Evidence map›Paper›PMID 40957671›Full record

ArticleHeart (British Cardiac Society)2026

Circulating soluble LOX-1 and patient prognosis after an acute coronary syndrome.

Alexandru Schiopu, Sara Svedlund, Gayathri Narasimhan, Bi Juin Loong, Troels Yndigegn, Vijayalakshmi Varma, Emily L Ongstad, Isabel Goncalves, Anna Collén, Jan Nilsson and 1 more

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In one paragraph

Article in Heart (British Cardiac Society), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Alexandru SchiopuDepartment of Translational Medicine, Lund University, Malmö, Sweden Alexandru.Schiopu@med.lu.se.ORCID 0000-0002-7587-5050
Sara SvedlundDepartment of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Gayathri NarasimhanDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Bi Juin LoongDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Troels YndigegnDepartment of Cardiology, Skåne University Hospital, Lund, Sweden.ORCID 0000-0002-8960-2125
Vijayalakshmi VarmaTranslational Science and Experimental Medicine, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, Maryland, USA.
Emily L OngstadBioscience Cardiovascular, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, Maryland, USA.
Isabel GoncalvesDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Anna CollénProjects, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
Jan NilssonDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Li-Ming GanDepartment of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe lectin-like oxidised low-density lipoprotein receptor-1 (LOX-1) mediates atherosclerotic plaque inflammation and vulnerability. On activation, LOX-1 sheds its extracellular domain into the circulation as soluble LOX-1 (sLOX-1). sLOX-1 is markedly elevated in patients with acute coronary syndrome (ACS).

methodsWe prospectively assessed the associations between plasma sLOX-1 and the development of heart failure (HF), major adverse cardiovascular events (MACE) and coronary and left ventricular (LV) dysfunction in two cohorts of patients with ACS. The first cohort comprised 524 patients recruited during the acute index event at the coronary care unit of Skåne University Hospital, Malmö, Sweden. The second cohort included 363 patients with ACS treated with acute percutaneous intervention at Sahlgrenska University Hospital, Gothenburg, Sweden. Additionally, we examined the anti-inflammatory effects of LOX-1 blockade in vitro using human umbilical vein endothelial cells (HUVECs).

resultsIn the first cohort, acute-phase sLOX-1 was associated with incident HF and MACE independently of cardiovascular risk factors, revascularisation and medication (HR per 1-SD sLOX-1 increase: 1.57 (95% CI: 1.10 to 2.23; p=0.012) for HF and 1.36 (1.08 to 1.71; p=0.009) for MACE). Elevated sLOX-1 was also associated with lower LV ejection fraction and accelerated remodelling, as measured by echocardiography at 1-year post-ACS. In the second cohort, sLOX-1 was negatively associated with left anterior descending coronary artery flow reserve and LV systolic function, and positively correlated with soluble markers of systemic inflammation and cardiac overload at 4 and 16 weeks post-ACS. In vitro, antibody-mediated LOX-1 blockade prevented oxidised low-density lipoprotein-induced HUVEC activation.

conclusionsElevated plasma sLOX-1 at baseline and during follow-up is associated with incident HF and MACE, as well as cardiac and coronary dysfunction in patients with ACS. As plasma sLOX-1 levels may reflect the intensity of LOX-1 expression on vascular and immune cells, these findings support LOX-1 as a potentially important therapeutic target to improve prognosis in patients with ACS.

Indexed as

Acute Coronary SyndromeHeart FailureScavenger Receptors, Class EAgedBiomarkersFemaleHumansHuman Umbilical Vein Endothelial CellsMaleMiddle AgedPrognosisProspective StudiesRisk FactorsSwedenVentricular Dysfunction, LeftBiomarkersOLR1 protein, humanScavenger Receptors, Class EAcute Coronary SyndromeBiomarkersCohort StudiesHeart failureInflammation

Identifiers

PMID40957671
PMCPMC13539867

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.