Pathophysiology and diagnosis of coronary microvascular dysfunction in ST-elevation myocardial infarction

Author:

Konijnenberg Lara S F1ORCID,Damman Peter1,Duncker Dirk J2ORCID,Kloner Robert A34,Nijveldt Robin1,van Geuns Robert-Jan M1,Berry Colin56ORCID,Riksen Niels P7,Escaned Javier8ORCID,van Royen Niels1

Affiliation:

1. Department of Cardiology, Radboud University Medical Center, Postbus 9101, 6500 HB Nijmegen, The Netherlands

2. Department of Radiology and Cardiology, Erasmus Medical Center, Rotterdam, The Netherlands

3. Huntington Medical Research Institutes, Pasadena, CA, USA

4. Division of Cardiovascular Medicine, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA

5. West of Scotland Heart and Lung Centre, Golden Jubilee National Hospital, Clydebank, UK

6. British Heart Foundation, Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK

7. Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

8. Department of Cardiology, Hospital Clínico San Carlos IDISSC, Universidad Complutense de Madrid, Madrid, Spain

Abstract

Abstract Early mechanical reperfusion of the epicardial coronary artery by primary percutaneous coronary intervention (PCI) is the guideline-recommended treatment for ST-elevation myocardial infarction (STEMI). Successful restoration of epicardial coronary blood flow can be achieved in over 95% of PCI procedures. However, despite angiographically complete epicardial coronary artery patency, in about half of the patients perfusion to the distal coronary microvasculature is not fully restored, which is associated with increased morbidity and mortality. The exact pathophysiological mechanism of post-ischaemic coronary microvascular dysfunction (CMD) is still debated. Therefore, the current review discusses invasive and non-invasive techniques for the diagnosis and quantification of CMD in STEMI in the clinical setting as well as results from experimental in vitro and in vivo models focusing on ischaemic-, reperfusion-, and inflammatory damage to the coronary microvascular endothelial cells. Finally, we discuss future opportunities to prevent or treat CMD in STEMI patients.

Funder

CVON

Netherlands Heart Foundation

Dutch Heart Foundation

European Union’s Horizon 2020 research and innovation programme

Netherlands heart Foundation

British Heart Foundation

Publisher

Oxford University Press (OUP)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

Reference208 articles.

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3. Microvascular reperfusion injury: rapid expansion of anatomic no reflow during reperfusion in the rabbit;Reffelmann;Am J Physiol Circ Physiol,2002

4. Microvascular obstruction and left ventricular remodeling early after acute myocardial infarction;Lima;Circulation,2012

5. The ‘no reflow’ phenomenon after temporary coronary occlusion in the dog;Kloner;J Clin Invest,1974

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