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Archives of cardiovascular diseases
Volume 108, n° 12
pages 661-674 (décembre 2015)
Doi : 10.1016/j.acvd.2015.09.006
Received : 23 July 2015 ;  accepted : 7 September 2015
The no-reflow phenomenon: State of the art
Le no-reflow  : état de l’art
 

Figure 1




Figure 1 : 

No-reflow pathophysiology. No-reflow or microvascular obstruction/reperfusion injury is a dynamic and complex phenomenon that starts with lethal ischaemia and ends ultimately with replacement of the injured myocardial tissue with a dense fibrotic scar. The phenomenon takes its seeds in a prolonged (>30minutes) lethal ischaemia to the healthy myocardium, resulting in cell death. The second phase is caused by the brutal reperfusion of the ischaemic myocardium. In the following 24hours, a cascade of deleterious phenomena take place, including intra- and extracellular oedema, microvessel obstruction with atherothrombotic material as well as cell debris, vasoconstriction induced by platelet hyperactivation and important cytotoxic signals delivered by the different myocardial cell components. After 24hours, an important inflammatory response in the ischaemic injured myocardium as well as the non-infarcted remote myocardium occurs and can cause additional damage to the myocardium.


Figure 2




Figure 2 : 

Myocardial tissue characterization and cardiac magnetic resonance (CMR) techniques to assess microvascular obstruction with contrast-enhanced CMR. Mid-ventricular short-axis views in an anterior STEMI patient with optimal reperfusion on CMR performed 48hours after admission. A. T2-weighted (T2W) acquisition showing transmural extensive oedema in the anteroseptal wall (arrow). B. First-pass perfusion acquisition, at the same time as gadolinium intravenous bolus, where the hypoperfused area appears hypointense (red contour) in the subendocardium of the anteroseptal wall. C & D. Subsequent delayed enhancement views, performed (C) 3minutes and (D) 10minutes after gadolinium administration. The microvascular obstruction area on these views is hypointense (red contour); on the 10-minute acquisition it is surrounded by hyperintense myocardium that corresponds to the myocardial infarcted tissue. As gadolinium passively and slowly diffuses to the infarct core, the hypointense area shrinks, and the 10-minute microvascular obstruction area (D) is roughly half the size of the early microvascular obstruction area (C).


Figure 3




Figure 3 : 

Short-axis view of early and late contrast-enhanced cardiac magnetic resonance imaging in a patient with acute reperfused lateral myocardial infarction. The infarcted myocardium appears hyperintense on the late enhancement image, with a subendocardial area with persistent low signal intensity (black arrow) corresponding to severe microvascular obstruction (right panel). On the early late gadolinium enhancement (LGE) sequence (left panel), the whole myocardium is still saturated with gadolinium, but the microvascular obstruction area already appears hypointense (black arrow).

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