Evidence map›Paper›PMID 8675707›Full record

ArticleThe Journal of clinical investigation1996

Increased coronary heart disease in Japanese-American men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels.

S Zhong, D S Sharp, J S Grove, C Bruce, K Yano, J D Curb, A R Tall

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 1 pooled it
19.0field-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

129 citing papers in PubMed, 1 synthesis or guideline pooled it, 584 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Drug designed to raise HDL levels falls down.The Journal of clinical investigation · 2007
    Trial
  5. Review
  6. Article
  7. Article
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  12. Article
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  17. Sphingolipids in Atherosclerosis: Chimeras in Structure and Function.International journal of molecular sciences · 2022
    Review
  18. Article
  19. HDL and Lipid Metabolism.Advances in experimental medicine and biology · 2022
    Article
  20. HDL Receptor inFrontiers in cell and developmental biology · 2022
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

S ZhongDepartment of Medicine, Columbia University, New York 10032, USA.
D S Sharp
J S Grove
C Bruce
K Yano
J D Curb
A R Tall
Columbia University · USKuakini Medical Center · USNational Heart Lung and Blood Institute · USUniversity of Hawaiʻi at Mānoa · USUniversity of Hawaii System · US

Funding

STRUCTURE AND FUNCTION OF HIGH DENSITY LIPOPROTEINSR01HL022682 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TALL, ALAN RICHARD · 1985 to 2010
$5.0M
STRUCTURE/FUNCTION OF HIGH DENSITY LIPOPROTEINSR37HL022682 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TALL, ALAN RICHARD · 1992 to 2001
$1.0M
VITAMIN A TRANSPORT AND RETINOL-BINDING PROTEIN METABOLISMP50HL021006 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TALL, ALAN RICHARD · 1985 to 1996
–
NHLBI NIH HHS HL-21006NHLBI NIH HHS HL-22682
6 · The paper itself

Abstract

Plasma high density lipoprotein (HDL) levels are strongly genetically determined and show a general inverse relationship with coronary heart disease (CHD). The cholesteryl ester transfer protein (CETP) mediates the transfer of cholesteryl esters from HDL to other lipoproteins and is a key participant in the reverse transport of cholesterol from the periphery to the liver. A high prevalence of two different CETP gene mutations (D442G, 5.1%; intron 14G:A, 0.5%), was found in 3,469 men of Japanese ancestry in the Honolulu Heart Program and mutations were associated with decreased CETP (-35%) and increased HDL chol levels (+10% for D442G). However, the overall prevalence of definite CHD was 21% in men with mutations and 16% in men without mutations. The relative risk (RR) of CHD was 1.43 in men with mutations (P < .05); after adjustment for CHD risk factors, the RR was 1.55 (P = .02); after additional adjustment for HDL levels, the RR was 1.68 (P = .008). Similar RR values were obtained for the D442G mutation alone. Increased CHD in men with mutations was primarily observed for HDL chol 41-60 mg/dl; for HDL chol > 60 mg/dl men with and without mutations had low CHD prevalence. Thus, genetic CETP deficiency appears to be an independent risk factor for CHD, primarily due to increased CHD prevalence in men with the D442G mutation and HDL cholesterol between 41 and 60 mg/dl. The findings suggest that both HDL concentration and the dynamics of cholesterol transport through HDL (i.e., reverse cholesterol transport) determine the anti-atherogenicity of the HDL fraction.

Indexed as

GlycoproteinsMutationAgedAsianCarrier ProteinsCholesterol EstersCholesterol Ester Transfer ProteinsCholesterol, HDLCoronary DiseaseHumansJapanMaleCarrier ProteinsCETP protein, humanCholesterol EstersCholesterol Ester Transfer ProteinsCholesterol, HDLGlycoproteins

Identifiers

PMID8675707
PMCPMC507389
OpenAlexW2125757745

What OpenQuestion holds

Textmetadata
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.