ReviewCurrent atherosclerosis reports2016
Genetics-Current and Future Role in the Prevention and Management of Coronary Artery Disease.
Review in Current atherosclerosis reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Polygenic Risk Based Detection and Treatment of Subclinical Coronary Atherosclerosis in the PROACT Clinical Trials.Journal of the American College of Cardiology · 2026Trial
- VEGF-A related SNPs: a cardiovascular context.Frontiers in cardiovascular medicine · 2023Review
- Mendelian Randomization Studies Promise to Shorten the Journey to FDA Approval.JACC. Basic to translational science · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewThe purpose of this study is to review genetic risk variants for coronary artery disease (CAD) and how they will change the management and prevention of CAD currently and in the future. RECENT
findingsThrough the efforts of international consortia, 58 genetic risk variants for CAD of genome-wide significance have been replicated in appropriate independent populations. Only one third of these variants mediate their risk through known conventional risk factors for CAD. Thus, unknown mechanisms contribute to CAD. Secondly, the genetic risk is proportional to the total number of risk variants rather than the intensity of any risk factor. Thirdly, the availability of the genetic risk variants enables one to perform Mendelian randomization (MR) studies since they are randomized at conception, not confounded, fixed for life, and can be used to determine if a risk factor is causative or just a marker. MR can also be used to determine the safety and efficacy of a gene product targeted for drug therapy. Genetic risk variants have been shown to successfully risk stratify for CAD in both primary and secondary preventions. Contrary to dogma, MR documents that plasma HDL-C is not protective of CAD. The use of genetic risk score (GRS) for CAD is shown to be more effective in risk stratifying for CAD than the Framingham risk score and independent of the conventional risk factors including family history. Furthermore, the GRS predicts the response to statin therapy in primary and secondary preventions. The use of GRS could represent a paradigm shift in the prevention of CAD.
Indexed as
Identifiers
27815829What 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.