ReviewHerz2025
[Role of genetics in precision medicine of coronary artery disease].
Review in Herz, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Clinical and Genetic Factors Associated with Multivessel Coronary Artery Disease: A Cross-Sectional Study of CYP2C19 Polymorphisms and Metabolic Comorbidities.International journal of general medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary artery disease (CAD) develops multifactorially through an interplay of lifestyle, environmental and genetic factors. Smoking, hypertension, hyperlipidemia, obesity and diabetes mellitus are modifiable risk factors for CAD. In addition, both rare mutations and multiple frequently occurring genetic variants can cause CAD, whereby the heritability of CAD is ca. 50%. Genetic diagnostics enable the early identification of affected children and adults and, based on a greatly increased cardiovascular risk, initiation of preventive treatment. In recent years, genome-wide association studies have identified hundreds of significant variants that together greatly increase the risk of CAD. In the general population the many frequently occurring risk alleles in combination with modifiable risk factors result in a widespread genetic predisposition to CAD. Their relevance arises in the context of an integrative risk assessment, whereby the additional genetic risk can be calculated by polygenic risk scores (PRS), which provide a hazard ratio that can be multiplied with the clinically determined risk. This overview article discusses the diagnostic principles of rare and frequent genetic causes of CAD as well as their implications in the precision treatment of the disease.
Indexed as
Identifiers
40019575What 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.