Circulating lectin pathway proteins do not predict short-term cardiac outcomes after myocardial infarction

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Despite improvements in treatment, coronary artery disease is still responsible for one-third of all deaths globally, due predominantly to myocardial infarction (MI) and stroke. There is an important potential in developing new strategies for treatment of patients with these conditions. Inflammation, and in particular the actions of the complement system, has emerged as part of the pathogenesis in reperfusion injury in patients with MI. To further qualify this, we examined the association between the plasma levels of lectin pathway proteins and myocardial end-points, left ventricular ejection fraction (LVEF) and infarct size in a cohort of patients with ST-elevation myocardial infarction (STEMI). A blood sample was drawn the day after percutaneous coronary intervention from 73 patients with STEMI. The primary end-points, LVEF and infarct size, were measured with magnetic resonance imaging 6–9 days after the infarct. Complement pattern-recognition molecules of the lectin pathway (mannan-binding lectin, H-ficolin, L-ficolin and M-ficolin) were analysed along with soluble membrane attack complex (sMAC) and C-reactive protein (CRP) in plasma with immunofluorometric assays <50%. CRP correlated negatively with LVEF, regression coefficient = –0·17 (P = 0·01). None of the lectin pathway proteins correlated to LVEF or infarct size, nor did soluble membrane attack complex (sMAC). There were no differences in plasma levels of these complement proteins when comparing patients with ejection fraction <50% to patients with ejection fraction <50%. Pattern-recognition molecules of the lectin pathway and sMAC do not predict short-term cardiac outcomes after MI.

Original languageEnglish
JournalClinical and Experimental Immunology
Pages (from-to)94-100
Number of pages7
Publication statusPublished - Oct 2019

Bibliographical note

© 2019 British Society for Immunology.

    Research areas

  • complement system, ischaemia/reperfusion injury, lectin pathway, myocardial infarction, C-REACTIVE PROTEIN, ACTIVATION, COMPLEMENT, REPERFUSION, reperfusion injury, MANNAN-BINDING LECTIN, ischaemia, THERAPY, FICOLIN, INHIBITOR, PENTRAXIN-3

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