Evidence map›Paper›PMID 14972088›Full record

ReviewCurrent hypertension reports2004

Genes for left ventricular hypertrophy.

Donna K Arnett, Lisa de las Fuentes, Ulrich Broeckel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 33% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Left ventricular cardiac geometry and ambulatory blood pressure in children.Journal of clinical hypertension (Greenwich, Conn.) · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Myocardial remodeling in hypertension.Journal of human hypertension · 2015
    Review
  11. Review
  12. Article
  13. Article
  14. Genetic epidemiology of left ventricular hypertrophy.American journal of cardiovascular disease · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

Donna K ArnettDivision of Epidemiology, School of Public Health, University of Minnesota, 1300 South Second Street, Suite 300, Minneapolis, MN 55454, USA. arnett@epi.umn.edu
Lisa de las Fuentes
Ulrich Broeckel
University of Minnesota · US

Funding

HYPERGEN: GENETICS OF LEFT VENTRICULAR HYPERTROPHYR01HL055673 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARNETT, DONNA K · 1996 to 2016
$18.1M
NHLBI NIH HHS L30 HL074749NHLBI NIH HHS R01 HL055673
6 · The paper itself

Abstract

Left ventricular (LV) hypertrophy is very common, particularly among hypertensives. The presence of LV hypertrophy profoundly affects morbidity and mortality from cardiovascular diseases and stroke, and is now recognized as the most important predictor of chronic heart failure. Hypertension, obesity, and diabetes are important determinants of LV hypertrophy, but they fail to identify many individuals with the condition, suggesting that other factors, likely genetic in origin, play a role. Although much research has been undertaken to understand the causes of hypertrophy and the medical treatments that can lead to its regression, much remains unknown about its genetic basis. LV hypertrophy is considered a complex genetic disease, likely representing an interaction of several genes with the environment. The heritability of LV mass, measured as a quantitative trait, falls between 0.3 and 0.7 in different populations, suggesting it has a familial component. Genes encoding proteins involved in LV structure, as well as genes encoding cell signal transduction, hormones, growth factors, calcium homeostasis, substrate metabolism, and blood pressure are likely candidates for the development of common forms of LV hypertrophy. An overview of the pathophysiology of LV hypertrophy and dysfunction is provided, in addition to evidence of the genetic basis for LV hypertrophy in humans and animal models.

Indexed as

Genetic Predisposition to DiseaseHumansHypertrophy, Left VentricularIncidencePolymorphism, Single NucleotideUnited StatesVentricular Dysfunction, Left

Identifiers

PMID14972088
OpenAlexW1990564736

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.