Evidence map›Paper›PMID 20347790›Full record

ReviewHeart failure clinics2010

The genetics of congestive heart failure.

Calum A MacRae

Abstract readReview
In one paragraph

Review in Heart failure clinics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

5 citing papers in PubMed.

  1. Article
  2. DNA methylation reprograms cardiac metabolic gene expression in end-stage human heart failure.American journal of physiology. Heart and circulatory physiology · 2019
    Article
  3. Article
  4. Review
  5. 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

1 author.

Calum A MacRaeCardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA. camacrae@bics.bwh.harvard.edu

Funding

The Genetic Basis of Lone Atrial FibrillationR01HL075431 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MACRAE, CALUM A. · 2005 to 2008
$1.5M
Development of a High-throughput Integrated In Vivo Heart Failure AssayR01HL109264 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MACRAE, CALUM A. · 2012 to 2014
$1.3M
Functional evaluation of GWAS loci for cardiovascular intermediate phenotypesR21HL098938 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MACRAE, CALUM A. · 2009 to 2010
$1.1M
NHLBI NIH HHS R01 HL075431NHLBI NIH HHS R01 HL109264NHLBI NIH HHS R21 HL098938
6 · The paper itself

Abstract

The heart failure syndrome is known to represent a final common pathway for a broad range of etiologies, but there is tremendous variation in the propensity to develop congestive heart failure after a given insult. This variation is thought to result in part from inherited differences in myocardial, vascular or systemic responses, but the nature of the underlying traits responsible ultimately for the development of heart failure has remained elusive. There has been limited progress in the genetic exploration of the key clinical phenotype itself: heart failure. In this article, the author attempts to place the results of genetic studies of cardiomyopathy in the broader context of the clinical syndrome of heart failure, highlighting some of the key questions for future study.

Indexed as

CardiomyopathiesGenome-Wide Association StudyHeart FailureHumansPhenotypeRisk FactorsSyndrome

Identifiers

PMID20347790
PMCPMC2847583

What OpenQuestion holds

Textmetadata
LicenceTDM
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.