Statins are a panacea for secondary prevention of atherosclerotic cardiovascular disease and primary prevention in high-risk individuals. They are very well tolerated and side effects like muscle toxicity and increased risk of new onset of diabetes are seen in a minority of cases. They are also recommended in diabetic patient because the benefit is many times more than the risk of diabetes. Statins reduce total cholesterol, LDL cholesterol, Apo B, non-HDL cholesterol, and triglycerides, and also increase high-density lipoprotein (HDL) cholesterol levels in most patients with hypercholesterolemia and combined hyperlipidemia. Statins are not indicated in individuals with Frederickson Class I and V hyperlipidemias. Extensive literature supports use of statins in coronary heart disease (CHD) patients for treatment of dyslipidemia and secondary prevention. It has also been recognized that in secondary prevention and ACS populations lower LDL may be better. Trials have compared moderate with more robust LDL-C reduction, using maximum doses of atorvastatin or simvastatin. Available statins differ in their ability to reduce atherogenic lipoproteins and raise the level of high-density lipoprotein (HDL) cholesterol. Depending on dose used and specific statin, LDL cholesterol reduction of 18% to 55% can be expected. Atorvastatin and rosuvastatin are the most potent statins for lowering LDL-C cholesterol levels, yielding average reductions that approach 50% for atorvastatin and exceed 50% for rosuvastatin at the highest dose. Reduction in triglycerides with statins ranges from 7% to 30%, and is higher in hypertriglyceridemic populations and at higher statin doses. HDL levels usually rise by 5% to 10%. No consistent dose response relationship between statin dose and degree of HDL increase is seen.
Published in |
American Journal of Internal Medicine (Volume 9, Issue 2)
This article belongs to the Special Issue Dyslipidemia: Flash Back and Vision Ahead |
DOI | 10.11648/j.ajim.20210902.13 |
Page(s) | 76-82 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
Copyright |
Copyright © The Author(s), 2021. Published by Science Publishing Group |
Dyslipidemia, Statin, Atherosclerosis
[1] | GBD 2013 Risk factors Collaborators. Global, regional, and national comparative risk assessment of 79 behavioral, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet2015; 386: 2287-2323. |
[2] | Yusuf S, Hawken S, Ounpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004; 364: 937-52. |
[3] | O’Donnell MJ, Xavier D, Liu L, et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study. Lancet 2010; 376: 112-23. |
[4] | Weir HK, Anderson RN, Coleman King SM, et al. Heart disease and cancer deaths—trends and projections in the United States, 1969-2020. Prev Chronic Dis. 2016; 13: E157. |
[5] | Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356 222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT) JAMA. 1986; 256: 2823–8. |
[6] | Kannel WB, Castelli WP, Gordon T, et al. Serum cholesterol, lipoproteins, and the risk of coronary heart disease. The Framingham study. Ann Intern Med. 1971; 74: 1–12. |
[7] | 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. |
[8] | 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. |
[9] | Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC /AACVPR/ AAPA/ABC/ ACPM/ADA/ AGS/APhA/ ASPC/NLA/PCNA guideline on the management of blood cholesterol: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2018 Nov 10 [E-pub ahead of print]. |
[10] | Veerkamp MJ, de Graaf J, Bredie SJ, Hendriks JC, Demacker PN, Stalenhoef AF. Diagnosis of familial combined hyperlipidemia based on lipid phenotype expression in 32 families: results of a 5-year follow-up study. Arterioscler Thromb VascBiol 2002; 22: 274-282. |
[11] | Cuchel M, Bruckert E, Ginsberg HN, Raal FJ, Santos RD, Wiklund O, Chapman MJ, et al. European Atherosclerosis Society Consensus Panel on Familial Hypercholesterolaemia. Homozygous familial hypercholesterolaemia: new insights and guidance for clinicians to improve detection and clinical management. A position paper from the Consensus Panel on Familial Hypercholesterolaemia of the European Atherosclerosis Society. Eur HeartJ2014; 35: 2146-2157. |
[12] | Wiegman A, Gidding SS, Watts GF, Chapman MJ, Ginsberg HN, Cuchel M, et al. European Atherosclerosis Society Consensus Panel. Familial hypercholesterolaemia in children and adolescents: gaining decades of life by optimizing detection and treatment. Eur Heart J 2015; 36: 2425-2437. |
[13] | Moulin P, Dufour R, Averna M, Arca M, Cefalu AB, Noto D, D’Erasmo L, Di Costanzo A, Marcais C, Alvarez-Sala Walther LA, Banach M, Boren J, Cramb R, Gouni-Berthold I, Hughes E, Johnson C, Pinto X, Reiner Z, van Lennep JR, Soran H, Stefanutti C, Stroes E, Bruckert E. Identification and diagnosis of patients with familial chylomicronaemia syndrome (FCS): expert panel recommendations and proposal of an "FCS score". Atherosclerosis 2018; 275: 265_272. |
[14] | Meyers CD, Tremblay K, Amer A, Chen J, Jiang L, Gaudet D. Effect of the DGAT1 inhibitor pradigastat on triglyceride and apoB48 levels in patients with familial chylomicronemia syndrome. Lipids Health Dis 2015; 14: 8. |
[15] | Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2011; 123: 2292–333. |
[16] | 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. |
[17] | Amarenco P, Bogousslavsky J, Callahan A 3rd, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. 2006; 355: 549–59. |
[18] | Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe added to statin therapy after acute coronary syndromes. N Engl J Med. 2015; 372: 2387–97. |
[19] | Parker BA, Capizzi JA, Grimaldi AS, et al. Effect of statins on skeletal muscle function. Circulation. 2013; 127: 96–103. |
[20] | Navarese EP, Buffon A, Andreotti F, et al. Meta-analysis of impact of different types and doses of statins on new-onset diabetes mellitus. Am J Cardiol. 2013; 111: 1123–30. |
[21] | Preiss D, Seshasai SR, Welsh P, Murphy SA, Ho JE, Waters DD, DeMicco DA, Barter P, Cannon CP, Sabatine MS, Braunwald E, Kastelein JJ, de Lemos JA, Blazing MA, Pedersen TR, Tikkanen MJ, Sattar N, Ray KK. Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a metaanalysis. JAMA 2011; 305: 2556-2564. |
[22] | Waters DD, Ho JE, Boekholdt SM, DeMicco DA, Kastelein JJ, Messig M, Breazna A, Pedersen TR. Cardiovascular event reduction versus new-onset diabetes during atorvastatin therapy: effect of baseline risk factors for diabetes. J Am Coll Cardiol 2013; 61: 148-152. |
APA Style
Satyavir Yadav, Sundeep Mishra, Rajeev Agarwala. (2021). Statins: The Backbone of Treatment of Dyslipidemia. American Journal of Internal Medicine, 9(2), 76-82. https://doi.org/10.11648/j.ajim.20210902.13
ACS Style
Satyavir Yadav; Sundeep Mishra; Rajeev Agarwala. Statins: The Backbone of Treatment of Dyslipidemia. Am. J. Intern. Med. 2021, 9(2), 76-82. doi: 10.11648/j.ajim.20210902.13
AMA Style
Satyavir Yadav, Sundeep Mishra, Rajeev Agarwala. Statins: The Backbone of Treatment of Dyslipidemia. Am J Intern Med. 2021;9(2):76-82. doi: 10.11648/j.ajim.20210902.13
@article{10.11648/j.ajim.20210902.13, author = {Satyavir Yadav and Sundeep Mishra and Rajeev Agarwala}, title = {Statins: The Backbone of Treatment of Dyslipidemia}, journal = {American Journal of Internal Medicine}, volume = {9}, number = {2}, pages = {76-82}, doi = {10.11648/j.ajim.20210902.13}, url = {https://doi.org/10.11648/j.ajim.20210902.13}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajim.20210902.13}, abstract = {Statins are a panacea for secondary prevention of atherosclerotic cardiovascular disease and primary prevention in high-risk individuals. They are very well tolerated and side effects like muscle toxicity and increased risk of new onset of diabetes are seen in a minority of cases. They are also recommended in diabetic patient because the benefit is many times more than the risk of diabetes. Statins reduce total cholesterol, LDL cholesterol, Apo B, non-HDL cholesterol, and triglycerides, and also increase high-density lipoprotein (HDL) cholesterol levels in most patients with hypercholesterolemia and combined hyperlipidemia. Statins are not indicated in individuals with Frederickson Class I and V hyperlipidemias. Extensive literature supports use of statins in coronary heart disease (CHD) patients for treatment of dyslipidemia and secondary prevention. It has also been recognized that in secondary prevention and ACS populations lower LDL may be better. Trials have compared moderate with more robust LDL-C reduction, using maximum doses of atorvastatin or simvastatin. Available statins differ in their ability to reduce atherogenic lipoproteins and raise the level of high-density lipoprotein (HDL) cholesterol. Depending on dose used and specific statin, LDL cholesterol reduction of 18% to 55% can be expected. Atorvastatin and rosuvastatin are the most potent statins for lowering LDL-C cholesterol levels, yielding average reductions that approach 50% for atorvastatin and exceed 50% for rosuvastatin at the highest dose. Reduction in triglycerides with statins ranges from 7% to 30%, and is higher in hypertriglyceridemic populations and at higher statin doses. HDL levels usually rise by 5% to 10%. No consistent dose response relationship between statin dose and degree of HDL increase is seen.}, year = {2021} }
TY - JOUR T1 - Statins: The Backbone of Treatment of Dyslipidemia AU - Satyavir Yadav AU - Sundeep Mishra AU - Rajeev Agarwala Y1 - 2021/03/09 PY - 2021 N1 - https://doi.org/10.11648/j.ajim.20210902.13 DO - 10.11648/j.ajim.20210902.13 T2 - American Journal of Internal Medicine JF - American Journal of Internal Medicine JO - American Journal of Internal Medicine SP - 76 EP - 82 PB - Science Publishing Group SN - 2330-4324 UR - https://doi.org/10.11648/j.ajim.20210902.13 AB - Statins are a panacea for secondary prevention of atherosclerotic cardiovascular disease and primary prevention in high-risk individuals. They are very well tolerated and side effects like muscle toxicity and increased risk of new onset of diabetes are seen in a minority of cases. They are also recommended in diabetic patient because the benefit is many times more than the risk of diabetes. Statins reduce total cholesterol, LDL cholesterol, Apo B, non-HDL cholesterol, and triglycerides, and also increase high-density lipoprotein (HDL) cholesterol levels in most patients with hypercholesterolemia and combined hyperlipidemia. Statins are not indicated in individuals with Frederickson Class I and V hyperlipidemias. Extensive literature supports use of statins in coronary heart disease (CHD) patients for treatment of dyslipidemia and secondary prevention. It has also been recognized that in secondary prevention and ACS populations lower LDL may be better. Trials have compared moderate with more robust LDL-C reduction, using maximum doses of atorvastatin or simvastatin. Available statins differ in their ability to reduce atherogenic lipoproteins and raise the level of high-density lipoprotein (HDL) cholesterol. Depending on dose used and specific statin, LDL cholesterol reduction of 18% to 55% can be expected. Atorvastatin and rosuvastatin are the most potent statins for lowering LDL-C cholesterol levels, yielding average reductions that approach 50% for atorvastatin and exceed 50% for rosuvastatin at the highest dose. Reduction in triglycerides with statins ranges from 7% to 30%, and is higher in hypertriglyceridemic populations and at higher statin doses. HDL levels usually rise by 5% to 10%. No consistent dose response relationship between statin dose and degree of HDL increase is seen. VL - 9 IS - 2 ER -