Genetic variants associated with Lp(a) lipoprotein level and coronary disease.

By R. Clarke, J. Peden, J. Hopewell, T. Kyriakou, A. Goel, S. Heath, S. Parish, S. Barlera, M. Franzosi, S. Rust and 13 more. New England Journal of Medicine, 2009

1,577 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/afb06e44c956a44da4262f87a863e55bada65ebe

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Citations in the corpus

Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of Atherothrombotic Disease. (2016, background): “This finding is consistent with triglycerides being associated with vascular risk through the cholesterol content of remnant particles.80 Recent genetic studies also support a causal role of triglyceride-mediated pathways in IHD.81 Lipoprotein(a) (Lp[a]) is an LDL cholesterol particle attached to an”
A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease (2015, positive): “The LPA SNPs have previously been shown to be strongly associated with CAD in candidate gene studies based on experimental genotype data 7,8 .”
Distribution and Medical Impact of Loss-of-Function Variants in the Finnish Founder Population (2014, methodology): “We adjusted the association for the composite LPA variant with a previously published risk variant (rs3798220) [22], but observed a similarly protective effect (N = 18,270, HR = 0.”
HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment (2013, background): “There is also evidence for a causal association between Lp(a) and CHD, with lower Lp(a) associated with lower CHD risk.(7) Niacin does, therefore, have multiple effects on lipid metabolism which might be beneficial.”
2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk. (2019, background): “In contrast, Mendelian randomization studies have consistently demonstrated that lifelong exposure to higher Lp(a) levels is strongly and causally associated with an increased risk of ASCVD.(74,75) While randomized trials evaluating therapies that lower Lp(a) by 20 30% (including niacin and CETP inh”
Diagnostic Yield of Sequencing Familial Hypercholesterolemia Genes in Severe Hypercholesterolemia (2016, background): “Manuscript received March 2, 2016; revised manuscript received March 22, Biology study (19), the ESP-EOMI (Exome Sequencing Project Early–Onset Myocardial Infarction) study (20), a nested case-control of the JHS (Jackson Heart Study) (21), the Munich Myocardial Infarction study (22), the Ottawa Hear”
Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement (2022, positive): “This was largely derived from Mendelian randomization studies which used genetic tools that strongly predict Lp(a) levels, including apo(a) isoforms determined by the number of K-IV repeats on Western blots,(118,119) the number or sum of K-IV repeats,(74,120) and SNPs (notably rs10455872 and rs37982”
Lipoprotein(a) as a cardiovascular risk factor: current status (2010, background): “Later in 2009, a further key paper on this topic including 8000 CHD cases and 8000 controls was published.(4) On the basis of”
Multivariable Mendelian Randomization: The Use of Pleiotropic Genetic Variants to Estimate Causal Effects (2015, positive): “factor are of interest; for example, in cardiovascular disease, the concentration of lipoprotein(a) and the size of lipoprotein(a) particles (7).”