Evidence map›Paper›PMID 22936369›Full record

ReviewHerz2012

Genetics and metabolic cardiomyopathies.

E C Wicks, P M Elliott

Abstract readReview
PubMed Publisher
In one paragraph

Review in Herz, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Chromosomal regulation by MeCP2: structural and enzymatic considerations.Cellular and molecular life sciences : CMLS · 2004
    Review
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.

E C WicksThe Heart Hospital, 16-18 Westmoreland Street, W1G 8PH, London, UK.
P M Elliott

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic disorders encompass a heterogeneous group of conditions that commonly affect the heart and contribute adversely to cardiovascular outcomes. As the heart is a metabolically active organ, inborn errors in metabolism (IEMs) often present with cardiac manifestations such as cardiomyopathy, arrhythmia, and valvular dysfunction. More than 40 IEMs are reported to cause cardiomyopathy, including fatty acid oxidation defects, glycogen, lysosomal and perioxisome storage diseases, mitochondrial cardiomyopathies, organic acidaemias, aminoacidopathies and congenital disorders of glycosylation. Studies suggest that IEM account for only 5% of cardiomyopathies; however, their diagnosis is imperative to enable the effective institution of disease-specific management strategies. This review describes the more common genetic defects that affect metabolic pathways and give rise to heart muscle disease.

Indexed as

Models, CardiovascularModels, GeneticCardiomyopathiesComputer SimulationGenetic Predisposition to DiseaseHeartHumansMetabolism, Inborn Errors

Identifiers

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.