Evidence mapPaperPMID 39257198Full record

ArticleThe Journal of clinical endocrinology and metabolism2025

Incremental Value of Blood-Based Markers of Liver Fibrosis in Cardiovascular Risk Stratification.

Georgios Georgiopoulos, Stavros Athanasopoulos, Georgios Mavraganis, Christina Konstantaki, Maria Papaioannou, Dimitrios Delialis, Lasthenis Angelidakis, Marco Sachse, Dimitrios Papoutsis, Beyza Cavlan and 6 more

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
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

9 citing papers in PubMed.

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  5. Amyloid-beta (1-40) peptide is associated with systemic metabolic health.European journal of clinical investigation · 2026
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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

16 authors.

Georgios GeorgiopoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Stavros AthanasopoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Georgios MavraganisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Christina KonstantakiDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Maria PapaioannouDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Dimitrios DelialisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Lasthenis AngelidakisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Marco SachseDepartment of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Dimitrios PapoutsisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Beyza CavlanDepartment of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Simon Tual-ChalotBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, NE1 7RU Newcastle Upon Tyne, UK.ORCID 0000-0002-9307-7175
Georgios ZervasDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Kateryna SopovaDepartment of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Asimina MitrakouDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.
Konstantinos StellosDepartment of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.ORCID 0000-0002-0194-0825
Kimon StamatelopoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, 11528 Athens, Greece.ORCID 0000-0001-6444-8734

Funding

British Heart Foundation PG/23/11093German Research Foundation CRC1366 C07Royal Society RG\R1\241197
6 · The paper itself

Abstract

contextNonalcoholic fatty liver disease (NAFLD) with advanced liver fibrosis is associated with cardiovascular disease (CVD).

objectiveThis work aimed to examine if markers of vascular injury mediate the link between liver fibrosis noninvasive tests (LFNITs) and CVD events, and to compare the incremental predictive value of LFNITs over established CVD risk scores.

methodsConsecutively recruited individuals (n = 1692) with or without clinically overt coronary artery disease (CAD) from the Athens Cardiometabolic Cohort, were analyzed. Fibrosis-4 index (FIB-4), NAFLD Fibrosis score (NFS), and BARD score were evaluated for direct and indirect associations with indices of subclinical arterial injury including carotid maximal wall thickness (maxWT) and pulse wave velocity (PWV) and with a composite of major adverse cardiovascular events (MACE) that consisted of cardiac death, acute myocardial infarction, or coronary revascularization (39-month median follow-up).

resultsFIB-4 was the only LFNIT that was consistently associated with multiple markers of vascular injury, irrespective of CAD presence and after controlling for traditional risk factors, surrogates of insulin resistance, or obesity (adjusted P < .05 for all). FIB-4 was also independently associated with CAD presence (adjusted odds ratio [OR] 6.55; 3.48-12.3; P < .001). Increased FIB-4 greater than 2.67 was incrementally associated with an increased risk for MACE (OR [95% CI] 2.00 [1.12-3.55], ΔAUC [95% CI] 0.014 [0.002-0.026]). These associations were mediated by maxWT rather than PWV. Only FIB-4 (>3.25) was independently and incrementally associated with all-cause mortality (adjusted P < 0.05).

conclusionIn a cardiometabolically diverse population, the incremental associations of LFNITs with CVD outcomes were mediated by atherosclerotic burden rather than arterial stiffening. FIB-4 consistently demonstrated associations with all study end points. These findings provide mechanistic insights and support the clinical applicability of FIB-4 in CVD prevention.

Indexed as

BiomarkersCardiovascular DiseasesLiver CirrhosisNon-alcoholic Fatty Liver DiseaseAdultAgedCohort StudiesCoronary Artery DiseaseFemaleHeart Disease Risk FactorsHumansMaleMiddle AgedPredictive Value of TestsPrognosisPulse Wave AnalysisBiomarkersarterial damagecardiovascular eventscardiovascular risk biomarkerFibrosis-4 indexliver fibrosisnoninvasive tests

Identifiers

PMID39257198
PMCPMC11913098

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.