Document Detail

Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-A magnetic resonance study.
MedLine Citation:
PMID:  23399387     Owner:  NLM     Status:  Publisher    
BACKGROUND: Lectin complement pathway (LP) activation is an important mechanism in myocardial ischemia reperfusion injury (IRI). LP is activated via the recognition molecules mannose-binding lectin (MBL), ficolins-2 and-3 and is regulated by MBL/Ficolin-associated Protein-1 (MAP-1). Also, C-reactive protein (CRP) and ficolin-2 interact in vitro, but the role of the ficolins in IRI is unknown. METHODS AND RESULTS: In 55 patients with ST segment elevation myocardial infarction, we investigated the association of LP components and CRP in plasma samples with left ventricular (LV) end systolic and diastolic volumes (ESV and EDV) and infarct size, assessed by cardiac magnetic resonance early at 1-3 days after primary percutaneous coronary intervention and at 6 months follow-up. Opposed to MBL, ficolin-3 and MAP-1, ficolin-2 levels were low at baseline. At baseline, ficolin-2>median was associated with ESV and EDV increases by 7.83ml/m(2) (p=0.004) and 14.04ml/m(2) (p<0.001). MBL and MAP-1 were not associated with LV dilatation, yet ficolin-2 and MBL worked synergistically and the combination of their levels>median was associated with ESV (11.21ml/m(2); p=0.017) and EDV increases (14.72ml/m(2); p=0.006). MAP-1<median+ficolin-2>median had the greatest LV dilatation (17.61ml/m(2)). The ficolin-2×CRP interaction variable was positively associated with infarct size and inversely associated with EDV change over 6 months (p=0.006). There was no interaction between CRP and the other LP molecules. CONCLUSION: The LP initiator molecule ficolin-2 and combinations of ficolin-2, MBL and MAP-1 are associated with LV dilatation after myocardial infarction. Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling, indicating a potential role for LP and LP-pentraxin cross-activation in IRI and LV remodeling.
Mikkel Malby Schoos; Lea Munthe-Fog; Mikkel-Ole Skjoedt; Rasmus Sejersten Ripa; Jacob Lønborg; Jens Kastrup; Henning Kelbæk; Peter Clemmensen; Peter Garred
Related Documents :
23278527 - Simulation of changes in myocardial tissue properties during left ventricular assistanc...
23255277 - Percutaneous hemodynamic support with impella 2.5 during scar-related ventricular tachy...
7553707 - Diagnostic evaluation of women with suspected coronary artery disease.
2299487 - Coronary arteriosclerosis in pediatric heart transplant survivors: limitation of long-t...
15605677 - The use of recombinant human b-type natriuretic peptide (nesiritide) in the management ...
3791617 - Pharmacologic vasodilators in the coronary circulation.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-2-8
Journal Detail:
Title:  Molecular immunology     Volume:  54     ISSN:  1872-9142     ISO Abbreviation:  Mol. Immunol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-2-12     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905289     Medline TA:  Mol Immunol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  408-414     Citation Subset:  -    
Copyright Information:
Copyright © 2013 Elsevier Ltd. All rights reserved.
Department of Cardiology, Rigshospitalet, Copenhagen University Hospital, Denmark. Electronic address:
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  The binding of soluble recombinant human Fc? receptor I for human immunoglobulin G is conferred by i...
Next Document:  The control of the complement lectin pathway activation revisited: Both C1-inhibitor and antithrombi...