Chronic stable angina treatment anti-lipid agents
Chronic stable angina Microchapters | ||
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Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
Diagnosis | ||
Alternative Therapies for Refractory Angina | ||
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Guidelines for Asymptomatic Patients | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Phone:617-632-7753; Associate Editor(s)-In-Chief: John Fani Srour, M.D.; Jinhui Wu, M.D.; Lakshmi Gopalakrishnan, M.B.B.S.
Overview
The incidence of major cardiovascular mortality was reduced by 30% with the use of simvastatin[1] and pravastatin[2][3] in patients with coronary artery disease and hence may be used for both primary and secondary prevention.[4] However, there are no trials specifically performed on patients with stable angina but they form a significant portion in other major trials studying the efficacy of lipid-lowering drugs on the overall mortality from cardiovascular events.[5]
Mechanisms of benefit
- Statins have also been postulated to have anti-inflammatory and anti-thrombotic effects.[6] [7] [8] [9]
- The non-lipid properties of statins have shown to provide myocardial protection and hence lower the risk of procedural myocardial injury in elective coronary intervention. Such short-term myocardial protection is achieved by pre-treatment with atorvastatin 40mg/day for 7 days.[10]
- Long-term statin therapy have shown to reduce major cardiovascular events such as MI, stroke, and risk of revascularization in patients with different serum cholesterol levels.[2] [5] [11]
Anti-lipid agents
If baseline LDL-Cholesterol is ≥100 mg/dL, LDL lowering drug therapy should be initiated in addition to therapeutic lifestyle changes. When LDL lowering medications are used in high risk or moderately high risk persons, it is recommended that intensity of therapy be sufficient to achieve a 30% to 40% reduction in LDL-Cholesterol levels.
If baseline LDL-C is 70 to 100 mg/dL, it is reasonable to treat LDL-C to <70 mg/dL. If on-treatment LDL-C is ≥100 mg/dL, LDL lowering drug therapy should be intensified.
If Triglycerides are 200-499 mg/dL, the sum of non–HDL-Cholesterol levels should be <130 mg/dL. Moreover this, further reduction of non–HDL Cholesterol to <100 mg/dL is reasonable, if Triglycerides are ≥200 to 499 mg/dL.
Therapeutic options to reduce non–HDL-C are: ’’’Niacin”’ can be useful as a therapeutic option to reduce non–HDL-C (after LDL-C lowering therapy) or ’’’Fibrate”’ therapy as a therapeutic option can be useful to reduce non–HDL-C (after starting to LDL-C–lowering therapy).
If Triglycerides are ≥500 mg/dL, therapeutic options to lower the Triglycerides to reduce the risk of pancreatitis are fibrate or niacin; these should be initiated before LDL-Choesterol lowering therapy. The goal is to achieve non–HDL-C <130 mg/dL if possible.
If LDL-Cholesterol <70 mg/dL is the chosen target, consider drug titration to achieve this level to minimize side effects and cost of therapy. When LDL-Cholesterol level of <70 mg/dL is not achievable because of high baseline LDL-Cholesterol levels, it is generally possible to achieve reductions of >50% in LDL-Cholesterol levels by either statins or any other LDL-Cholesterol –lowering drug combinations. Treatment with anti lipid drug combinations is beneficial for patients on lipid lowering therapy who are unable to achieve LDL-Cholesterol <100 mg/dL.
ACC/AHA Guidelines- Pharmacotherapy to Prevent MI and Death and Reduce Symptoms (DO NOT EDIT) [12] [13] [14]
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Class I1. Dietary therapy for all patients should include reduced intake of saturated fats (to less than 7% of total calories), transfatty acids, and cholesterol (to less than 200 mg per day). (Level of Evidence: B) 2. Daily physical activity and weight management are recommended for all patients. (Level of Evidence: B) 3. Recommended lipid management includes assessment of a fasting lipid profile.
4. Drug combinations are beneficial for patients on lipid lowering therapy who are unable to achieve LDL-C less than 100 mg per dL. (Level of Evidence: C) 5. Lipid-lowering therapy in patients with documented CAD and LDL-LDL cholesterol greater than 130 mg/dL with a target LDL of less than 100 mg/dL. (Level of Evidence: A) Class IIa1. Adding plant stanol or sterols (2 g per day) and/or viscous fiber (greater than 10 g per day) is reasonable to further lower LDL-C. (Level of Evidence: B) 2. Lipid-lowering therapy in patients with documented CAD and LDL cholesterol 100 to 129 mg/dL, with a target LDL of 100 mg/dL. (Level of Evidence: B) 3. Recommended lipid management includes assessment of a fasting lipid profile.
4. Therapeutic options to reduce non–HDL-C are:
5. The following lipid management strategies can be beneficial:
Class IIb1. For all patients, encouraging consumption of omega-3 fatty acids in the form of fish or in capsule form (1 g per day) for risk reduction may be reasonable. For treatment of elevated TG, higher doses are usually necessary for risk reduction. (Level of Evidence: B) |
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ESC Guidelines- Pharmacological therapy to improve prognosis in patients with stable angina (DO NOT EDIT) [15]
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Class I1. Statin therapy for all patients with coronary disease. (Level of Evidence: A) Class IIa1. High dose statin therapy in high-risk (more than 2% annual CV mortality) patients with proven coronary disease. (Level of Evidence: B) Class IIb1. Fibrate therapy in patients with low HDL and high triglycerides who have diabetes or the metabolic syndrome. (Level of evidence: B) 2. Fibrate or nicotinic acid as adjunctive therapy to statin in patients with low HDL and high triglycerides at high risk (more than 2% annual CV mortality). (Level of evidence: C) |
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Vote on and Suggest Revisions to the Current Guidelines
Sources
- The ACC/AHA/ACP–ASIM Guidelines for the Management of Patients With Chronic Stable Angina [12]
- TheACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina [13]
- The 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable Angina [14]
- Guidelines on the management of stable angina pectoris: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology [15]
References
- ↑ (1994) Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) Lancet 344 (8934):1383-9. PMID: 7968073
- ↑ 2.0 2.1 Sacks FM, Tonkin AM, Shepherd J, Braunwald E, Cobbe S, Hawkins CM et al. (2000) Effect of pravastatin on coronary disease events in subgroups defined by coronary risk factors: the Prospective Pravastatin Pooling Project. Circulation 102 (16):1893-900. PMID: 11034935
- ↑ (1998) Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. N Engl J Med 339 (19):1349-57. DOI:10.1056/NEJM199811053391902 PMID: 9841303
- ↑ 4.0 4.1 Grundy SM, Cleeman JI, Merz CN, Brewer HB, Clark LT, Hunninghake DB et al. (2004) Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. J Am Coll Cardiol 44 (3):720-32. DOI:10.1016/j.jacc.2004.07.001 PMID: 15358046
- ↑ 5.0 5.1 Heart Protection Study Collaborative Group (2002) 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. DOI:10.1016/S0140-6736(02)09327-3 PMID: 12114036
- ↑ Faggiotto A, Paoletti R (1999) State-of-the-Art lecture. Statins and blockers of the renin-angiotensin system: vascular protection beyond their primary mode of action. Hypertension 34 (4 Pt 2):987-96. PMID: 10523396
- ↑ Bonetti PO, Lerman LO, Napoli C, Lerman A (2003) Statin effects beyond lipid lowering--are they clinically relevant? Eur Heart J 24 (3):225-48. PMID: 12590901
- ↑ Rosenson RS, Tangney CC (1998) Antiatherothrombotic properties of statins: implications for cardiovascular event reduction. JAMA 279 (20):1643-50. PMID: 9613915
- ↑ Ridker PM, Cannon CP, Morrow D, Rifai N, Rose LM, McCabe CH et al. (2005) C-reactive protein levels and outcomes after statin therapy. N Engl J Med 352 (1):20-8. DOI:10.1056/NEJMoa042378 PMID: 15635109
- ↑ Pasceri V, Patti G, Nusca A, Pristipino C, Richichi G, Di Sciascio G et al. (2004) Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study. Circulation 110 (6):674-8. DOI:10.1161/01.CIR.0000137828.06205.87 PMID: 15277322
- ↑ Colhoun HM, Betteridge DJ, Durrington PN, Hitman GA, Neil HA, Livingstone SJ et al. (2004) Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet 364 (9435):685-96. DOI:10.1016/S0140-6736(04)16895-5 PMID: 15325833
- ↑ 12.0 12.1 Gibbons RJ, Chatterjee K, Daley J, Douglas JS, Fihn SD, Gardin JM et al. (1999)guidelines for the management of patients with chronic stable angina: executive summary and recommendations. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Chronic Stable Angina).Circulation 99 (21):2829-48. PMID: 10351980
- ↑ 13.0 13.1 Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS et al. (2003) ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Chronic Stable Angina). Circulation 107 (1):149-58. PMID: 12515758
- ↑ 14.0 14.1 Fraker TD, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J et al. (2007)2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina. Circulation 116 (23):2762-72.[1] PMID: 17998462
- ↑ 15.0 15.1 Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F; et al. (2006). "Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology". Eur Heart J. 27 (11): 1341–81. doi:10.1093/eurheartj/ehl001. PMID 16735367.