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Cardiovascular Research Advance Access first published online on June 5, 2009
This version [Corrected Proof] published online on June 17, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp185
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Lethal reperfusion injury in acute myocardial infarction: facts and unresolved issues

David Garcia-Dorado1,*, Marisol Ruiz-Meana1 and Hans Michael Piper2

1 Laboratory of Experimental Cardiology, Area del Cor, Hospital Universitari Vall d'Hebron, Barcelona 08035, Spain
2 Institute of Physiology, Justus Liebig University, Giessen, Germany

* Corresponding author. Tel: +34 93 489 4038; Fax: +34 93 489 4032. E-mail address: dgdorado@vhebron.net

The first 150 words of the full text of this article appear below.


   1. The concept of lethal myocardial reperfusion injury
 
1.1 Definitions
‘Reperfusion injury’ has been for some time an imprecise and controversial term referring to a variety of alterations occurring at the time of restoration of blood flow, from functional impairment to cell death. The term ‘lethal reperfusion injury’ specifically refers to cell death associated with transient ischaemia that can be prevented by interventions applied at the time of reperfusion.1 Therefore, it is the component of cell death occurring as a consequence of reperfusion. There are aspects of lethal reperfusion injury upon which there is general agreement based on solid information.

1.2 Existence and relevance
The existence of lethal myocardial reperfusion injury has been demonstrated by an overwhelming body of evidence obtained mainly in laboratory experiments, but also, and increasingly, in humans.2 Different interventions have consistently been shown to limit myocardial necrosis when applied at the time of reperfusion in a variety of models and preparations, and it is unquestionable that, at least under certain . . . [Full Text of this Article]

1.3 Initial minutes after reperfusion
1.4 Necrosis
1.5 Open questions
1.5.1 Relevance to patients
1.5.2 Relevance of late cell death and apoptosis
1.5.3 Contribution of microvascular injury and no-reflow

   2. The mechanisms of reperfusion-induced cardiomyocyte death
 
2.1 Mechanisms already defined
2.2 Open questions
2.2.1 The molecular identity of the mitochondrial pore
2.2.2 The relationship between mitochondrial permeability transition and other mechanisms of cell death in lethal reperfusion injury
2.2.3 The pathways of postconditioning protection

   3. The clinical application of cardioprotection
 
3.1 Progress achieved
3.2 Open questions
3.2.1 Effectiveness
3.2.2 Overall clinical value

   4. The future
 

   Funding
 

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