ReviewClinical cardiology2012
Genetics of coronary artery disease in the 21st century.
Review in Clinical cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses 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
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- Association of ANRIL polymorphisms with coronary artery disease: A systemic meta-analysis.Medicine · 2020Pooled it
- Association between Toll-like receptor 4 Asp299Gly polymorphism and coronary heart disease susceptibility.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Pooled it
- Comprehensive Analysis of Cardiovascular Diseases: Symptoms, Diagnosis, and AI Innovations.Bioengineering (Basel, Switzerland) · 2024Review
- The focal adhesion protein Testin modulates KCNE2 potassium channel β subunit activity.Channels (Austin, Tex.) · 2021Article
- Article
- Implications of ACE (I/D) Gene Variants to the Genetic Susceptibility of Coronary Artery Disease in Asian Indians.Indian journal of clinical biochemistry : IJCB · 2017Article
- Sports engagement and age at first myocardial infarction in men under 55 years of age.PloS one · 2017Article
- Genetics of coronary artery disease and myocardial infarction.World journal of cardiology · 2016Review
- Rationale, Design, and Methodological Aspects of the BUDAPEST-GLOBAL Study (Burden of Atherosclerotic Plaques Study in Twins-Genetic Loci and the Burden of Atherosclerotic Lesions).Clinical cardiology · 2015Article
- The Genetic Basis of Coronary Artery Disease and Atrial Fibrillation: A Search for Disease Mechanisms and Therapeutic Targets.Journal of cardiothoracic and vascular anesthesia · 2015Review
- The reduction of vascular disease risk mutations contributes to longevity in the Chinese population.Meta gene · 2014Article
- Towards a molecular systems model of coronary artery disease.Current cardiology reports · 2014Review
- Molecular sources of residual cardiovascular risk, clinical signals, and innovative solutions: relationship with subclinical disease, undertreatment, and poor adherence: implications of new evidence upon optimizing cardiovascular patient outcomes.Vascular health and risk management · 2013Review
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 1 institution in 1 country.
Funding
Abstract
Coronary artery disease (CAD) is still the number-one killer in the world, and clinical trials indicate that it is preventable. Mortality and morbidity can be reduced by at least 30% to 40% by treating known risk factors. Genetic susceptibility is claimed to account for 50% of predisposition. The challenge of preventing CAD in this century, as claimed by some investigators, will require a more comprehensive prevention and treatment of environmental and genetic risk factors. Part of that challenge has been met by genome-wide association studies, which have identified 36 genetic variants with increased risk for CAD. All of these genetic variants have reached genome-wide significance (5 × 10(-8) ) and replicate in independent populations with large sample sizes. More than 50% of these variants occur in >50% of the population, with 10 occurring in >75% of the population. The challenge and the opportunity lie in the observation that >66% of these risk variants do not mediate their risk through known conventional risk factors. These results suggest that genetic predisposition for CAD is conferred by common DNA variants and many factors contributing to the pathogenesis of CAD are yet to be determined. Comprehensive prevention of CAD will most likely require combating genetic and environmental risk factors. We are on the cusp of genetic screening, and new therapeutic targets are becoming available to manage both genetic and environmental risk factors for CAD.
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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.