Evidence map›Paper›PMID 22388920›Full record

ArticleDer Internist2012

[Clinical and genetic aspects of hypertrophic and dilated cardiomyopathy].

B Meder, H A Katus

Open access · greenAbstract readEnglish Abstract
PubMed Publisher
In one paragraph

Article in Der Internist, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

3 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

2 authors at 2 institutions in 1 country.

B MederAbteilung Innere Medizin III (Schwerpunkt Kardiologie, Angiologie und Pneumologie), Universitätsklinikum Heidelberg.
H A Katus
Chirurgische Universitätsklinik Heidelberg · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary cardiomyopathies are frequent heart diseases with an estimated prevalence of 0.3-0.4% in the general population, significantly contributing to systolic heart failure and sudden cardiac death in the young. Molecular genetic studies have identified 49 different disease genes for hypertrophic and dilated cardiomyopathy, often involving proteins of the sarcomere, the cardiac Z-disc and the cytoskeleton. With the development of new, advanced technologies based on next-generation sequencing, it is now possible to efficiently screen all known disease genes in an individual patient. The clinical workup of cardiomyopathies should always include the investigation of the patient's family to account for the familial aggregation of cardiomyopathies and identify diseased as well as asymptomatic carriers of mutations. The detection of specific genotypes facilitates diagnostic classification and can improve risk stratification in affected patients.

Indexed as

Cardiomyopathy, DilatedCardiomyopathy, Hypertrophic, FamilialGenetic Predisposition to DiseaseGenetic TestingHumansPolymorphism, Single Nucleotide

Identifiers

PMID22388920
OpenAlexW103428130

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.