Evidence map›Paper›PMID 23173100›Full record

ArticleAmerican journal of cardiovascular disease2012

Genetic epidemiology of left ventricular hypertrophy.

Jonathan N Bella, Harald Hh Göring

Open access · greenAbstract read
In one paragraph

Article in American journal of cardiovascular disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Article
  4. Article
  5. Article
  6. Review
  7. Cardiovascular Risk Factors Track From Mother to Child.Journal of the American Heart Association · 2018
    Article
  8. XRCC3 polymorphism is associated with hypertension-induced left ventricular hypertrophy.Hypertension research : official journal of the Japanese Society of Hypertension · 2018
    Article
  9. Article
  10. Review
  11. Article
  12. Factors independently associated with cardiac troponin I levels in young and healthy adults from the general population.Clinical research in cardiology : official journal of the German Cardiac Society · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

2 authors at 1 institution in 1 country.

Jonathan N BellaDivision of Cardiology, Department of Medicine, Bronx-Lebanon Hospital Center and Albert Einstein College of Medicine Bronx, NY, USA.
Harald Hh Göring
Bronx-Lebanon Hospital Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Left ventricular (LV) hypertrophy is a strong independent predictor of increased cardiovascular morbidity and mortality in clinical and population-based samples. Clinical and hemodynamic stimuli to LV hypertrophy induce not only an increase in cardiac mass and wall thickness but also a fundamental reconfiguration of the protein, cellular and molecular components of the myocardium. Several studies have indicated that LV mass is influenced by genetic factors. The substantial heritability (h(2)) for LV mass in population-based samples of varying ethnicity indicates robust genetic influences on LV hypertrophy. Genome-wide linkage and association studies in diverse populations have been performed to identify genes influencing LV mass, and although several chromosomal regions have been found to be significantly associated with LV mass, the specific genes and functional variants contained in these chromosomal regions have yet to be identified. In addition, multiple studies have tried to link single-nucleotide polymorphisms (SNPs) in regulatory and pathway genes with common forms of LV hypertrophy, but there is little evidence that these genetic variations are functional. Up to this point in time, the results obtained in genetic studies are of limited clinical value. Much of the heritability remains unexplained, the identity of the underlying gene pathways, genes, and functional variants remains unknown, and the promise of genetically-based risk prediction and personalized medicine remain unfulfilled. However, molecular biological technologies continue to improve rapidly, and the long-term potential of sophisticated genetic investigations using these modern genomic technologies, coupled with smart study designs, remains intact. Ultimately, genetic investigations offer much promise for future prevention, early intervention and treatment of this major public health issue.

Indexed as

genetic epidemiologyGenome-wide linkage and association studiesLeft ventricular (LV) hypertrophy

Identifiers

PMID23173100
PMCPMC3499934
OpenAlexW12248668

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.