SynthesisCirculation2018
LPA Variants Are Associated With Residual Cardiovascular Risk in Patients Receiving Statins.
Synthesis in Circulation, 2018. The graph read 1 number from its abstract, feeding 1 cell of the map, but none could be read as for or against, so it casts no vote. It also reports an association that does not count as treatment evidence, such as OR 1.58 (1.35 to 1.86) for lipids. Cited by 43 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.
Read, but not usablea number the graph found but could not read as for or against
The most significant association was for an intronic single nucleotide polymorphism within LPA/PLG (rs10455872; minor allele frequency, 0.069; odds ratio, 1.58; 95% confidence interval, 1.35-1.86; P=2.6×10 CONCLUSIONS: Genetic variations at the LPA locus are associated with CHD events during statin therapy independently of the extent of low-density lipoprotein cholesterol lowering.
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Where it lands on the map
Rows are treatments, columns are outcomes. The coloured squares are the cells this paper feeds, coloured by the vote it casts there. Click one to jump to what this paper adds to it.
What it adds to each cell
For every cell the paper feeds: the belief in the claim with and without this paper, and this paper's estimate drawn against every other readable study in the cell. The ringed dot is this paper.
Statins×lipids
No readable resultOpen on the map →What to test next →38 readable studies in this cell: 26 favour the treatment, 5 find no difference, 7 favour the comparator.
This paper's own estimate is on a different scale from the rest of the cell, so it is not drawn here.
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
43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 citations in OpenAlex.
- Integrative bioinformatics frameworks for abdominal aortic aneurysm using GWAS meta-analysis, biological network construction, and structural modeling.Scientific reports · 2025Pooled it
- Atherogenic Lipoproteins for the Statin Residual Cardiovascular Disease Risk.International journal of molecular sciences · 2022Pooled it
- Revealing the genetic architectures underlying organ-specific aging based on proteomic data.Nature communications · 2025Article
- Impact of clinical pharmacist-led pharmacotherapy on long-term outcomes in cardiovascular in-patients: A three-year cohort study.Medicine · 2025Observational
- Cardiovascular Implications of Lipoprotein(a) and its Genetic Variants: A Critical Review From the Middle East.JACC. Asia · 2025Review
- Novel lipid profiles and atherosclerotic cardiovascular disease risk: insights from a latent profile analysis.Lipids in health and disease · 2025Article
- Biomedical literature-based clinical phenotype definition discovery using large language models.Database : the journal of biological databases and curation · 2025Article
- Efficacy of Traditional Anti-lipidemic Drugs in Lowering Lipoprotein(a) Levels: A Systematic Review.Cureus · 2024Review
- Genetics and Pathophysiological Mechanisms of Lipoprotein(a)-Associated Cardiovascular Risk.Journal of the American Heart Association · 2024Review
- Article
- Improving reporting standards for phenotyping algorithm in biomedical research: 5 fundamental dimensions.Journal of the American Medical Informatics Association : JAMIA · 2024Article
- Haplotype of the Lipoprotein(a) Gene Variants rs10455872 and rs3798220 Is Associated with Parameters of Coagulation, Fibrinolysis, and Inflammation in Patients after Myocardial Infarction and Highly Elevated Lipoprotein(a) Values.International journal of molecular sciences · 2024Article
- Lipoprotein (a) as a Biomarker for Cardiovascular Diseases and Potential New Therapies to Mitigate Risk.Current vascular pharmacology · 2024Review
- Assessment of Apolipoprotein(a) Isoform Size Using Phenotypic and Genotypic Methods.International journal of molecular sciences · 2023Review
- Baseline Lipoprotein(a) Levels and Long-Term Cardiovascular Outcomes After Acute Myocardial Infarction.Journal of Korean medical science · 2023Article
- Genetic Factors for Coronary Heart Disease and Their Mechanisms: A Meta-Analysis and Comprehensive Review of Common Variants from Genome-Wide Association Studies.Diagnostics (Basel, Switzerland) · 2022Review
- How Do Lipoprotein(a) Concentrations Affect Clinical Outcomes for Patients With Stable Coronary Artery Disease Who Underwent Different Dual Antiplatelet Therapy After Percutaneous Coronary Intervention?Journal of the American Heart Association · 2022Article
- GLUT4 gene rs5418 polymorphism is associated with increased coronary heart disease risk in a Uygur Chinese population.BMC cardiovascular disorders · 2022Article
- Treatment and prevention of lipoprotein(a)-mediated cardiovascular disease: the emerging potential of RNA interference therapeutics.Cardiovascular research · 2022Review
- Sex, age, and ethnic dependency of lipoprotein variants as the risk factors of ischemic heart disease: a detailed study on the different age-classes and genders in Tehran Cardiometabolic Genetic Study (TCGS).Biology of sex differences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors at 15 institutions in 3 countries.
Funding
Abstract
The marked sentences are the ones the graph read a number from.
backgroundCoronary heart disease (CHD) is a leading cause of death globally. Although therapy with statins decreases circulating levels of low-density lipoprotein cholesterol and the incidence of CHD, additional events occur despite statin therapy in some individuals. The genetic determinants of this residual cardiovascular risk remain unknown.
methodsWe performed a 2-stage genome-wide association study of CHD events during statin therapy. We first identified 3099 cases who experienced CHD events (defined as acute myocardial infarction or the need for coronary revascularization) during statin therapy and 7681 controls without CHD events during comparable intensity and duration of statin therapy from 4 sites in the Electronic Medical Records and Genomics Network. We then sought replication of candidate variants in another 160 cases and 1112 controls from a fifth Electronic Medical Records and Genomics site, which joined the network after the initial genome-wide association study. Finally, we performed a phenome-wide association study for other traits linked to the most significant locus.
resultsThe meta-analysis identified 7 single nucleotide polymorphisms at a genome-wide level of significance within the LPA/PLG locus associated with CHD events on statin treatment. The most significant association was for an intronic single nucleotide polymorphism within LPA/PLG (rs10455872; minor allele frequency, 0.069; odds ratio, 1.58; 95% confidence interval, 1.35-1.86; P=2.6×10
conclusionsGenetic variations at the LPA locus are associated with CHD events during statin therapy independently of the extent of low-density lipoprotein cholesterol lowering. This finding provides support for exploring strategies targeting circulating concentrations of lipoprotein(a) to reduce CHD events in patients receiving statins.
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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 Socratic graph.