Evidence map›Paper›PMID 27831500›Full record

ArticleCirculation2017

LPA Gene, Ethnicity, and Cardiovascular Events.

Sang-Rok Lee, Anand Prasad, Yun-Seok Choi, Chao Xing, Paul Clopton, Joseph L Witztum, Sotirios Tsimikas

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

Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 3 pooled it
8.8field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 3 syntheses or guidelines pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. An integrated cardiometabolic genetic testing program in a predominantly Hispanic population within a community setting.Genetics in medicine : official journal of the American College of Medical Genetics · 2026
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. The biology of lipoprotein(a): From genetics to molecular mechanisms.European journal of clinical investigation · 2026
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

13 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

7 authors at 5 institutions in 2 countries.

Sang-Rok LeeFrom Division of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla (S.-R.L., Y.-S.C., S.T.); Division of Cardiology, Chonbuk National University Hospital and Chonbuk School of Medicine, Jeonju, Korea (S.-R.L.); Division of Cardiology, Department of Medicine, The University of Texas Health Science Center San Antonio (A.P.); Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul (Y.-S.C.); Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center at Dallas (C.X.); Veterans Affairs Medical Center, San Diego, CA (P.C.); and Division of Endocrinology and Metabolism, University of California San Diego, La Jolla (J.L.W.).
Anand PrasadFrom Division of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla (S.-R.L., Y.-S.C., S.T.); Division of Cardiology, Chonbuk National University Hospital and Chonbuk School of Medicine, Jeonju, Korea (S.-R.L.); Division of Cardiology, Department of Medicine, The University of Texas Health Science Center San Antonio (A.P.); Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul (Y.-S.C.); Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center at Dallas (C.X.); Veterans Affairs Medical Center, San Diego, CA (P.C.); and Division of Endocrinology and Metabolism, University of California San Diego, La Jolla (J.L.W.).
Yun-Seok ChoiFrom Division of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla (S.-R.L., Y.-S.C., S.T.); Division of Cardiology, Chonbuk National University Hospital and Chonbuk School of Medicine, Jeonju, Korea (S.-R.L.); Division of Cardiology, Department of Medicine, The University of Texas Health Science Center San Antonio (A.P.); Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul (Y.-S.C.); Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center at Dallas (C.X.); Veterans Affairs Medical Center, San Diego, CA (P.C.); and Division of Endocrinology and Metabolism, University of California San Diego, La Jolla (J.L.W.).
Chao XingFrom Division of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla (S.-R.L., Y.-S.C., S.T.); Division of Cardiology, Chonbuk National University Hospital and Chonbuk School of Medicine, Jeonju, Korea (S.-R.L.); Division of Cardiology, Department of Medicine, The University of Texas Health Science Center San Antonio (A.P.); Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul (Y.-S.C.); Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center at Dallas (C.X.); Veterans Affairs Medical Center, San Diego, CA (P.C.); and Division of Endocrinology and Metabolism, University of California San Diego, La Jolla (J.L.W.).
Paul CloptonFrom Division of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla (S.-R.L., Y.-S.C., S.T.); Division of Cardiology, Chonbuk National University Hospital and Chonbuk School of Medicine, Jeonju, Korea (S.-R.L.); Division of Cardiology, Department of Medicine, The University of Texas Health Science Center San Antonio (A.P.); Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul (Y.-S.C.); Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center at Dallas (C.X.); Veterans Affairs Medical Center, San Diego, CA (P.C.); and Division of Endocrinology and Metabolism, University of California San Diego, La Jolla (J.L.W.).
Joseph L WitztumFrom Division of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla (S.-R.L., Y.-S.C., S.T.); Division of Cardiology, Chonbuk National University Hospital and Chonbuk School of Medicine, Jeonju, Korea (S.-R.L.); Division of Cardiology, Department of Medicine, The University of Texas Health Science Center San Antonio (A.P.); Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul (Y.-S.C.); Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center at Dallas (C.X.); Veterans Affairs Medical Center, San Diego, CA (P.C.); and Division of Endocrinology and Metabolism, University of California San Diego, La Jolla (J.L.W.).
Sotirios TsimikasFrom Division of Cardiovascular Diseases, Sulpizio Cardiovascular Center, Department of Medicine, University of California San Diego, La Jolla (S.-R.L., Y.-S.C., S.T.); Division of Cardiology, Chonbuk National University Hospital and Chonbuk School of Medicine, Jeonju, Korea (S.-R.L.); Division of Cardiology, Department of Medicine, The University of Texas Health Science Center San Antonio (A.P.); Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul (Y.-S.C.); Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center at Dallas (C.X.); Veterans Affairs Medical Center, San Diego, CA (P.C.); and Division of Endocrinology and Metabolism, University of California San Diego, La Jolla (J.L.W.). stsimikas@ucsd.edu.
Veterans Health Administration · USCatholic University of Korea · KRJeonbuk National University Hospital · KRThe University of Texas Health Science Center at San Antonio · USThe University of Texas Southwestern Medical Center · US

Funding

ROLE OF LIPOXYGENASES IN ATHEROGENESIS IN DIABETES MELLITUSP01HL055798 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI HEDRICK, CATHERINE C · 1995 to 2016
$28.4M
Transcriptional GenomicsP01HL088093 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WITZTUM, JOSEPH L. · 2008 to 2018
$26.4M
UT Southwestern Center for Translational Medicine (UL1/KL2/TL1)UL1TR001105 · NCATS · UT SOUTHWESTERN MEDICAL CENTER · PI TOTO, ROBERT DANIEL · 2013 to 2017
$24.5M
Oxidation-specific nanoparticles for imaging atherosclerosisR01HL119828 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TSIMIKAS, SOTIRIOS · 2013 to 2017
$2.0M
NCATS NIH HHS UL1 TR001105NHLBI NIH HHS P01 HL055798NHLBI NIH HHS P01 HL088093NHLBI NIH HHS R01 HL119828
6 · The paper itself

Abstract

backgroundThe relationship of LPA single nucleotide polymorphisms (SNPs), apolipoprotein(a) isoforms, and lipoprotein(a) [Lp(a)] levels with major adverse cardiovascular events (MACE) in different ethnic groups is not well known.

methodsLPA SNPs, apolipoprotein(a) isoforms, Lp(a), and oxidized phospholipids on apolipoprotein B-100 (OxPL-apoB) levels were measured in 1792 black, 1030 white, and 597 Hispanic subjects enrolled in the Dallas Heart Study. Their interdependent relationships and prospective association with MACE after median 9.5-year follow-up were determined.

resultsLPA SNP rs3798220 was most prevalent in Hispanics (42.38%), rs10455872 in whites (14.27%), and rs9457951 in blacks (32.92%). The correlation of each of these SNPs with the major apolipoprotein(a) isoform size was highly variable and in different directions among ethnic groups. In the entire cohort, Cox regression analysis with multivariable adjustment revealed that quartiles 4 of Lp(a) and OxPL-apoB were associated with hazard ratios (95% confidence interval) for time to MACE of 2.35 (1.50-3.69, P<0.001) and 1.89 (1.26-2.84, P=0.003), respectively, versus quartile 1. Addition of the major apolipoprotein(a) isoform and the 3 LPA SNPs to these models attenuated the risk, but significance was maintained for both Lp(a) and OxPL-apoB. Evaluating time to MACE in specific ethnic groups, Lp(a) was a positive predictor and the size of the major apolipoprotein(a) isoform was an inverse predictor in blacks, the size of the major apolipoprotein(a) isoform was an inverse predictor in whites, and OxPL-apoB was a positive predictor in Hispanics.

conclusionsThe prevalence and association of LPA SNPs with size of apolipoprotein(a) isoforms, Lp(a), and OxPL-apoB levels are highly variable and ethnicity-specific. The relationship to MACE is best explained by elevated plasma Lp(a) or OxPL-apoB levels, despite significant ethnic differences in LPA genetic markers.

Indexed as

AdultCardiovascular DiseasesEthnicityFemaleHumansLipoprotein(a)MalePolymorphism, Single NucleotideProspective StudiesRisk FactorsLipoprotein(a)cardiovascular eventsethnicityisoformslipoprotein(a)oxidized phospholipidssingle nucleotide polymorphisms

Identifiers

PMID27831500
PMCPMC5241172
OpenAlexW2557177692

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.