Evidence map›Paper›PMID 28826666›Full record

ArticleJournal of clinical lipidology

Paradoxical coronary artery disease in humans with hyperalphalipoproteinemia is associated with distinct differences in the high-density lipoprotein phosphosphingolipidome.

William Hancock-Cerutti, Marie Lhomme, Carolane Dauteuille, Sora Lecocq, M John Chapman, Daniel J Rader, Anatol Kontush, Marina Cuchel

Open access · greenAbstract read
In one paragraph

Article in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Deciphering Acute Coronary Syndromes Pathobiology Through Proteomics.Journal of cardiovascular development and disease · 2025
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  9. Genome-Wide Association Study Identifies a FunctionalArteriosclerosis, thrombosis, and vascular biology · 2021
    Article
  10. Article
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

8 authors at 4 institutions in 2 countries.

William Hancock-CeruttiNational Institute for Health and Medical Reserch (INSERM), Research Unit 1166 ICAN, Paris, France; University of Pierre and Marie Curie - Paris 6, Paris, France; AP-HP, Groupe Hospitalier Pitié Salpétrière, Paris, France; ICAN Analytics, ICAN Institute, Paris, France; Division of Translational Medicine and Human Genetics, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Marie LhommeICANalytics, Institute of Cardiometabolism and Nutrition, ICAN, Pitié-Salpêtrière Hospital, Paris, France.
Carolane DauteuilleNational Institute for Health and Medical Reserch (INSERM), Research Unit 1166 ICAN, Paris, France; University of Pierre and Marie Curie - Paris 6, Paris, France; AP-HP, Groupe Hospitalier Pitié Salpétrière, Paris, France; ICAN Analytics, ICAN Institute, Paris, France.
Sora LecocqNational Institute for Health and Medical Reserch (INSERM), Research Unit 1166 ICAN, Paris, France; University of Pierre and Marie Curie - Paris 6, Paris, France; AP-HP, Groupe Hospitalier Pitié Salpétrière, Paris, France; ICAN Analytics, ICAN Institute, Paris, France.
M John ChapmanNational Institute for Health and Medical Reserch (INSERM), Research Unit 1166 ICAN, Paris, France; University of Pierre and Marie Curie - Paris 6, Paris, France; AP-HP, Groupe Hospitalier Pitié Salpétrière, Paris, France; ICAN Analytics, ICAN Institute, Paris, France.
Daniel J RaderDivision of Translational Medicine and Human Genetics, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Anatol KontushNational Institute for Health and Medical Reserch (INSERM), Research Unit 1166 ICAN, Paris, France; University of Pierre and Marie Curie - Paris 6, Paris, France; AP-HP, Groupe Hospitalier Pitié Salpétrière, Paris, France; ICAN Analytics, ICAN Institute, Paris, France. Electronic address: anatol.kontush@upmc.fr.
Marina CuchelDivision of Translational Medicine and Human Genetics, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: mcuchel@mail.med.upenn.edu.
Inserm · FRSorbonne Université · FRTranslational Therapeutics (United States) · USUniversity of Pennsylvania · US

Funding

INSTITUTIONAL CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR024134 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2006 to 2011
$70.4M
ZDV VS ZDV + DDL VS ZDV + DDL + NVP IN ASYMPTOMATIC HIV PATIENTSM01RR000040 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 1985 to 2006
$21.1M
Mechanistic study of CHD risk in subjects with high HDLCK23HL077146 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI CUCHEL, MARINA · 2004 to 2008
$662k
NCRR NIH HHS M01 RR000040NCRR NIH HHS UL1 RR024134NHLBI NIH HHS K23 HL077146
6 · The paper itself

Abstract

backgroundPlasma high-density lipoprotein cholesterol (HDL-C) levels are inversely associated with risk of coronary artery disease (CAD) in epidemiologic studies. Despite this, the directionality of this relationship and the underlying biology behind it remain to be firmly established, especially at the extremes of HDL-C levels.

objectiveWe investigated differences in the HDL phosphosphingolipidome in a rare population of subjects with premature CAD despite high HDL-C levels to gain insight into the association between the HDL lipidome and CAD disease status in this unusual phenotype. We sought to assess differences in HDL composition that are associated with CAD in subjects with HDL-C >90th percentile. We predicted that quantitative lipidomic analysis of HDL particles would reveal novel differences between CAD patients and healthy subjects with matched HDL-C levels.

methodsWe collected plasma samples from 25 subjects with HDL-C >90th percentile and clinically manifest CAD and healthy controls with HDL-C >90th percentile and without self-reported CAD. More than 140 individual HDL phospholipid and sphingolipid species were analyzed by LC/MS/MS.

resultsSignificant reductions in HDL phosphatidylcholine (-2.41%, Q value = 0.025) and phosphatidylinositol (-10.7%, Q value = 0.047) content, as well as elevated sphingomyelin (+10.0%, Q value = 0.025) content, and sphingomyelin/phosphatidylcholine ratio (+12.8%, P value = .005) were associated with CAD status in subjects with high HDL-C.

conclusionsThese differences may lay the groundwork for further analysis of the relationship between the HDL lipidome and disease states, as well as for the development of biomarkers of CAD status and HDL function.

Indexed as

AdultAgedCholesterol Ester Transfer ProteinsCoronary Artery DiseaseFemaleHumansLipid Metabolism, Inborn ErrorsLipoproteins, HDLMaleMiddle AgedPhosphatidylcholinesCholesterol Ester Transfer Proteinshigh density lipoprotein phosphatidylcholineLipoproteins, HDLPhosphatidylcholinesCoronary artery diseaseHDLHyperalphalipoproteinemiaLipidomicsPhospholipids

Identifiers

PMID28826666
PMCPMC10455038
OpenAlexW2727128957

What OpenQuestion holds

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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.