Chronic stable angina guidelines for pharmacotherapy to improve prognosis and reduce symptoms

Editors-In-Chief: C. Michael Gibson, M.S., M.D. [mailto:mgibson@perfuse.org] Phone:617-632-7753; Associate Editor-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S.

Overview
ACC/AHA and ESC guidelines for the use pharmacotherapy in the management of chronic stable angina, to improve symptoms and/or releive ischemia and provide better prognosis.

==ACC/AHA Guidelines- Pharmacotherapy to Prevent MI and Death and Reduce Symptoms (DO NOT EDIT)  == {{cquote|

Class I
1. Aspirin should be started at 75 to 162 mg per day and continued indefinitely in all patients unless contraindicated. (Level of Evidence: A)

2. Aspirin in the absence of contraindication in patients with prior MI. (Level of Evidence: A)

3. Use of warfarin in conjunction with aspirin and/or clopidogrel is associated with an increased risk of bleeding and should be monitored closely. (Level of Evidence: B)

4. Calcium antagonists (short-acting dihydropyridine calcium antagonists should be avoided) and/or long-acting nitrates as initial therapy for reduction of symptoms when beta-blockers are contraindicated. (Level of Evidence: B)

5. Calcium antagonists (short-acting dihydropyridine calcium antagonists should be avoided) and/or long-acting nitrates in combination with beta-blockers when initial treatment with beta-blockers is not successful. (Level of Evidence: B)

6. Calcium antagonists (short-acting dihydropyridine calcium antagonists should be avoided) and/or long-acting nitrates as a substitute for beta-blockers if initial treatment with beta-blockers leads to unacceptable side effects. (Level of Evidence: C)

7. Sublingual nitroglycerin or nitroglycerin spray for the immediate relief of angina. (Level of Evidence: C)

8. It is beneficial to start and continue beta-blocker therapy indefinitely in all patients who have had MI, acute coronary syndrome, or left ventricular dysfunction with or without heart failure symptoms, unless contraindicated. (Level of Evidence: A)

9. Beta-blockers as initial therapy in the absence of contraindications in patients with prior MI. (Level of Evidence: B)

10. ACE inhibitors in all patients with significant coronary artery disease by angiography or previous myocardial infarction who also have diabetes and/or left ventricular systolic dysfunction. (Level of Evidence: A)

11. ACE inhibitors should be started and continued indefinitely in all patients with left ventricular ejection fraction less than or equal to 40% and in those with hypertension, diabetes, or chronic kidney disease unless contraindicated. (Level of Evidence: A)

12. ACE inhibitors should be started and continued indefinitely in patients who are not lower risk (lower risk defined as those with normal left ventricular ejection fraction in whom cardiovascular risk factors are well controlled and revascularization has been performed), unless contraindicated. (Level of Evidence: B)

13. Angiotensin receptor blockers are recommended for patients who have hypertension, have indications for but are intolerant of ACE inhibitors, have heart failure, or have had a myocardial infarction with left ventricular ejection fraction less than or equal to 40%. (Level of Evidence: A)

14. Aldosterone blockade is recommended for use in post-MI patients without significant renal dysfunction (creatinine should be less than 2.5 mg per dL in men and less than 2.0 mg per dL in women) or hyperkalemia (potassium should be less than 5.0 mEq per L) who are already receiving therapeutic doses of an ACE inhibitor and a beta blocker, have a left ventricular ejection fraction less than or equal to 40%, and have either diabetes or heart failure. (Level of Evidence: A)

15. 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)

16. Daily physical activity and weight management are recommended for all patients. (Level of Evidence: B)

17. 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)

18. 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)

19. 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. Clopidogrel when aspirin is absolutely contraindicated. (Level of Evidence: B)

2. Long-acting non-dihydropyridine calcium antagonists (short-acting dihydropyridine calcium antagonists should be avoided) instead of beta-blockers as initial therapy. (Level of Evidence: B)

3. ACE inhibitor in patients with coronary artery disease by angiography or previous myocardial infarction or other vascular disease. (Level of Evidence: B)

4. It is reasonable to use ACE inhibitors among lower-risk patients with mildly reduced or normal left ventricular ejection fraction in whom cardiovascular risk factors are well controlled and revascularization has been performed. (Level of Evidence: B)

5. 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)

6. 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)

7. 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)

8. 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)

9. 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. Angiotensin receptor blockers may be considered in combination with ACE inhibitors for heart failure due to left ventricular systolic dysfunction. (Level of Evidence: B)

2. 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)

Class III
1. Dipyridamole. (Level of Evidence: B)

2. Chelation therapy (intravenous infusions of ethylenediamine tetraacetic acid or EDTA) is not recommended for the treatment of chronic angina or arteriosclerotic cardiovascular disease and may be harmful because of its potential to cause hypocalcemia. (Level of Evidence: C)}}

==ESC Guidelines- Pharmacotherapy to Improve Prognosis (DO NOT EDIT) == {{cquote|

Class I
1. Aspirin 75 mg daily in all patients without speciﬁc contraindications (i.e., active GI bleeding, aspirin allergy, or previous aspirin intolerance). (Level of Evidence: A)

2. Oral beta-blocker therapy in patients post-MI or with heart failure. (Level of Evidence: A)

3. ACE-inhibitor therapy in patients with coincident indications for ACE-inhibition, such as hypertension, heart failure, LV dysfunction, prior MI with LV dysfunction, or diabetes. (Level of Evidence: A)

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

Class IIa
1. Clopidogrel as an alternative antiplatelet agent in patients with stable angina who cannot take aspirin (e.g., aspirin allergic). (Level of Evidence: B)

2. ACE-inhibitor therapy in all patients with angina and proven coronary disease. (Level of Evidence: B)

3. 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)}}

==ESC Guidelines- Pharmacotherapy to Improve Symptoms and/or Reduce Ischaemia in patients with stable angina (DO NOT EDIT) ==

{{cquote|

Class I
1. Provide short-acting nitroglycerin for acute symptom relief and situational prophylaxis, with appropriate instructions on how to use the treatment. (Level of Evidence: B)

2. Test the effects of a beta-1 blocker, and titrate to full dose; consider the need for 24 h protection against ischaemia. (Level of Evidence: A)

3. In case of beta-blocker intolerance or poor efﬁcacy attempt monotherapy with a CCB (Level of Evidence: A), long-acting nitrate (Level of Evidence: C), or nicorandil. (Level of Evidence: C)

4. If the effects of beta-blocker monotherapy are insufﬁcient, add a dihydropyridine CCB. (Level of Evidence: B)

Class IIa
1. In case of beta-blocker intolerance try sinus node inhibitor. (Level of Evidence: B)

2. If CCB monotherapy or combination therapy (CCB with beta-blocker) is unsuccessful, substitute the CCB with a long-acting nitrate or nicorandil. Be careful to avoid nitrate tolerance. (Level of Evidence: C)

Class IIb
1. Metabolic agents may be used, where available, as add-on therapy, or as substitution therapy when conventional drugs are not tolerated. (Level of Evidence: B)}}

Vote on and Suggest Revisions to the Current Guidelines

 * The Chronic Stable Angina Living Guidelines: Vote on current recommendations and suggest revisions to the guidelines

Guidelines Resource

 * The ACC/AHA/ACP–ASIM Guidelines for the Management of Patients With Chronic Stable Angina


 * The ACC/AHA 2002 Guideline Update for the Management of Patients With Chronic Stable Angina


 * Guidelines on the management of stable angina pectoris: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology


 * The 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable Angina