Evidence map›Paper›PMID 18803426›Full record

ReviewMolecular diagnosis & therapy2008

Molecular signatures of cardiovascular disease risk: potential for test development and clinical application.

Heribert Schunkert, Inke R König, Jeanette Erdmann

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular diagnosis & therapy, 2008. 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
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. 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

3 authors.

Heribert SchunkertMedicine Clinic II, University of Lübeck, Lübeck, Germany. heribert.schunker@uk-sh.de
Inke R König
Jeanette Erdmann

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most cardiovascular diseases are multifactorial by etiology. As an example, the development of myocardial infarction is promoted by numerous risk factors, ranging from rather modifiable lifestyle habits (e.g. smoking, physical activity) to genetic predisposition. With respect to the latter, 15 years of candidate gene analyses have failed to explain the molecular basis for the genetic predisposition to myocardial infarction. By contrast, recent genome-wide association studies have identified chromosomal loci that reproducibly displayed some association with myocardial infarction risk. When molecular genetic studies of coronary artery disease were first begun, it was assumed that genetic factors would soon be routinely incorporated into risk prediction scores. A number of biomarkers have been identified and tested in combination with the classical risk factors for refined risk prediction. However, the strategy for individualized risk prediction by incorporation of new biomarkers in established scores has so far proven to be more difficult than at first hoped.

Indexed as

Genetic MarkersGenetic Predisposition to DiseaseCardiovascular DiseasesGenome, HumanHumansMolecular Diagnostic TechniquesMyocardial InfarctionPhenotypeRisk FactorsGenetic Markers

Identifiers

PMID18803426

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.