Skip to main content

Advertisement

SpringerLink
Log in

Comprehensive Lipid Management in the Coronary Artery Disease Patient

  • Published:
Current Cardiovascular Risk Reports Aims and scope Submit manuscript

Abstract

Low-density lipoprotein cholesterol (LDL-C) is the lipoprotein most implicated in atherosclerosis, and aggressive statin therapy remains the cornerstone of treatment. Adjunct therapies are often required to reach LDL-C goals, and recent studies have only fueled the debate over ezetimibe versus niacin. Alternate dosing regimens of high-potency statins can be used in those who cannot tolerate side effects. Residual risk may remain after LDL-C goals are achieved. Non–high-density lipoprotein cholesterol (non–HDL-C) must be calculated in patients with elevated triglycerides. Omega-3 fatty acids are most effective in lowering non–HDL-C. Low HDL-C levels can be raised with niacin, but clinical events may not be significantly reduced. Newer therapeutic targets, such as cholesteryl ester transfer protein (CETP) inhibitors, raise HDL-C and are being evaluated for safety and efficacy. Several ongoing, randomized controlled trials are investigating the relative efficacy of adjunctive therapies for reducing coronary heart disease events in high-risk patients.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

Papers of particular interest, published recently, have been highlighted as: • Of importance

  1. Lloyd-Jones D, Adams RJ, Brown TM, et al. Heart disease and stroke statistics—2010 update. Circulation. 2010;121:e46–e215.

    Article  PubMed  Google Scholar 

  2. Fletcher B, Berra K, Ades P, et al. Managing abnormal blood lipids: a collaborative approach. Circulation. 2005;112:3184–209.

    Article  PubMed  Google Scholar 

  3. Smith SC, Allen J, Blair SN, et al. AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease. Circulation. 2006;113:2363–72.

    Article  PubMed  Google Scholar 

  4. Hochholzer W, Giugliano RP. Lipid lowering goals: back to nature? Ther Adv Cardiovasc Dis. 2010;4:185–91.

    Article  PubMed  CAS  Google Scholar 

  5. Cannon CP, Braunwald E, McCabe CH, et al. Comparison of intensive and moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350:1495–502.

    Article  PubMed  CAS  Google Scholar 

  6. Lardizabal JA, Deedwania PC. Benefits of statin therapy and compliance in high risk cardiovascular patients. Vasc Health Risk Manag. 2010;6:843–53.

    PubMed  CAS  Google Scholar 

  7. Delles C, Dymott JA, Neisius U, et al. Reduced LDL-cholesterol levels in patients with coronary artery disease are paralleled by improved endothelial function: an observational study in patients from 2003 to 2007. Atherosclerosis. 2010;211:271–7.

    Article  PubMed  CAS  Google Scholar 

  8. LaRosa JC, Deedwania PC, Shepherd J, et al. Comparison of 80 versus 10 mg of atorvastatin on occurrence of cardiovascular events after the first event (from the Treating to New Targets [TNT] Trial). Am J Cardiol. 2010;105:283–7.

    Article  PubMed  CAS  Google Scholar 

  9. Pedersen TR, Faergeman O, Kastelein JJ, et al. High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction. The IDEAL study: a randomized controlled trial. JAMA. 2005;294:2437–45.

    Article  PubMed  CAS  Google Scholar 

  10. Pedersen TR, Cater NB, Faergeman O, et al. Comparison of atorvastatin 80 mg/day versus simvastatin 20 to 40 mg/day on frequency of cardiovascular events late (5 Years) after acute myocardial infarction (from the Incremental Decrease in End Points through Aggressive Lipid Lowering [IDEAL] Trial). Am J Cardiol. 2010;106:354–9.

    Article  PubMed  CAS  Google Scholar 

  11. Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) Collaborative Group, et al. Intensive Lowering of LDL Cholesterol with 80 mg versus 20 mg Simvastatin daily in 12,064 survivors of myocardial infarction: a double-blinded randomised trial. Lancet. 2010; 376: 1658–1669.

    Google Scholar 

  12. Munoz D, Blumenthal RS. Statins for secondary prevention: might less in fact be more? Nat Rev Endocrinol. 2011;7:131–2.

    Article  PubMed  CAS  Google Scholar 

  13. Degreef LE et al. The tolerability and efficacy of low-dose simvastatin in statin-intolerant patients. Eur J Intern Med. 2010;21:293–6.

    Article  PubMed  CAS  Google Scholar 

  14. • Silverman MG, Blaha MJ, Blumenthal RS. Adjunctive Lipid Lowering Therapy in the Era of Surrogate Endpoints. Cardiol Rev. 2011; 19: 17–22. Many clinicians are making clinical decisions based on the outcomes of surrogate endpoint trials. It is important to recognize the difference between surrogate and hard endpoints. This review calls to attention several adjunct lipid-lowering strategies and the possible shortcomings of surrogate endpoints.

  15. Howard WJ. The role of ezetimibe in the prevention of cardiovascular disease: where do we stand after ARBITER 6-HALTS. Nutr Metab Cardiovasc Dis. 2010;20:295–300.

    Article  PubMed  CAS  Google Scholar 

  16. Murphy SA, Cannon CP, Wiviott SD, et al. Reduction in recurrent cardiovascular events with intensive lipid-lowering statin therapy compared with moderate lipid-lowering statin therapy after acute coronary syndromes from the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) trial. J Am Coll Cardiol. 2009;54:2358–62.

    Article  PubMed  CAS  Google Scholar 

  17. LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352:1425–35.

    Article  PubMed  CAS  Google Scholar 

  18. Chapman MJ, Redfern JS, McGovern ME, et al. Niacin and fibrates in atherogenic dyslipidemia: pharmacotherapy to reduce cardiovascular risk. Pharmacol Ther. 2010;126:314–45.

    Article  PubMed  CAS  Google Scholar 

  19. • Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and Cardiovascular Risk: A Scientific Statement From the American Heart Association. Circulation. 2011; 123: 000–000. Published ahead of publication online at http://circ.ahajournals.org. The AHA recently released an adjustment to previous triglyceride guidelines. This statement is an important reference for clinicians and provides a biochemical and epidemiologic basis for current recommendations.

  20. The ACCORD Study Group. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362:1563–74.

    Article  Google Scholar 

  21. Jun M, Foote C, Lv J, et al. Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis. Lancet. 2010 May 29;375(9729):1875–84. Epub 2010 May 10.

  22. Blaha MJ, Blumenthal RS, Brinton EA, Jacobson TA; National Lipid Association Taskforce on Non-HDL Cholesterol. The importance of non-HDL cholesterol reporting in lipid management. J Clin Lipidol. 2008; 2:267–73. Epub 2008 Jun 28.

    Google Scholar 

  23. • Alla VM, Kaushik M, Mooss A. Targeting Residual Risk: The Rationale for the Use of Non-HDL Cholesterol. South Med J. 2010; 103: 434–437. Non–HDL-C is an important measure of atherogenic risk, and it should be measured for all CHD patients. This article provides a current review of the use of non–HDL-C.

  24. Lavie CJ, Milani RV, Mehra MR, et al. Omega-3 polyunsaturated fatty acids and cardiovascular diseases. J Am Coll Cardiol. 2009;54:585–94.

    Article  PubMed  CAS  Google Scholar 

  25. Roth EM, Harris WS. Fish oil for primary and secondary prevention of coronary heart disease. Curr Atheroscler Rep. 2010;12:66–72.

    Article  PubMed  CAS  Google Scholar 

  26. Zampelas A. Eicosapentaenoic acid (EPA) from highly concentrated n-3 fatty acid ethyl esters in incorporated into advanced atherosclerotic plaques and higher plaque EPA is associated with decreased plaque inflammation and increased stability. Atherosclerosis. 2010;212:34–5.

    Article  PubMed  CAS  Google Scholar 

  27. • Filion KB, El Khoury F, Bielinski M, et al. Omega-3 fatty acids in high-risk cardiovascular patients: a meta-analysis of randomized controlled trials. BMC Cardiovasc Disord. 2010; 10:24. Future research is targeting omega-3 fatty acids. This meta-analysis provides evidence for the importance of this group of therapies and further information for the provider with regards to use and effectiveness.

  28. Bays HE, McKenney J, Maki KC. Effects of prescription omega-3-acid ethyl esters on non-high-density lipoprotein cholesterol when coadministered with escalating doses of atorvastatin. Mayo Clin Proc. 2010;85:122–8.

    Article  PubMed  CAS  Google Scholar 

  29. Natarajan P, Ray KK, Cannon CP. High-density lipoprotein and coronary heart disease. J Am Coll Cardiol. 2010;55:1283–99.

    Article  PubMed  CAS  Google Scholar 

  30. Fazio S, Linton MF. High-density lipoprotein therapeutics and cardiovascular prevention. J Clin Lipidol. 2010;4:411–9.

    Article  PubMed  Google Scholar 

  31. Jaffer FA. Assessing niacin as an atherosclerosis therapeutic agent. J Am Coll Cardiol. 2009;54:1795–6.

    Article  PubMed  CAS  Google Scholar 

  32. Rubenfire M, Brook RD, Rosenson RS. Treating mixed hyperlipidemia and the atherogenic lipid phenotype for prevention of cardiovascular events. Am J Med. 2010;123:892–8.

    Article  PubMed  CAS  Google Scholar 

  33. Guyton JR. Combination regimens with statin, niacin, and intestinally active LDL-lowering drugs: alternatives to high-dose statin therapy? Curr Opin Lipidol. 2010;21:372–7.

    Article  PubMed  CAS  Google Scholar 

  34. Toth PP. Pharmacomodulation of high-density lipoprotein metabolism as a therapeutic intervention for atherosclerotic disease. Curr Cardiol Rep. 2010;12:481–7.

    Article  PubMed  Google Scholar 

  35. Tomlinson B. Raising high-density lipoprotein: for better or worse. Heart. 2010;96:1339–40.

    Article  PubMed  Google Scholar 

  36. Negi S, Ballantyne CM. Insights from recent meta-analysis: role of high-density lipoprotein cholesterol in reducing cardiovascular events and rates of atherosclerotic disease progression. J Clin Lipidol. 2010;4:365–70.

    Article  PubMed  Google Scholar 

  37. Brown BG, McBride R, Boden WE, Probstfield J. AIM HIGH: niacin plus statin to prevent vascular events. http://clinicaltrials.gov/ct/show/NCT00120289.

  38. • NIH stops clinical trial on combination cholesterol treatment. NIH News. May 26, 2011. http://public.nhlbi.nih.gov/newsroom/home/GetPressRelease.aspx?id=2792.Low HDL-C is a cardiovascular risk factor; however, the NIH prematurely halted a trial that was designed to raise HDL-C with niacin therapy. The formal results of the AIM HIGH trial are still in process. Niacin is used commonly as an adjunct therapy, but the clinician should be aware of possible controversies regarding its use.

  39. • Cannon CP, Shah S, Dansky HM, et al. Safety of Anacetrapib in Patients with or at High Risk for Coronary Heart Disease. N Engl J Med. 2010; 363: 2406–2415. Because low HDL-C is associated with higher CVD risk, many new therapies are designed to increase HDL-C. This new therapy is better tolerated than its earlier counterpart, and this article discusses the safety and efficacy of this medication. Future event-driven trials will further elucidate the effect of CETP inhibitors on CVD risk.

  40. Armitage J, Baigent C, Chen Z, Landray M. A randomized trial of the long-term clinical effects of raising HDL cholesterol with extended release niacin/laropiprant. http://clinicaltrials.gov/ct2/show/NCT00461630.

  41. Califf RM, Lokhnygina Y, Cannon CP, Stepanavage ME, McCabe CH, Musliner TA, et al. An update on the improved reduction of outcomes: vytorin efficacy international trial (IMPROVE-IT) design. Am Heart J. 2010;159(5):705–9.

    Article  PubMed  Google Scholar 

  42. Ben-Yehuda, O. Atorvastatin versus atorvastatin/ezetimibe in patients with hypo-response to initial dose statin therapy. http://clinicaltrials.gov/ct2/show/NCT00965055.

  43. Glueck C. Dose related decrease in triglycerides in patients with hypertriglyceridemia and treated with Lovaza. http://clinicaltrials.gov/ct2/show/NCT00934219.

  44. The ORIGIN Trial Investigators. Rationale, design, and baseline characteristics for a large international trial of cardiovascular disease prevention in people with dysglycemia: the ORIGIN trial (Outcome Reduction with an Initial Clargine Intervention). Am Heart J. 2008;155:26–32.

    Google Scholar 

Download references

Disclosure

No conflicts of interest relevant to this article were reported.

Author information

Authors and Affiliations

  1. The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, 600 North Wolfe Street Carnegie 568 Cardiology, Baltimore, MD, 21287, USA

    Nivee P. Amin, Michael J. Blaha, Grant V. Chow, Roger S. Blumenthal & Dominique Ashen

Authors
  1. Nivee P. Amin
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Michael J. Blaha
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Grant V. Chow
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Roger S. Blumenthal
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Dominique Ashen
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Nivee P. Amin.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Amin, N.P., Blaha, M.J., Chow, G.V. et al. Comprehensive Lipid Management in the Coronary Artery Disease Patient. Curr Cardiovasc Risk Rep 5, 399–406 (2011). https://doi.org/10.1007/s12170-011-0191-3

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s12170-011-0191-3

Keywords

Search

Navigation