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European Heart Journal Advance Access published online on July 10, 2008
European Heart Journal, doi:10.1093/eurheartj/ehn281
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

No-reflow: the next challenge in treatment of ST-elevation acute myocardial infarction

Antonio Abbate1,*, Michael C. Kontos1 and Giuseppe G.L. Biondi-Zoccai2

1 VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA 23298-0281, USA
2 Division of Cardiology, University of Turin, Turin, Italy

* Corresponding author. Tel: +1 804 2702946, Fax +1 360 3231204, Email: aabbate@mcvh-vcu.com

This editorial refers to ‘Plasma levels of thromboxane A2 on admission are associated with no-reflow after primary percutaneous coronary intervention’{dagger} by G. Niccoli et al., on page 1843

The first 10% of the full text of this article appears below.

Coronary revascularization is not synonymous with myocardial reperfusion. DeWood et al.1 almost three decades ago showed that ~90% of patients with transmural myocardial infarction had total coronary occlusion at angiography associated with acute thrombosis. This and other studies have paved the way for the use of fibrinolytics in the treatment of transmural or ST-segment elevation myocardial infarction (STEMI). Despite the clear benefits observed with fibrinolysis, a significant proportion of patients failed to achieve adequate reperfusion as witnessed by persistence of total coronary occlusion, slow epicardial flow at angiography, or failure of regression of other signs of ischaemia such as ST-segment elevation. The advances of percutaneous coronary intervention (PCI) led to the use of balloon angioplasty . . . [Full Text of this Article]

Pathophysiology of no-reflow

Clinical perspective


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