard{at}chu.ulg.ac.be

Statistics from Altmetric.com

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

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

REPERFUSION VERSUS NO REFLOW

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 partial or complete reocclusion or for repetitive episodes of ischaemia and post-ischaemic myocardial and microvascular stunning.4 Primary PCI may be accompanied by distal embolisation of platelet aggregates, neutrophil accumulation, and capillary plugging inducing progressive microvascular obstruction despite initial reperfusion.5 In other patients, restoration of the blood supply leads to reactive hyperaemia, but also possibly to post-reperfusion injury by oxygen-free radicals, inducing cellular oedema. After optimisation of vessel patency by successful stent placement, early and sustained improvement of coronary flow reserve is usually observed, consistent with gradual resolution of post-ischaemic vascular stunning.6 In other words, after early recanalisation, myocardial perfusion can dynamically evolve in two opposite …

View Full Text

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.