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European Heart Journal Advance Access originally published online on March 19, 2009
European Heart Journal 2009 30(10):1180-1186; doi:10.1093/eurheartj/ehp070
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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

C-reactive protein, infarct size, microvascular obstruction, and left-ventricular remodelling following acute myocardial infarction

Stein Ørn1,2,*, Cord Manhenke1,2, Thor Ueland3,4, Jan K. Damås3,5, Tom Eirik Mollnes6, Thor Edvardsen7, Pål Aukrust3,5 and Kenneth Dickstein2

1 Division of Cardiology, Stavanger University Hospital, PO 8400, 4068 Stavanger, Norway
2 Institute of Internal Medicine, University of Bergen, Bergen, Norway
3 Research Institute of Internal Medicine, Rikshospitalet, University of Oslo, Oslo, Norway
4 Department of Endocrinology, Institute of Immunology, Rikshospitalet, University of Oslo, Oslo, Norway
5 Section of Clinical Immunology and Infectious Diseases, Rikshospitalet, University of Oslo, Oslo, Norway
6 Institute of Immunology, Rikshospitalet, University of Oslo, Oslo, Norway
7 Department of Cardiology, Rikshospitalet, University of Oslo, Oslo, Norway

Received 16 July 2008; revised 5 December 2008; accepted 28 January 2009; online publish-ahead-of-print 19 March 2009.

* Corresponding author. Tel: +47 45 21 96 53, Fax: +47 51 51 99 05, Email: drsteinorn{at}hotmail.com

Aims: This study assessed the relationship between inflammatory mediators and indices of infarct size and left-ventricular (LV) remodelling following successful primary percutaneous coronary intervention (PCI) in patients with first time ST elevation myocardial infarction (MI).

Methods and results: Forty-two patients admitted with an occluded single vessel were recruited consecutively. Cardiac magnetic resonance was used for serial assessment (2 days, 1 week, 2 months) of infarct size, microvascular obstruction (MO), and LV remodelling. Inflammatory mediators were analysed before and after PCI. Our major findings were: (1) Following PCI, there was a marked increase in plasma levels of C-reactive protein, closely correlated with an increase in interleukin-6 and terminal complement complex, reaching maximum 2 days after PCI; (2) C-reactive protein 2 days after PCI was significantly correlated with infarct size and parameters of LV remodelling 2 months after PCI; (3) Patients with persistent MO had significantly higher C-reactive protein levels 2 days following PCI.

Conclusion: We suggest that the rapid increase in C-reactive protein levels in this model of successful revascularization of a single, totally occluded vessel reflects the degree of inflammation within the infarcted area. Our findings support a role for C-reactive protein-mediated complement activation as both a marker and mediator of myocardial damage following MI.

Clinical study no.: NCT 00465868.

Key Words: Inflammation • C-reactive protein • Interleukin-6 • Terminal complement complex • Acute myocardial infarction • Remodelling • Primary percutaneous intervention • Cardiac magnetic resonance


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C-reactive protein: not only a marker but also a mediator of myocardial damage following acute myocardial infarction
Eur. Heart J., November 2, 2009; 30(22): 2813 - 2813.
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