ReviewCurrent atherosclerosis reports2007
Progress in unraveling the genetics of coronary artery disease and myocardial infarction.
Review in Current atherosclerosis reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed, 17 citations in OpenAlex.
- Genome-based exome sequencing analysis identifies GYG1, DIS3L and DDRGK1 are associated with myocardial infarction in Koreans.Journal of genetics · 2017Article
- Family coronary heart disease: a call to action.Clinical cardiology · 2010Article
- An evaluation of nine genetic variants related to metabolism and mechanism of action of warfarin as applied to stable dose prediction.Journal of thrombosis and thrombolysis · 2010Article
- Time trends in cardiovascular disease mortality in Russia and Germany from 1980 to 2007 - are there migration effects?BMC public health · 2010Article
- Joint effects of common genetic variants from multiple genes and pathways on the risk of premature coronary artery disease.American heart journal · 2010Article
- Role of somatic mutations in vascular disease formation.Expert review of molecular diagnostics · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a leading cause of morbidity and mortality. Coronary artery disease (CAD) and its clinical manifestation, myocardial infarction (MI), are equally determined by interacting environmental and (largely unknown) multigenic factors. Genome-wide and candidate gene searches for single nucleotide polymorphism (SNP) associations with CAD/MI (ie, coronary heart disease) often have resulted in nonreproducible or weak associations. Associations with intermediate surrogates have not ensured clinical event predictions. Linked SNP groups (haplotypes) can be more informative than individual SNPs unless the functional gene variant is known with certainty. Recent results of genetic association studies challenge the "common disease-common variant" hypothesis and suggest that multiple, relatively uncommon alleles often determine variation in coronary risk factors (eg, low high-density lipoprotein). Genetic risk scores, generated by considering several functional SNPs or haplotypes in multiple genes within a biologic pathway implicated in coronary heart disease, could improve predictive ability. Despite the complexity of coronary heart disease genetics, steady progress can be expected.
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.