Evidence map›Paper›PMID 41779128›Full record

ArticleClinical research in cardiology : official journal of the German Cardiac Society2026

Collagen type I degradation peptide as a predictive biomarker for mortality in ST-elevated myocardial infarction.

Emily M Martin, Elisavet Angeli, Federica Genovese, Martin Frydland, Morten A Karsdal, Jacob Eifer Møller, Christian Hassager

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Article in Clinical research in cardiology : official journal of the German Cardiac Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Emily M MartinNordic Bioscience A/S, Herlev Hovedgade 205, 2730, Herlev, Denmark. emma@nordicbio.com.ORCID http://orcid.org/0009-0001-0971-913X
Elisavet AngeliNordic Bioscience A/S, Herlev Hovedgade 205, 2730, Herlev, Denmark.
Federica GenoveseNordic Bioscience A/S, Herlev Hovedgade 205, 2730, Herlev, Denmark.
Martin FrydlandDepartment of Cardiology, Rigshospitalet, Copenhagen, Denmark.
Morten A KarsdalNordic Bioscience A/S, Herlev Hovedgade 205, 2730, Herlev, Denmark.
Jacob Eifer MøllerDepartment of Cardiology, Odense University Hospital, Odense, Denmark.
Christian HassagerDepartment of Cardiology, Rigshospitalet, Copenhagen, Denmark.

Funding

HORIZON EUROPE Marie Sklodowska-Curie Actions 101072828
6 · The paper itself

Abstract

BACKGROUND AND

aimsTissue remodelling and extracellular matrix (ECM) changes are primary consequences of ST-elevated myocardial infarction (STEMI), leading to an increased risk of developing heart failure and mortality. Collagen type I is the top constituent of the cardiac ECM and is rapidly degraded at sites of tissue injury occurring in STEMI. We aimed to investigate the prognostic potential of a novel biomarker of a collagen type I-derived signalling peptide (C1SIG) shown to be involved in left ventricular remodelling after MI and compare this against another collagen type I fragment quantified by the established C1M assay in a large STEMI cohort.

methodsPlasma C1SIG and C1M were quantified using specific enzyme-linked immunosorbent assays in 1616 individuals upon admittance to hospital with STEMI. Patients were then followed up for all-cause mortality over 1 year, and survival analyses were performed.

resultsShort-term biomarker changes assessed in a subgroup (n = 140) showed increased circulating C1M and C1SIG in the short period from admission with STEMI up to 12 h post-admission (both, p < 0.0001). High C1M levels, defined by the highest quartile, and high C1SIG levels, defined by the median, were associated with reduced survival probability at 1 year (both, p < 0.0001) post-admission. The association was further supported in univariate and maintained for C1M only in multivariate Cox proportional hazard regression models adjusted for multiple confounders (HR [95% CI] 1.46 [1.15-1.85]). Added value analysis determined the additional predictive value of C1M to the clinically used GRACE risk score for cardiovascular event prediction (p = 0.0002).

conclusionC1M and C1SIG are dynamic biomarkers of collagen type I degradation, where C1SIG is also suspected to be a collagen signal. C1M is an independent predictor of all-cause mortality within a year of a MI.

Indexed as

BiomarkerCardiovascular outcomeCollagen type IExtracellular matrixST-elevated myocardial infarction

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