[1. Fitzgerald K et al. A Highly Durable RNAi Therapeutic Inhibitor of PCSK9. N Engl J Med, 2017, 376(1):41-51.]Search in Google Scholar
[2. Abifadel M et al. Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. Nat Genet, 2003,34(2):154-6.]Search in Google Scholar
[3. Qiu C et al. What is the impact of PCSK9 rs505151 and rs11591147 polymorphisms on serum lipids level and cardiovascular risk: a meta-analysis. Lipids Health Dis, 2017,16(1):111.]Search in Google Scholar
[4. Cai G et al. The associations between proprotein convertase subtilisin/kexin type 9 E670G polymorphism and the risk of coronary artery disease and serum lipid levels: a meta-analysis. Lipids Health Dis, 2015,14:149.]Search in Google Scholar
[5. Adi D et al. Relationships between genetic polymorphisms of E670G in PCSK9 gene and coronary artery disease: a metaanalysis. Int J Clin Exp Med, 2015, 8(8):13251-8.]Search in Google Scholar
[6. Thygesen K, Alpert J, Jaffe A, et al. Third universal definition of myocardial infarction. Circulation. 2012;126;2020-35.]Search in Google Scholar
[7. Thygesen K, Alpert J, Jaffe A, et al. Fourth universal definition of myocardial infarction (2018). European Heart Journal. 2019; 40: 237-69.]Search in Google Scholar
[8. Mach F, Baigent C, Catapano A, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: the Tak Force for the management of Dyslipidaemias of the European Society of Cardiology {ESC} and European Atherosclerosis Society (EAS). European Heart Journal. 2020; 41: 111-88.]Search in Google Scholar
[9. Peterson AS, Fong LG, Young SG. PCSK9 function and physiology. J Lipid Res, 2008,49(7):1595-9.6.]Search in Google Scholar
[10. Stein R, Ferrari F, Scolari F, Genetics, Dyslipidemia, and Cardiovascular Disease: New Insights. Curr Cardiol Rep, 2019,21(8):68.7.]Search in Google Scholar
[11. Mega JL et al. Genetic risk, coronary heart disease events, and the clinical benefit of statin therapy: an analysis of primary and secondary prevention trials. Lancet, 2015,385(9984): 2264-2271.8.]Search in Google Scholar
[12. McPherson R, Tybjaerg-Hansen. Generics of Coronary Artery Disease. Circulation Research. 2016; 118: 564-78.]Search in Google Scholar
[13. Findley A, Richards A, Petrini C, et al. Interpreting coronary artery disease risk through gene-environment interactions in gene regulation. Genetics. 2019; 213: 651-63.]Search in Google Scholar
[14. Findley A, Monziani A, Richards A, et al. Functional dynamic genetic effects on gene regulation are specific to particular cell types and environmental conditions. eLife. 2021; 10: e67077.]Search in Google Scholar
[15. Zhu L, Ji X, Jiang L, et al. Utility of genetic variants to predict prognosis in coronary artery disease patietns receiving statin treatment. Int J Clin Exp Pathol. 2017; 10: 8795-8803.]Search in Google Scholar
[16. Kathiresan, S. et al. Genome-wide association of early-onset myocardial infarction with single nucleotide polymorphisms and copy number variants. Nat Genet. 2009; 41, 334-41.]Search in Google Scholar
[17. Knuuti J, Wijns W, Saraste A, et al. 2019 ESC Guidleines for the diagnosis and management of chronic coronary syndromes: The Task Force for diagnosis and management of chronic coronary syndromes of the European Society of Cardiology (ESC). Eur Heart J. 2020; 41: 407-77.]Search in Google Scholar
[18. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidlienes for the management of acute myocardial infarction in patients presenting with CT segment elevation: The Task Force for the management of acute Myocardial infarction in patients presenting with ST – segment elevation of the European Society of Cardiology.Eur Heart J, 2018; 39: 119-77.]Search in Google Scholar
[19. Collet J, Thiele H, Barbato E, et al. 2020 ESC Guideliens for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). 2021; 42: 1289-1367]Search in Google Scholar
[20. Lloyd-Jones DM et al. Lifetime risk of coronary heart disease by cholesterol levels at selected ages. Arch Intern Med, 2003,163(16): 1966-72.9.]Search in Google Scholar
[21. Kathiresan S et al. A genome-wide association study for blood lipid phenotypes in the Framingham Heart Study. BMC Med Genet, 2007,8 Suppl 1: S17.10.]Search in Google Scholar
[22. Zhou Li, He M, Mo Z, et al. A genome wide association study identifies common variants associated with lipid levels in the Chinese population. PLoS One. 2013; 8(12): e82420.]Search in Google Scholar
[23. Teslovich TM et al. Biological, clinical and population relevance of 95 loci for blood lipids. Nature, 2010.,466(7307):707-13. 11.]Search in Google Scholar
[24. Guella I et al. Effects of PCSK9 genetic variants on plasma LDL cholesterol levels and risk of premature myocardial infarction in the Italian population. J Lipid Res, 2010,51(11):3342-9.12.]Search in Google Scholar
[25. Willer CJ et al. Newly identified loci that influence lipid concentrations and risk of coronary artery disease. Nat Genet, 2008,40(2):161-9.13.]Search in Google Scholar
[26. Schunkert H et al. Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease. Nat Genet, 2011,43(4):333-8.14.]Search in Google Scholar
[27. Waterworth DM et al. Genetic variants influencing circulating lipid levels and risk of coronary artery disease. Arterioscler Thromb Vasc Biol, 2010,30(11):2264-76. 15.]Search in Google Scholar
[28. Kathiresan S et al. Common variants at 30 loci contribute to polygenic dyslipidemia. Nat Genet, 2009,41(1):56-65. 16.]Search in Google Scholar
[29. Reilly MP et al. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies. Lancet, 2011,377(9763):383-92.17.]Search in Google Scholar
