p.44 抽出テキスト
Circulation. 2019;139:e1082–e1143. DOI: 10.1161/CIR.0000000000000625 June 18/25, 2019 e1125 CLINICAL STATEMENTS AND GUIDELINES S2.2-5. Di Angelantonio E, Sarwar N, Perry P, et al. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009;302:1993–2000. S2.2-6. Doran B, Guo Y, Xu J, et al. Prognostic value of fasting versus nonfasting low-density lipoprotein cholesterol levels on long-term mortality: insight from the National Health and Nutrition Examination Survey III (NHANES-III). Circulation. 2014;130:546–53. S2.2-7. Martin SS, Blaha MJ, Elshazly MB, et al. Friedewald-estimated versus directly measured low-density lipoprotein cholesterol and treatment implications. J Am Coll Cardiol. 2013;62:732–9. S2.2-8. Martin SS, Blaha MJ, Elshazly MB, et al. Comparison of a novel method vs the Friedewald equation for estimating low-density lipoprotein cholesterol levels from the standard lipid profile. JAMA. 2013;310:2061–8. S2.2-9. Sathiyakumar V, Park J, Golozar A, et al. Fasting versus nonfasting and low-density lipoprotein cholesterol accuracy. Circulation. 2018;137:10–9. S2.2-10. Nordestgaard BG, Langsted A, Mora S, et al. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points—a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. Eur Heart J. 2016;37:1944–58. S2.2-11. Mora S, Rifai N, Buring JE, et al. Fasting compared with nonfasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation. 2008;118:993–1001. S2.2-12. Brunzell JD, Albers JJ, Chait A, et al. Plasma lipoproteins in familial combined hyperlipidemia and monogenic familial hypertriglyceridemia. J Lipid Res. 1983;24:147–55. S2.2-13. Sniderman AD, Tremblay A, De Graaf J, et al. Phenotypes of hyper- triglyceridemia caused by excess very-low-density lipoprotein. J Clin Lipidol. 2012;6:427–33. 2.3 Measurements of Apolipoprotein B and Lipoprotein (a) S2.3-1. Sniderman AD, Williams K, Contois JH, et al. A meta-analysis of lowdensity lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes. 2011;4:337–45. S2.3-2. Grundy SM, Vega GL, Tomassini JE, et al. Correlation of non-highdensity lipoprotein cholesterol and low-density lipoprotein cholesterol with apolipoprotein B during simvastatin + fenofibrate therapy in patients with combined hyperlipidemia (a subanalysis of the SAFARI trial). Am J Cardiol. 2009;104:548–53. S2.3-3. Sniderman AD, Tremblay A, De Graaf J, et al. Phenotypes of hypertriglyceridemia caused by excess very-low-density lipoprotein. J Clin Lipidol. 2012;6:427–33. S2.3-4. Grundy SM, Vega GL, Tomassini JE, et al. Comparisons of apolipoprotein B levels estimated by immunoassay, nuclear magnetic resonance, vertical auto profile, and non-high-density lipoprotein cholesterol in subjects with hypertriglyceridemia (SAFARI Trial). Am J Cardiol. 2011;108:40–6. S2.3-5. Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2016 ACC expert consensus decision pathway on the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk: a report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol. 2016;68:92–125. S2.3-6. Tsimikas S. A Test in Context: Lipoprotein(a): diagnosis, prognosis, controversies, and emerging therapies. J Am Coll Cardiol. 2017;69:692–711. S2.3-7. Cook NR, Mora S, Ridker PM. Lipoprotein(a) and cardiovascular risk prediction among women. J Am Coll Cardiol. 2018;72:287–96. 2.4 Monitoring Response of LDL-C to Statin Therapy S2.4-1. Cholesterol Treatment Trialist’s (CTT) CollaborationBaigent C, Blackwell L, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170 000 participants in 26 randomised trials. Lancet. 2010;376:1670–81. S2.4-2. Boekholdt SM, Hovingh GK, Mora S, et al. Very low levels of ath- erogenic lipoproteins and the risk for cardiovascular events: a metaanalysis of statin trials. J Am Coll Cardiol. 2014;64:485–94. 3 THERAPEUTIC MODALITIES 3.1 Lifestyle Therapies 3.1.1 Diet Composition, Weight Control, and Physical Activity S3.1.1-1. Eckel RH, Jakicic JM, Ard JD, et al. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129:S76–99. S3.1.1-2. Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. Circulation. 2014;129:S102–38. S3.1.1-3. Estruch R, Ros E, Salas-Salvado J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368:1279–90. S3.1.1-4. Lichtenstein AH, Appel LJ, Brands M, et al. Summary of American Heart Association diet and lifestyle recommendations revision 2006. Arterioscler Thromb Vasc Biol. 2006;26:2186–91. S3.1.1-5. Warburton DE, Charlesworth S, Ivey A, et al. A systematic review of the evidence for Canada’s physical activity guidelines for adults. Int J Behav Nutr Phys Act. 2010;7:39. 3.1.2 Lifestyle Therapies and Metabolic Syndrome S3.1.2-1. Gami AS, Witt BJ, Howard DE, et al. Metabolic syndrome and risk of incident cardiovascular events and death: a systematic review and meta-analysis of longitudinal studies. J Am Coll Cardiol. 2007;49:403–14. S3.1.2-2. Kastelein JJ, Ginsberg HN, Langslet G, et al. ODYSSEY FH I and FH II: 78 week results with alirocumab treatment in 735 patients with heterozygous familial hypercholesterolaemia. Eur Heart J. 2015;36:2996–3003. S3.1.2-3. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640–5. S3.1.2-4. Grundy SM. Metabolic syndrome: a multiplex cardiovascular risk factor. J Clin Endocrinol Metab. 2007;92:399–404. S3.1.2-5. Aguilar M, Bhuket T, Torres S, et al. Prevalence of the metabolic syn- drome in the United States, 2003–2012 JAMA. 2015;313:1973–4. 3.2 Lipid-Lowering Drugs S3.2-1. Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and cardio- vascular disease: a scientific statement from the American Heart Association. Circulation. 2011;123:2292–333. 3.2.1 Statin Therapy S3.2.1-1. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129:S1–45. S3.2.1-2. Karlson BW, Wiklund O, Palmer MK, et al. Variability of low-density lipoprotein cholesterol response with different doses of atorvastatin, rosuvastatin, and simvastatin: results from VOYAGER. Eur Heart J Cardiovasc Pharmacother. 2016;2:212–7. S3.2.1-3. Pedersen TR, Faergeman O, Kastelein JJ, et al. High-dose atorv- astatin vs usual-dose simvastatin for secondary prevention after Downloaded from http://ahajournals.org by on October 7, 2026