Evidence map›Paper›PMID 27135400›Full record

ArticleNature genetics2016

Variants with large effects on blood lipids and the role of cholesterol and triglycerides in coronary disease.

Anna Helgadottir, Solveig Gretarsdottir, Gudmar Thorleifsson, Eirikur Hjartarson, Asgeir Sigurdsson, Audur Magnusdottir, Aslaug Jonasdottir, Helgi Kristjansson, Patrick Sulem, Asmundur Oddsson and 23 more

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 9 pooled it
27.6field-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

124 citing papers in PubMed, 9 syntheses or guidelines pooled it, 264 citations in OpenAlex.

  1. Pooled it
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64 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

33 authors at 7 institutions in 4 countries.

Anna HelgadottirdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Solveig GretarsdottirdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Gudmar ThorleifssondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Eirikur HjartarsondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Asgeir SigurdssondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Audur MagnusdottirdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Aslaug JonasdottirdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Helgi KristjanssondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Patrick SulemdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.ORCID 0000-0001-7123-6123
Asmundur OddssondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Gardar SveinbjornssondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Valgerdur SteinthorsdottirdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Thorunn RafnardeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Gisli MassondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Ingileif JonsdottirdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Isleifur OlafssonDepartment of Clinical Biochemistry, Landspítali-National University Hospital, Reykjavik, Iceland.
Gudmundur I EyjolfssonLaboratory in Mjódd (RAM), Reykjavik, Iceland.
Olof SigurdardottirDepartment of Clinical Biochemistry, Akureyri Hospital, Akureyri, Iceland.
Maryam S DaneshpourCellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Davood KhaliliPrevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Fereidoun AziziEndocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Dorine W SwinkelsDepartment for Laboratory Medicine, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences, Nijmegen, the Netherlands.
Lambertus KiemeneyRadboud University Medical Center, Radboud Institute for Health Sciences, Nijmegen, the Netherlands.
Arshed A QuyyumiEmory University School of Medicine, Atlanta, Georgia, USA.
Allan I LeveyEmory University School of Medicine, Atlanta, Georgia, USA.
Riyaz S PatelEmory University School of Medicine, Atlanta, Georgia, USA.
Salim S HayekEmory University School of Medicine, Atlanta, Georgia, USA.
Ingibjorg J GudmundsdottirDivision of Cardiology, Department of Internal Medicine, Landspítali-National University Hospital, Reykjavik, Iceland.
Gudmundur ThorgeirssonFaculty of Medicine, University of Iceland, Reykjavik, Iceland.ORCID 0000-0002-7146-1395
Unnur ThorsteinsdottirdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Daniel F GudbjartssondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.ORCID 0000-0002-5222-9857
Hilma HolmdeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
Kari StefanssondeCODE Genetics/Amgen, Inc., Reykjavik, Iceland.
deCODE Genetics (Iceland) · ISEmory University · USResearch Institute for Endocrine Sciences · IRNational University Hospital of Iceland · ISRadboud University Nijmegen · NLAkureyri Hospital · ISUniversity of Iceland · IS

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR025008 · NCRR · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2007 to 2011
$29.0M
ENNCF - Viral Vector CoreP30NS055077 · NINDS · EMORY UNIVERSITY · PI LEVEY, ALLAN I · 2008 to 2018
$6.8M
Genome-wide association study of MI in CaucasiansR01HL089650 · NHLBI · DECODE GENETICS, INC. · PI GULCHER, JEFFREY R · 2007 to 2010
$2.3M
British Heart Foundation FS/14/76/30933NCRR NIH HHS UL1 RR025008NHLBI NIH HHS R01 HL089650NINDS NIH HHS P30 NS055077
6 · The paper itself

Abstract

Sequence variants affecting blood lipids and coronary artery disease (CAD) may enhance understanding of the atherogenicity of lipid fractions. Using a large resource of whole-genome sequence data, we examined rare and low-frequency variants for association with non-HDL cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides in up to 119,146 Icelanders. We discovered 13 variants with large effects (within ANGPTL3, APOB, ABCA1, NR1H3, APOA1, LIPC, CETP, LDLR, and APOC1) and replicated 14 variants. Five variants within PCSK9, APOA1, ANGPTL4, and LDLR associate with CAD (33,090 cases and 236,254 controls). We used genetic risk scores for the lipid fractions to examine their causal relationship with CAD. The non-HDL cholesterol genetic risk score associates most strongly with CAD (P = 2.7 × 10(-28)), and no other genetic risk score associates with CAD after accounting for non-HDL cholesterol. The genetic risk score for non-HDL cholesterol confers CAD risk beyond that of LDL cholesterol (P = 5.5 × 10(-8)), suggesting that targeting atherogenic remnant cholesterol may reduce cardiovascular risk.

Indexed as

CholesterolCoronary Artery DiseaseHumansLipidsTriglyceridesCholesterolLipidsTriglycerides

Identifiers

PMID27135400
PMCPMC9136713
OpenAlexW2345410714

What OpenQuestion holds

Textmetadata
LicenceTDM
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.