ReviewCurrent cardiology reports2014
The role of genetic risk factors in coronary artery disease.
Review in Current cardiology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Meta-Analysis of Polymyositis and Dermatomyositis Microarray Data Reveals Novel Genetic Biomarkers.Genes · 2019Pooled it
- Association of fibrinogen and plasmin inhibitor, but not coagulation factor XIII gene polymorphisms with coronary artery disease.Journal of medical biochemistry · 2021Article
- Genetics of sudden cardiac death.Current cardiology reports · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Genome-wide association studies for coronary artery disease utilizing the case control association study approach has identified 50 genetic risk variants associated with coronary artery disease or myocardial infarction. All of these genetic variants are of genome wide significance and replicated in an independent population. It is of note that 35 of these 50 genetic risk variants act through mechanisms as yet unknown. These findings have great implications for the pathogenesis of atherosclerosis, as well as new targets for the development of novel therapies for the prevention and treatment of CAD. The genetic variant PCSK9 has already led to the development of a monoclonal anti-body which is undergoing assessment in phases I, II, and III clinical trials. This therapy shows very promising results and since it increases removal of LDL-C, it is complementary to current statin therapy. Assessing the beneficial or deleterious effects of a lifelong exposure to a genetic risk variant (Mendelian randomization) will be an important adjunct to clinical trials.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.