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Coronary heart disease secondary prevention lipid management

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

2011 AHA/ACCF Guidelines for Secondary Prevention and Risk Reduction Therapy for Patients with Coronary and other Atherosclerotic Vascular Disease (DO NOT EDIT) [1]

2011 AHA/ACCF Guidelines for Secondary Prevention and Risk Reduction Therapy for Patients with Coronary and other Atherosclerotic Vascular Disease (DO NOT EDIT) [1]

Lipid Management (DO NOT EDIT) [1]

“ Goal: Treatment with statin therapy; use statin therapy to achieve an LDL-C of <100 mg/dL; for very high risk* patients an LDL-C <70 mg/dL is reasonable; if triglycerides are ≥200 mg/dL, non–HDL-C† should be <130 mg/dL, whereas non–HDL-C <100 mg/dL for very high risk patients is reasonable. ”
Class I
“1. A lipid profile in all patients should be established, and for hospitalized patients, lipid-lowering therapy as recommended below should be initiated before discharge. [2] (Level of Evidence: B)”
“2. Lifestyle modifications including daily physical activity and weight management are strongly recommended for all patients. [3][4] (Level of Evidence: B)”
“3. Dietary therapy for all patients should include reduced intake of saturated fats (to <7% of total calories), transfatty acids (to <1% of total calories), and cholesterol (to <200 mg/d). [5][6][7][8][4] (Level of Evidence: B)”
“4. In addition to therapeutic lifestyle changes, statin therapy should be prescribed in the absence of contraindications or documented adverse effects. [9][10][11][12][4] (Level of Evidence: A)”
“5. An adequate dose of statin should be used that reduces LDL-C to <100 mg/dL AND achieves at least a 30% lowering of LDL-C. [9][10][11][12][4] (Level of Evidence: C)”
“6. Patients who have triglycerides ≥200 mg/dL should be treated with statins to lower non–HDL-C to <130 mg/dL. [9][10][11][13] (Level of Evidence: B)”
“7. Patients who have triglycerides >500 mg/dL should be started on fibrate therapy in addition to statin therapy to prevent acute pancreatitis. (Level of Evidence: C)”
Class IIa
“1. If treatment with a statin (including trials of higher-dose statins and higher-potency statins does not achieve the goal selected for a patient, intensification of LDL-C-lowering drug therapy with a bile acid sequestrant‡ or niacin§ is reasonable. [14][15][16] (Level of Evidence: B)”
“2. For patients who do not tolerate statins, LDL-C–lowering therapy with bile acid sequestrants‡ and/or niacin§ is reasonable. [17][18] (Level of Evidence: B)”
“3. It is reasonable to treat very high-risk* patients with statin therapy to lower LDL-C to <70 mg/dL. [10][11][12][19][20][19] (Level of Evidence: C)”
“4. In patients who are at very high risk* and who have triglycerides ≥200 mg/dL, a non–HDL-C goal of <100 mg/dL is reasonable. [9][10][11][13] (Level of Evidence: B)”
Class IIb
“1. The use of ezetimibe may be considered for patients who do not tolerate or achieve target LDL-C with statins, bile acid sequestrants‡ , and/or niacin§. (Level of Evidence:C) ”
“2. For patients who continue to have an elevated non–HDL-C while on adequate statin therapy , niacin§ or fibrate∥ therapy [15][21] (Level of Evidence:B) or fish oil (Level of Evidence:C) may be reasonable. ”
“3. For all patients, it may be reasonable to recommend omega-3 fatty acids from fish¶ or fish oil capsules (1 g/d) for cardiovascular disease risk reduction. [22][23][24] (Level of Evidence:B) ”
“ * Presence of established CVD plus (1) multiple major risk factors (especially diabetes), (2) severe and poorly controlled risk factors (especially continued cigarette smoking), (3) multiple risk factors of the metabolic syndrome (especially high triglycerides ≥200 mg/dL plus non–HDL-C ≥130 mg/dL with low HDL-C <40 mg/dL), and (4) patients with ACSs. ”
“ † Non–HDL-C is equal to total cholesterol minus HDL-C. ”
“ ‡ The use of bile acid sequestrants is relatively contraindicated when triglycerides are ≥200 mg/dL and is contraindicated when triglycerides are ≥500 mg/dL. ”
“ § Dietary supplement niacin must not be used as a substitute for prescription niacin. ”
“ ∥ The combination of high-dose statin plus fibrate (especially gemfibrozil) can increase risk for severe myopathy. Statin doses should be kept relatively low with this combination. ”
“ ¶ Pregnant and lactating women should limit their intake of fish to minimize exposure to methylmercury. ”
References

References

  1. ↑ 1.0 1.1 Smith SC, Benjamin EJ, Bonow RO, Braun LT, Creager MA, Franklin BA; et al. (2011). “AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients with Coronary and other Atherosclerotic Vascular Disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation”. Circulation. 124 (22): 2458–73. doi:10.1161/CIR.0b013e318235eb4d. PMID 22052934.
  2. ↑ Murphy SA, Cannon CP, Wiviott SD, McCabe CH, Braunwald E (2009). “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. 54 (25): 2358–62. doi:10.1016/j.jacc.2009.10.005. PMID 20082923. Unknown parameter |month= ignored (help)
  3. ↑ Dattilo AM, Kris-Etherton PM (1992). “Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis”. Am. J. Clin. Nutr. 56 (2): 320–8. PMID 1386186. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 4.2 4.3 “Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report”. Circulation. 106 (25): 3143–421. 2002. PMID 12485966. Unknown parameter |month= ignored (help)
  5. ↑ Ginsberg HN, Kris-Etherton P, Dennis B; et al. (1998). “Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: the DELTA Study, protocol 1”. Arterioscler. Thromb. Vasc. Biol. 18 (3): 441–9. PMID 9514413. Unknown parameter |month= ignored (help)
  6. ↑ Schaefer EJ, Lamon-Fava S, Ausman LM; et al. (1997). “Individual variability in lipoprotein cholesterol response to National Cholesterol Education Program Step 2 diets”. Am. J. Clin. Nutr. 65 (3): 823–30. PMID 9062535. Unknown parameter |month= ignored (help)
  7. ↑ Schaefer EJ, Lichtenstein AH, Lamon-Fava S; et al. (1995). “Efficacy of a National Cholesterol Education Program Step 2 diet in normolipidemic and hypercholesterolemic middle-aged and elderly men and women”. Arterioscler. Thromb. Vasc. Biol. 15 (8): 1079–85. PMID 7627699. Unknown parameter |month= ignored (help)
  8. ↑ Yu-Poth S, Zhao G, Etherton T, Naglak M, Jonnalagadda S, Kris-Etherton PM (1999). “Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis”. Am. J. Clin. Nutr. 69 (4): 632–46. PMID 10197564. Unknown parameter |month= ignored (help)
  9. ↑ 9.0 9.1 9.2 9.3 “MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial”. Lancet. 360 (9326): 7–22. 2002. doi:10.1016/S0140-6736(02)09327-3. PMID 12114036. Unknown parameter |month= ignored (help)
  10. ↑ 10.0 10.1 10.2 10.3 10.4 LaRosa JC, Grundy SM, Waters DD; et al. (2005). “Intensive lipid lowering with atorvastatin in patients with stable coronary disease”. N. Engl. J. Med. 352 (14): 1425–35. doi:10.1056/NEJMoa050461. PMID 15755765. Unknown parameter |month= ignored (help)
  11. ↑ 11.0 11.1 11.2 11.3 11.4 Pedersen TR, Faergeman O, Kastelein JJ; et al. (2005). “High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial”. JAMA. 294 (19): 2437–45. doi:10.1001/jama.294.19.2437. PMID 16287954. Unknown parameter |month= ignored (help)
  12. ↑ 12.0 12.1 12.2 Baigent C, Blackwell L, Emberson J; et al. (2010). “Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials”. Lancet. 376 (9753): 1670–81. doi:10.1016/S0140-6736(10)61350-5. PMC 2988224. PMID 21067804. Unknown parameter |month= ignored (help)
  13. ↑ 13.0 13.1 Robinson JG, Wang S, Smith BJ, Jacobson TA (2009). “Meta-analysis of the relationship between non-high-density lipoprotein cholesterol reduction and coronary heart disease risk”. J. Am. Coll. Cardiol. 53 (4): 316–22. doi:10.1016/j.jacc.2008.10.024. PMID 19161879. Unknown parameter |month= ignored (help)
  14. ↑ Zhao XQ, Brown BG, Hillger L; et al. (1993). “Effects of intensive lipid-lowering therapy on the coronary arteries of asymptomatic subjects with elevated apolipoprotein B”. Circulation. 88 (6): 2744–53. PMID 8252687. Unknown parameter |month= ignored (help)
  15. ↑ 15.0 15.1 Brown BG, Zhao XQ, Chait A; et al. (2001). “Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease”. N. Engl. J. Med. 345 (22): 1583–92. doi:10.1056/NEJMoa011090. PMID 11757504. Unknown parameter |month= ignored (help)
  16. ↑ Campeau L, Hunninghake DB, Knatterud GL; et al. (1999). “Aggressive cholesterol lowering delays saphenous vein graft atherosclerosis in women, the elderly, and patients with associated risk factors. NHLBI post coronary artery bypass graft clinical trial. Post CABG Trial Investigators”. Circulation. 99 (25): 3241–7. PMID 10385497. Unknown parameter |month= ignored (help)
  17. ↑ Canner PL, Berge KG, Wenger NK; et al. (1986). “Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin”. J. Am. Coll. Cardiol. 8 (6): 1245–55. PMID 3782631. Unknown parameter |month= ignored (help)
  18. ↑ “The Lipid Research Clinics Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease”. JAMA. 251 (3): 351–64. 1984. PMID 6361299. Unknown parameter |month= ignored (help)
  19. ↑ 19.0 19.1 Cannon CP, Braunwald E, McCabe CH; et al. (2004). “Intensive versus moderate lipid lowering with statins after acute coronary syndromes”. N. Engl. J. Med. 350 (15): 1495–504. doi:10.1056/NEJMoa040583. PMID 15007110. Unknown parameter |month= ignored (help)
  20. ↑ Cannon CP, Steinberg BA, Murphy SA, Mega JL, Braunwald E (2006). “Meta-analysis of cardiovascular outcomes trials comparing intensive versus moderate statin therapy”. J. Am. Coll. Cardiol. 48 (3): 438–45. doi:10.1016/j.jacc.2006.04.070. PMID 16875966. Unknown parameter |month= ignored (help)
  21. ↑ Robins SJ, Rubins HB, Faas FH; et al. (2003). “Insulin resistance and cardiovascular events with low HDL cholesterol: the Veterans Affairs HDL Intervention Trial (VA-HIT)”. Diabetes Care. 26 (5): 1513–7. PMID 12716814. Unknown parameter |month= ignored (help)
  22. ↑ Kris-Etherton PM, Harris WS, Appel LJ (2002). “Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease”. Circulation. 106 (21): 2747–57. PMID 12438303. Unknown parameter |month= ignored (help)
  23. ↑ Bucher HC, Hengstler P, Schindler C, Meier G (2002). “N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials”. Am. J. Med. 112 (4): 298–304. PMID 11893369. Unknown parameter |month= ignored (help)
  24. ↑ Mosca L, Benjamin EJ, Berra K; et al. (2011). “Effectiveness-based guidelines for the prevention of cardiovascular disease in women–2011 update: a guideline from the american heart association”. Circulation. 123 (11): 1243–62. doi:10.1161/CIR.0b013e31820faaf8. PMC 3182143. PMID 21325087. Unknown parameter |month= ignored (help)


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