Evidence map›Paper›PMID 19729614›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2009

Ion mobility analysis of lipoprotein subfractions identifies three independent axes of cardiovascular risk.

Kiran Musunuru, Marju Orho-Melander, Michael P Caulfield, Shuguang Li, Wael A Salameh, Richard E Reitz, Göran Berglund, Bo Hedblad, Gunnar Engström, Paul T Williams and 3 more

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 5 pooled it
6.3field-weighted citation impact, top 3% 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

91 citing papers in PubMed, 5 syntheses or guidelines pooled it, 170 citations in OpenAlex.

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  15. The effects of extended release niacin on lipoprotein sub-particle concentrations in HIV-infected patients.Hawai'i journal of medicine & public health : a journal of Asia Pacific Medicine & Public Health · 2013
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31 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

13 authors at 1 institution in 1 country.

Kiran MusunuruCenter for Human Genetic Research, Cardiology Division, Massachusetts General Hospital, Boston, MA, USA.
Marju Orho-Melander
Michael P Caulfield
Shuguang Li
Wael A Salameh
Richard E Reitz
Göran Berglund
Bo Hedblad
Gunnar Engström
Paul T Williams
Sekar Kathiresan
Olle Melander
Ronald M Krauss
Children’s Institute · US

Funding

Pharmacogenomics and Risk of Cardiovascular DiseaseU01HL069757 · NHLBI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI KRAUSS, RONALD M · 2001 to 2009
$24.7M
NHLBI NIH HHS U01 HL069757NHLBI NIH HHS U01HL069757
6 · The paper itself

Abstract

objectiveWhereas epidemiological studies show that levels of low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) predict incident cardiovascular disease (CVD), there is limited evidence relating lipoprotein subfractions and composite measures of subfractions to risk for CVD in prospective cohort studies. METHODS AND

resultsWe tested whether combinations of lipoprotein subfractions independently predict CVD in a prospective cohort of 4594 initially healthy men and women (the Malmö Diet and Cancer Study, mean follow-up 12.2 years, 377 incident cardiovascular events). Plasma lipoproteins and lipoprotein subfractions were measured at baseline with a novel high-resolution ion mobility technique. Principal component analysis (PCA) of subfraction concentrations identified 3 major independent (ie, zero correlation) components of CVD risk, one representing LDL-associated risk, a second representing HDL-associated protection, and the third representing a pattern of decreased large HDL, increased small/medium LDL, and increased triglycerides. The last corresponds to the previously described "atherogenic lipoprotein phenotype." Several genes that may underlie this phenotype-CETP, LIPC, GALNT2, MLXIPL, APOA1/A5, LPL-are suggested by SNPs associated with the combination of small/medium LDL and large HDL.

conclusionsPCA on lipoprotein subfractions yielded three independent components of CVD risk. Genetic analyses suggest these components represent independent mechanistic pathways for development of CVD.

Indexed as

AdultAgedBiomarkersCardiovascular DiseasesCholesterol, HDLCholesterol, LDLChromatography, High Pressure LiquidChromatography, Ion ExchangeCohort StudiesFemaleHumansIon TransportLipoproteins, VLDLLogistic ModelsMaleMiddle AgedBiomarkersCholesterol, HDLCholesterol, LDLLipoproteins, VLDL

Identifiers

PMID19729614
PMCPMC2772123
OpenAlexW2101573428

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.