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Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
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Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery

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Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in

Mikkel Malby Schoos1, Lea Munthe-Fog, Mikkel-Ole Skjoedt

  • 1Department of Cardiology, Rigshospitalet, Copenhagen University Hospital, Denmark. mikkel.schoos@gmail.com

Molecular Immunology
|February 13, 2013
PubMed

Insights

Ficolin-2, a lectin pathway component, is linked to left ventricular enlargement after myocardial infarction. Its interaction with C-reactive protein may influence infarct size and cardiac remodeling.

Area of Science:

  • Immunology
  • Cardiology
  • Complement System

Background:

  • Lectin pathway (LP) activation contributes to myocardial ischemia reperfusion injury (IRI).
  • LP involves mannose-binding lectin (MBL), ficolins-2 and -3, and MBL/Ficolin-associated Protein-1 (MAP-1).
  • The role of ficolins in IRI and their interaction with C-reactive protein (CRP) remain unclear.

Purpose of the Study:

  • To investigate the association of LP components and CRP with left ventricular (LV) volumes and infarct size in ST-segment elevation myocardial infarction (STEMI) patients.
  • To explore potential synergistic effects and interactions between LP components and CRP in the context of myocardial IRI and LV remodeling.

Main Methods:

  • Analysis of plasma samples from 55 STEMI patients.
  • Measurement of LP components (ficolin-2, MBL, ficolin-3, MAP-1) and CRP levels.
  • Assessment of LV end-systolic and end-diastolic volumes (ESV, EDV) and infarct size using cardiac magnetic resonance at 1-3 days and 6 months post-primary percutaneous coronary intervention.

Main Results:

  • Lower baseline ficolin-2 levels were observed compared to other LP components.
  • Elevated ficolin-2 levels correlated with increased LV ESV and EDV.
  • Synergistic association between high ficolin-2 and MBL levels with LV dilatation was noted.
  • The interaction between ficolin-2 and CRP was linked to larger infarct size and altered LV remodeling over 6 months.

Conclusions:

  • Ficolin-2, alone and in combination with MBL and MAP-1, is associated with LV dilatation post-myocardial infarction.
  • The interaction between ficolin-2 and CRP suggests a role in infarct size and LV remodeling, highlighting potential LP-pentraxin cross-activation in IRI.
Abstract

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