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Complement factor concentrations in patients with acute myocardial infarction: time course and ability to predict

Roman Brenner1, Micha T Maeder, Lukas Trachsel

  • 1Division of Cardiology, Kantonsspital St. Gallen, Rorschacherstrasse 95, CH-9007 St. Gallen, Switzerland.

Biomarkers in Medicine
|February 14, 2014
PubMed

Insights

Total hemolytic complement (CH50) levels at hospital admission may predict left ventricular (LV) dysfunction after myocardial infarction (MI). Higher CH50 indicates increased risk for developing LV dysfunction post-MI.

Area of Science:

  • Cardiology
  • Immunology
  • Biochemistry

Background:

  • Inflammatory processes are implicated in myocardial ischemia/reperfusion injury following myocardial infarction (MI).
  • Left ventricular (LV) dysfunction is a significant complication after MI, impacting patient prognosis.
  • Predictive biomarkers for post-MI LV dysfunction are crucial for timely intervention.

Purpose of the Study:

  • To investigate the predictive capability of complement factor concentrations for the development of LV dysfunction post-MI.
  • To assess the association between complement factors and C-reactive protein (CRP) with LV ejection fraction in acute MI patients.

Main Methods:

  • Fifty-five patients with acute myocardial infarction were enrolled.
  • Complement factors and CRP were measured at hospital admission (HA) and during the first 3 days.
  • LV ejection fraction was assessed via echocardiography before hospital discharge.

Main Results:

  • Elevated total hemolytic complement (CH50) at HA and peak CRP levels were observed in patients who developed LV dysfunction (LV ejection fraction ≤45%).
  • Individual complement factor concentrations or their temporal changes did not correlate with LV dysfunction occurrence.
  • CH50 concentration at HA independently predicted LV dysfunction.

Conclusions:

  • CH50 concentration at hospital admission may serve as a valuable biomarker for identifying acute MI patients at high risk of developing LV dysfunction.
  • This finding generates a hypothesis for further validation in larger cohorts.
  • Understanding the role of complement in MI pathophysiology can guide therapeutic strategies.
Abstract

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