Chronic stable angina treatment anti-lipid agents

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Phone:617-632-7753; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S.

Overview

Statins by inhibiting HMG-CoA reductase subsequently reduce serum cholesterol levels and hence have been shown to be effective in the primary prevention of various hyperlipidemias and secondary prevention of ischemic heart disease.[1][2] The most commonly used statins are simvastatin, atorvastatin, pravastatin and rosuvastatin. The incidence of major cardiovascular mortality was reduced by 30% with the use of simvastatin[1] and pravastatin[3][4] in patients with coronary artery disease and hence may be used for both primary and secondary prevention.[5] 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.[6]

Mechanisms of benefit

  • Statins competitively inhibit HMG-CoA reductase which is the rate-limiting enzyme of cholesterol synthesis and hence reduce intracellular cholesterol levels, subsequently, leading to increased clearance of serum LDL.[7] [5]
  • Direct evidence of statin-based cholesterol lowering effect on atherosclerosis was presented in the ASTEROID trial, which demonstrated reduction in LDL-C with accompanied significant increase in HDL-C and subsequently resulting in the regression of atheroma in patients with coronary artery disease.[8]
  • Statins have also been postulated to have anti-inflammatory and anti-thrombotic effects.[9] [10] [11] [12]
  • Improving endothelial function,
  • Modulate inflammatory responses,
  • Maintain plaque stability and
  • Prevent thrombus formation.
  • 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.[14]
  • 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.[3] [6] [15]

Indications

  • In all patients with coronary artery disease, statins are indicated both for primary and secondary prevention, irrespective of the serum cholesterol concentrations, owing to its property of reducing over-all cardiovascular mortality.[3][5][6][15]
  • Pre-treatment with atorvastatin in patients with stable angina was shown to reduce procedural myocardial injury, as assessed by biochemical markers.[14]
  • Two randomized placebo-controlled trials reported that the use of simvastatin 40 mg/day and atorvastatin 10 mg/day provided similar primary protection against major cardiovascular events in diabetic patients.[16] [15]

Drug interactions

Concomitant use of fibrate, antibiotics (such as clarithromycins and erythromycins), anti-fungals (such as ketaconazole and itraconazole with any of the statins, increase the risk of myopathy and rhabdomyolysis.[17]

ACC/AHA Guidelines- Pharmacotherapy to Prevent MI and Death and Reduce Symptoms (DO NOT EDIT) [18] [19] [20]

“

Class I

1. 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.

a. LDL-C should be less than 100 mg per dL. (Level of Evidence: A)
b. If baseline LDL-C is greater than or equal to 100 mg per 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-C levels. (Level of Evidence: A)
c. If on-treatment LDL-C is greater than or equal to 100 mg per dL, LDL-lowering drug therapy should be intensified. (Level of Evidence: A)
d. If TG are 200 to 499 mg per dL, non–HDL-C should be less than 130 mg per dL. (Level of Evidence: B)
e. If TG are greater than or equal to 500 mg per dL, therapeutic options to lower the TG to reduce the risk of pancreatitis are fibrate or niacin; these should be initiated before LDL-C lowering therapy. The goal is to achieve non–HDL-C less than 130 mg per dL if possible. (Level of Evidence: C)

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 IIa

1. 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.

a. Reduction of LDL-C to less than 70 mg per dL or high-dose statin therapy is reasonable. (Level of Evidence: A)
b. If baseline LDL-C is 70 to 100 mg per dL, it is reasonable to treat LDL-C to less than 70 mg per dL. (Level of Evidence: B)
c. Further reduction of non–HDL-C to less than 100 mg per dL is reasonable, if TG are greater than or equal to 200 to 499 mg per dL. (Level of Evidence: B)

4. Therapeutic options to reduce non–HDL-C are:

a. Niacin can be useful as a therapeutic option to reduce non–HDL-C (after LDL-C–lowering therapy) (Level of Evidence: B)
b. Fibrate therapy as a therapeutic option can be useful to reduce non–HDL-C (after LDL-C–lowering therapy). (Level of Evidence: B)

5. The following lipid management strategies can be beneficial:

a. If LDL-C less than 70 mg per dL is the chosen target, consider drug titration to achieve this level to minimize side effects and cost. When LDL-C less than 70 mg per dL is not achievable because of high baseline LDL-C levels, it generally is possible to achieve reductions of greater than 50% in LDL-C levels by either statins or LDL-C–lowering drug combinations. ((Level of Evidence: C)

Class IIb

1. 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)

”

ESC Guidelines- Pharmacological therapy to improve prognosis in patients with stable angina (DO NOT EDIT) [21]

“

Class I

1. Statin therapy for all patients with coronary disease. (Level of Evidence: A)

Class IIa

1. High dose statin therapy in high-risk (more than 2% annual CV mortality) patients with proven coronary disease. (Level of Evidence: B)

Class IIb

1. 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)

”

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 [18]
  • TheACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina [19]
  • The 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable Angina [20]
  • Guidelines on the management of stable angina pectoris: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology [21]

References

  1. ↑ 1.0 1.1 (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. ↑ Baigent C, Keech A, Kearney PM, Blackwell L, Buck G, Pollicino C et al. (2005) Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 366 (9493):1267-78. DOI:10.1016/S0140-6736(05)67394-1 PMID: 16214597
  3. ↑ 3.0 3.1 3.2 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
  4. ↑ (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
  5. ↑ 5.0 5.1 5.2 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
  6. ↑ 6.0 6.1 6.2 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
  7. ↑ Ma PT, Gil G, Südhof TC, Bilheimer DW, Goldstein JL, Brown MS (1986) Mevinolin, an inhibitor of cholesterol synthesis, induces mRNA for low density lipoprotein receptor in livers of hamsters and rabbits. Proc Natl Acad Sci U S A 83 (21):8370-4. PMID: 3464957
  8. ↑ Nissen SE, Nicholls SJ, Sipahi I, Libby P, Raichlen JS, Ballantyne CM et al. (2006) Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA 295 (13):1556-65. DOI:10.1001/jama.295.13.jpc60002 PMID: 16533939
  9. ↑ 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
  10. ↑ 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
  11. ↑ Rosenson RS, Tangney CC (1998) Antiatherothrombotic properties of statins: implications for cardiovascular event reduction. JAMA 279 (20):1643-50. PMID: 9613915
  12. ↑ 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
  13. ↑ Furberg CD (1999) Natural statins and stroke risk. Circulation 99 (2):185-8. PMID: 9892578
  14. ↑ 14.0 14.1 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
  15. ↑ 15.0 15.1 15.2 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
  16. ↑ Collins R, Armitage J, Parish S, Sleigh P, Peto R, Heart Protection Study Collaborative Group (2003) MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial. Lancet 361 (9374):2005-16. PMID: 12814710
  17. ↑ Graham DJ, Staffa JA, Shatin D, Andrade SE, Schech SD, La Grenade L et al. (2004) Incidence of hospitalized rhabdomyolysis in patients treated with lipid-lowering drugs. JAMA 292 (21):2585-90. DOI:10.1001/jama.292.21.2585 PMID: 15572716
  18. ↑ 18.0 18.1 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
  19. ↑ 19.0 19.1 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
  20. ↑ 20.0 20.1 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
  21. ↑ 21.0 21.1 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.


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