Evidence map›Paper›PMID 32119801›Full record

ReviewMetabolic syndrome and related disorders2020

High-Risk Atherosclerosis and Metabolic Phenotype: The Roles of Ectopic Adiposity, Atherogenic Dyslipidemia, and Inflammation.

Katharina Lechner, Amy L McKenzie, Nicolle Kränkel, Clemens Von Schacky, Nicolai Worm, Uwe Nixdorff, Benjamin Lechner, Johannes Scherr, Oliver Weingärtner, Ronald M Krauss

Open access · hybridAbstract readReview
In one paragraph

Review in Metabolic syndrome and related disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 3 pooled it
12.1field-weighted citation impact, top 1% of its field
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

75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 137 citations in OpenAlex.

  1. Pooled it
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  6. Review
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  16. Pathophysiology of Maternal Obesity and Hypertension in Pregnancy.Journal of cardiovascular development and disease · 2025
    Review
  17. Review
  18. Review
  19. Article
  20. [Metabolic-associated fatty liver disease (MAFLD): a multisystemic disease beyond the liver].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Review

15 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 3 countries.

Katharina LechnerDepartment of Prevention, Rehabilitation and Sports Medicine, School of Medicine, Technical University of Munich, Munich, Germany.
Amy L McKenzieVirta Health, San Francisco, California, USA.
Nicolle KränkelKlinik Für Kardiologie, Campus Benjamin Steglitz, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Clemens Von SchackyPreventive Cardiology, Ludwig-Maximilians University, Munich, Germany.
Nicolai WormGerman University for Prevention and Health Care Management, Saarbrücken, Germany.
Uwe NixdorffEuropean Prevention Center, Düsseldorf, Germany.
Benjamin LechnerDepartment of Internal Medicine IV, Ludwig-Maximilians University, Munich, Germany.
Johannes ScherrDepartment of Prevention, Rehabilitation and Sports Medicine, School of Medicine, Technical University of Munich, Munich, Germany.
Oliver WeingärtnerKlinik Für Innere Medizin I, Universitätsklinikum Jena, Jena, Germany.
Ronald M KraussUniversity of California, San Francisco, San Francisco, California, USA.
German Centre for Cardiovascular Research · DELudwig-Maximilians-Universität München · DEJena University Hospital · DEUniversity of California, San Francisco · USUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current algorithms for assessing risk of atherosclerotic cardiovascular disease (ASCVD) and, in particular, the reliance on low-density lipoprotein (LDL) cholesterol in conditions where this measurement is discordant with apoB and LDL-particle concentrations fail to identify a sizeable part of the population at high risk for adverse cardiovascular events. This results in missed opportunities for ASCVD prevention, most notably in those with metabolic syndrome, prediabetes, and diabetes. There is substantial evidence that accumulation of ectopic fat and associated metabolic traits are markers for and pathogenic components of high-risk atherosclerosis. Conceptually, the subset of advanced lesions in high-risk atherosclerosis that triggers vascular complications is closely related to a set of coordinated high-risk traits clustering around a distinct metabolic phenotype. A key feature of this phenotype is accumulation of ectopic fat, which, coupled with age-related muscle loss, creates a milieu conducive for the development of ASCVD: atherogenic dyslipidemia, nonresolving inflammation, endothelial dysfunction, hyperinsulinemia, and impaired fibrinolysis. Sustained vascular inflammation, a hallmark of high-risk atherosclerosis, impairs plaque stabilization in this phenotype. This review describes how metabolic and inflammatory processes that are promoted in large measure by ectopic adiposity, as opposed to subcutaneous adipose tissue, relate to the pathogenesis of high-risk atherosclerosis. Clinical biomarkers indicative of these processes provide incremental information to standard risk factor algorithms and advanced lipid testing identifies atherogenic lipoprotein patterns that are below the discrimination level of standard lipid testing. This has the potential to enable improved identification of high-risk patients who are candidates for therapeutic interventions aimed at prevention of ASCVD.

Indexed as

AdiposityAtherosclerosisBiomarkersCardiometabolic Risk FactorsCardiovascular DiseasesChoristomaDyslipidemiasHumansInflammationMetabolic SyndromeObesityPhenotypeRisk FactorsBiomarkersatherosclerosisdyslipidemiaectopic adipose tissueinflammationlifestylemetabolic syndrome

Identifiers

PMID32119801
PMCPMC7196362
OpenAlexW3009253347

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.