Evidence map›Paper›PMID 23011600›Full record

ArticleHerzschrittmachertherapie & Elektrophysiologie2012

[Dilated cardiomyopathy].

Philipp Ehlermann, Hugo A Katus

Abstract readEnglish Abstract
PubMed Publisher
In one paragraph

Article in Herzschrittmachertherapie & Elektrophysiologie, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 53% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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 1 institution in 1 country.

Philipp EhlermannInnere Medizin III-Kardiologie, Angiologie und Pneumologie, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany. philipp.ehlermann@med.uni-heidelberg.de
Hugo A Katus
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dilated cardiomyopathy (DCM) has a familial accumulation in 20-50% of cases and, therefore, frequently has a genetic cause. Currently, numerous mutations are known in more than 40 genes, which account for around 20% of familial cases. The structured evaluation of family history with recording of a family tree is an obligatory part of the initial diagnosis of DCM. By evaluation of family members other persons at risk can be identified. With the exception of the lamin A/C gene (LMNA), genetic testing does not allow risk stratification. DCM caused by LMNA mutations is associated with a high risk of sudden cardiac death. In cases of familial conduction disease, sudden cardiac death and a concomitant muscle disease LMNA mutation should be excluded. Implantation of an ICD is indicated if the LVEF is chronically less than 35% independent from etiology. This applies with some restrictions for asymptomatic patients in NYHA class I. Patients should receive optimal drug therapy for 3-12 months before ICD implantation.

Indexed as

Cardiomyopathy, DilatedGenetic Predisposition to DiseaseGermanyHumansIncidenceRisk FactorsSurvival AnalysisSurvival Rate

Identifiers

PMID23011600
OpenAlexW3190533690

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.