Evidence map›Paper›PMID 21248783›Full record

ArticleJournal of human hypertension2012

Epistatic effects of ACE I/D and AGT gene variants on left ventricular mass in hypertensive patients: the HyperGEN study.

A I Lynch, W Tang, G Shi, R B Devereux, J H Eckfeldt, D K Arnett

Abstract readMulticenter Study
In one paragraph

Article in Journal of human hypertension, 2012. 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
0.6field-weighted citation impact, top 28% 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, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Association BetweenFrontiers in cardiovascular medicine · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Genetic epidemiology of left ventricular hypertrophy.American journal of cardiovascular disease · 2012
    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

6 authors at 4 institutions in 1 country.

A I LynchDepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
W Tang
G Shi
R B Devereux
J H Eckfeldt
D K Arnett
University of Minnesota · USCornell University · USUniversity of Alabama at Birmingham · USWashington University in St. Louis · US

Funding

HYPERGEN: GENETICS OF LEFT VENTRICULAR HYPERTROPHYR01HL055673 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARNETT, DONNA K · 1996 to 2016
$18.1M
HYPERGENU10HL054496 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARNETT, DONNA K. · 1995 to 1999
–
NHLBI NIH HHS R01 HL055673NHLBI NIH HHS U10 HL054496PHS HHS R01-555673
6 · The paper itself

Abstract

Identifying predictors of left ventricular hypertrophy has been an active study topic because of its association with cardiovascular morbidity and mortality. We examined the epistatic effect (gene-gene interaction) of two genes (angiotensin-converting enzyme (ACE) insertion/deletion (I/D); angiotensinogen (AGT) -6G-A, M235T, -20A-C) in the renin-angiotensin system on left ventricular mass (LVM) among hypertensive participants in the Hypertension Genetic Epidemiology Network study. Included were 2156 participants aged 20-87 years (60% women, 63% African American). We employed mixed linear regression models to assess main effects of four genetic variants on echocardigraphically determined LVM (indexed for height), and ACE-by-AGT epistatic effects. There was evidence that AGT -6G-A was associated with LVM among white participants: adjusted mean LVM (gm(-2.7)) increased with 'G' allele copy number ('AA':41.2, 'AG':42.3, 'GG':44.0; P=0.03). There was also evidence of an ACE I/D-by-AGT -20A-C epistatic effect among white participants (interaction P=0.03): among ACE 'DD' participants, AGT -20A-C 'C' allele carriers had lower mean LVM than 'AA' homozygotes ('DD/CC':39.2, 'DD/AC':39.9, 'DD/AA':43.9), with no similar significant effect among ACE 'I' allele carriers ('ID/CC':47.2, 'ID/AC':43.4, 'ID/AA':42.6; 'II/CC': NA, 'II/AC':41.3, 'II/AA':43.1). These findings indicate that renin-angiotensin system variants in at least two genes may interact to modulate LVM.

Indexed as

Epistasis, GeneticGenetic VariationAdultAgedAged, 80 and overAngiotensinogenBlack or African AmericanChi-Square DistributionFemaleGene FrequencyGenetic Predisposition to DiseaseHomozygoteHumansHypertensionHypertrophy, Left VentricularLinear ModelsAGT protein, humanAngiotensinogenPeptidyl-Dipeptidase A

Identifiers

PMID21248783
PMCPMC3775641
OpenAlexW2014043509

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.