Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study

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Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study. / Schoos, Mikkel Malby; Munthe-Fog, Lea; Skjoedt, Mikkel-Ole; Ripa, Rasmus Sejersten; Lønborg, Jacob; Kastrup, Jens; Kelbæk, Henning; Clemmensen, Peter; Garred, Peter.

In: Molecular Immunology, Vol. 54, No. 3-4, 07.2013, p. 408-14.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Schoos, MM, Munthe-Fog, L, Skjoedt, M-O, Ripa, RS, Lønborg, J, Kastrup, J, Kelbæk, H, Clemmensen, P & Garred, P 2013, 'Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study', Molecular Immunology, vol. 54, no. 3-4, pp. 408-14. https://doi.org/10.1016/j.molimm.2013.01.008

APA

Schoos, M. M., Munthe-Fog, L., Skjoedt, M-O., Ripa, R. S., Lønborg, J., Kastrup, J., Kelbæk, H., Clemmensen, P., & Garred, P. (2013). Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study. Molecular Immunology, 54(3-4), 408-14. https://doi.org/10.1016/j.molimm.2013.01.008

Vancouver

Schoos MM, Munthe-Fog L, Skjoedt M-O, Ripa RS, Lønborg J, Kastrup J et al. Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study. Molecular Immunology. 2013 Jul;54(3-4):408-14. https://doi.org/10.1016/j.molimm.2013.01.008

Author

Schoos, Mikkel Malby ; Munthe-Fog, Lea ; Skjoedt, Mikkel-Ole ; Ripa, Rasmus Sejersten ; Lønborg, Jacob ; Kastrup, Jens ; Kelbæk, Henning ; Clemmensen, Peter ; Garred, Peter. / Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study. In: Molecular Immunology. 2013 ; Vol. 54, No. 3-4. pp. 408-14.

Bibtex

@article{b861ca8bad0a4d7f8d2926ebce37dab8,
title = "Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study",
abstract = "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 resultsIn 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 7.83 ml/m2 (p = 0.004) and 14.04 ml/m2 (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 (11.21 ml/m2; p = 0.017) and EDV increases (14.72 ml/m2; p = 0.006). MAP-1 < median + ficolin-2 > median had the greatest LV dilatation (17.61 ml/m2). 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.ConclusionThe 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.",
author = "Schoos, {Mikkel Malby} and Lea Munthe-Fog and Mikkel-Ole Skjoedt and Ripa, {Rasmus Sejersten} and Jacob L{\o}nborg and Jens Kastrup and Henning Kelb{\ae}k and Peter Clemmensen and Peter Garred",
note = "Copyright {\textcopyright} 2013 Elsevier Ltd. All rights reserved.",
year = "2013",
month = jul,
doi = "10.1016/j.molimm.2013.01.008",
language = "English",
volume = "54",
pages = "408--14",
journal = "Molecular Immunology",
issn = "0161-5890",
publisher = "Pergamon Press",
number = "3-4",

}

RIS

TY - JOUR

T1 - Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study

AU - Schoos, Mikkel Malby

AU - Munthe-Fog, Lea

AU - Skjoedt, Mikkel-Ole

AU - Ripa, Rasmus Sejersten

AU - Lønborg, Jacob

AU - Kastrup, Jens

AU - Kelbæk, Henning

AU - Clemmensen, Peter

AU - Garred, Peter

N1 - Copyright © 2013 Elsevier Ltd. All rights reserved.

PY - 2013/7

Y1 - 2013/7

N2 - 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 resultsIn 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 7.83 ml/m2 (p = 0.004) and 14.04 ml/m2 (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 (11.21 ml/m2; p = 0.017) and EDV increases (14.72 ml/m2; p = 0.006). MAP-1 < median + ficolin-2 > median had the greatest LV dilatation (17.61 ml/m2). 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.ConclusionThe 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.

AB - 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 resultsIn 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 7.83 ml/m2 (p = 0.004) and 14.04 ml/m2 (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 (11.21 ml/m2; p = 0.017) and EDV increases (14.72 ml/m2; p = 0.006). MAP-1 < median + ficolin-2 > median had the greatest LV dilatation (17.61 ml/m2). 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.ConclusionThe 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.

U2 - 10.1016/j.molimm.2013.01.008

DO - 10.1016/j.molimm.2013.01.008

M3 - Journal article

C2 - 23399387

VL - 54

SP - 408

EP - 414

JO - Molecular Immunology

JF - Molecular Immunology

SN - 0161-5890

IS - 3-4

ER -

ID: 47424022