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Activation of the complement lectin pathway is associated with long-term cardiac dysfunction and incident heart failure in acute coronary syndrome patients

Zhong, Baojun LU ; King, Ben LU orcid ; Mares, Razvan Gheorghita LU ; Arbanasi, Emil Marian LU ; Yndigegn, Troels LU ; Engelbertsen, Daniel LU ; Björkbacka, Harry LU orcid ; Nilsson, Jan LU ; Goncalves, Isabel LU orcid and Blom, Anna LU orcid , et al. (2026) In International Journal of Cardiology 462.
Abstract

Background: Myocardial injury activates the complement lectin pathway (LP) in acute coronary syndrome (ACS) and LP inhibition improved cardiac function in experimental studies, suggesting a direct pathogenic role. The clinical consequences of LP activation are insufficiently defined. We investigated how plasma levels of the LP activators mannose-binding lectin (MBL) and ficolin-2 (FCN2) relate to cardiac recovery and prognosis in ACS patients. Methods: MBL and FCN2 were measured at baseline in a cohort of 546 ACS patients and at 6-weeks in 124 patients with available samples. Prospective associations with heart failure (HF), stroke, and major adverse cardiovascular events (MACE) during a median follow-up of 2.2 years were assessed by... (More)

Background: Myocardial injury activates the complement lectin pathway (LP) in acute coronary syndrome (ACS) and LP inhibition improved cardiac function in experimental studies, suggesting a direct pathogenic role. The clinical consequences of LP activation are insufficiently defined. We investigated how plasma levels of the LP activators mannose-binding lectin (MBL) and ficolin-2 (FCN2) relate to cardiac recovery and prognosis in ACS patients. Methods: MBL and FCN2 were measured at baseline in a cohort of 546 ACS patients and at 6-weeks in 124 patients with available samples. Prospective associations with heart failure (HF), stroke, and major adverse cardiovascular events (MACE) during a median follow-up of 2.2 years were assessed by multivariable Cox regression. Spearman correlation was used to assess relationships between MBL and FCN2 levels, inflammatory and fibrotic mediators in plasma, and echocardiographic parameters of left ventricular (LV) remodelling and dysfunction. Results: Baseline MBL was associated with incident HF (HR 1.50, 95% CI 1.04–2.16, p = 0.029), independently of clinical risk factors, revascularization, baseline troponin and renal function. Patients with persistently elevated MBL at baseline and follow-up had increased pro-inflammatory and pro-fibrotic mediators in plasma, dilated LV and reduced LV systolic function at 1-year post-ACS. FCN2 showed no association with the outcomes. Conclusions: ACS patients with persistently high plasma MBL levels suffer cardiac remodelling and dysfunction, and have an increased risk for HF. Our findings provide clinical support to experimental data suggesting that the complement LP might be a potential therapeutic target to prevent post-ACS HF.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Acute coronary syndrome, Complement lectin pathway, Ficolin-2 (FCN2), Heart failure, Mannose-binding lectin (MBL)
in
International Journal of Cardiology
volume
462
article number
134699
publisher
Elsevier
external identifiers
  • pmid:42498041
  • scopus:105046219788
ISSN
0167-5273
DOI
10.1016/j.ijcard.2026.134699
language
English
LU publication?
yes
additional info
Publisher Copyright: © 2026 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license. http://creativecommons.org/licenses/by/4.0/
id
8baad0c2-cafe-4258-be71-3f9a3fedecca
date added to LUP
2026-10-02 11:00:07
date last changed
2026-10-03 02:56:00
@article{8baad0c2-cafe-4258-be71-3f9a3fedecca,
  abstract     = {{<p>Background: Myocardial injury activates the complement lectin pathway (LP) in acute coronary syndrome (ACS) and LP inhibition improved cardiac function in experimental studies, suggesting a direct pathogenic role. The clinical consequences of LP activation are insufficiently defined. We investigated how plasma levels of the LP activators mannose-binding lectin (MBL) and ficolin-2 (FCN2) relate to cardiac recovery and prognosis in ACS patients. Methods: MBL and FCN2 were measured at baseline in a cohort of 546 ACS patients and at 6-weeks in 124 patients with available samples. Prospective associations with heart failure (HF), stroke, and major adverse cardiovascular events (MACE) during a median follow-up of 2.2 years were assessed by multivariable Cox regression. Spearman correlation was used to assess relationships between MBL and FCN2 levels, inflammatory and fibrotic mediators in plasma, and echocardiographic parameters of left ventricular (LV) remodelling and dysfunction. Results: Baseline MBL was associated with incident HF (HR 1.50, 95% CI 1.04–2.16, p = 0.029), independently of clinical risk factors, revascularization, baseline troponin and renal function. Patients with persistently elevated MBL at baseline and follow-up had increased pro-inflammatory and pro-fibrotic mediators in plasma, dilated LV and reduced LV systolic function at 1-year post-ACS. FCN2 showed no association with the outcomes. Conclusions: ACS patients with persistently high plasma MBL levels suffer cardiac remodelling and dysfunction, and have an increased risk for HF. Our findings provide clinical support to experimental data suggesting that the complement LP might be a potential therapeutic target to prevent post-ACS HF.</p>}},
  author       = {{Zhong, Baojun and King, Ben and Mares, Razvan Gheorghita and Arbanasi, Emil Marian and Yndigegn, Troels and Engelbertsen, Daniel and Björkbacka, Harry and Nilsson, Jan and Goncalves, Isabel and Blom, Anna and Schiopu, Alexandru}},
  issn         = {{0167-5273}},
  keywords     = {{Acute coronary syndrome; Complement lectin pathway; Ficolin-2 (FCN2); Heart failure; Mannose-binding lectin (MBL)}},
  language     = {{eng}},
  month        = {{11}},
  publisher    = {{Elsevier}},
  series       = {{International Journal of Cardiology}},
  title        = {{Activation of the complement lectin pathway is associated with long-term cardiac dysfunction and incident heart failure in acute coronary syndrome patients}},
  url          = {{http://dx.doi.org/10.1016/j.ijcard.2026.134699}},
  doi          = {{10.1016/j.ijcard.2026.134699}},
  volume       = {{462}},
  year         = {{2026}},
}