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Coronary heart disease secondary prevention

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

Overview

Overview

Patients who should be treated with secondary prevention are those with established atherosclerosis including peripheral artery disease; carotid artery disease; atherosclerotic aortic disease; diabetes and those with a Framingham Risk Score of > 20%. There are 12 aspects of secondary prevention: Smoking cessation; blood pressure control; lipid-lowering; increasing physical activity; weight loss; diabetes control; antiplatelet agents/anticoagulants; RAS blockers; beta-blockers; depression management; cardiac rehabilitation and influenza vaccine. Please note that secondary prevention guidelines, especially, those involving medication, may differ between UA/NSTEMI; STEMI; and Chronic Stable Angina. Please refer to appropriate page for more specific guidelines.

Target Population

Target Population

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

Overview

Patients who should be treated with secondary prevention are those with established atherosclerosis including peripheral artery disease; carotid artery disease; atherosclerotic aortic disease; diabetes and those with a Framingham Risk Score of > 20%.

2007 ACC/AHA Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction (DO NOT EDIT) [1]

Identification of Patients at Risk (DO NOT EDIT) [1]

Class I

“1. Patients with established CHD should be identified for secondary prevention efforts, and patients with a CHD risk equivalent (e.g., atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or 10-year risk greater than 20% as calculated by Framingham equations should receive equally intensive risk factor intervention as those with clinically apparent CHD. (Level of Evidence A)”

References

  1. ↑ 1.0 1.1 Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE, Chavey WE, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura R, Ornato JP, Page RL, Riegel B (2007). “ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine”. Journal of the American College of Cardiology. 50 (7): e1–e157. doi:10.1016/j.jacc.2007.02.013. PMID 17692738. Retrieved 2011-04-11. Unknown parameter |month= ignored (help)


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Patient Education

Patient Education

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

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2007 ACC/AHA Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction (DO NOT EDIT) [1]

Patient Education (DO NOT EDIT) [1]

Class I

” 1. Beyond the detailed instructions for daily exercise, patients should be given specific instruction on activities (e.g., heavy lifting, climbing stairs, yard work, and household activities) that are permissible and those that should be avoided. Specific mention should be made regarding resumption of driving, return to work, and sexual activity. (Level of Evidence: C)”

References

  1. ↑ 1.0 1.1 Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE, Chavey WE, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura R, Ornato JP, Page RL, Riegel B (2007). “ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine”. Journal of the American College of Cardiology. 50 (7): e1–e157. doi:10.1016/j.jacc.2007.02.013. PMID 17692738. Retrieved 2011-04-11. Unknown parameter |month= ignored (help)


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Smoking Cessation

Smoking Cessation

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]

Smoking Cessation (DO NOT EDIT) [1]

“ Goal: Complete cessation. No exposure to environmental tobacco smoke. ”
Class I
“1. Patients should be asked about tobacco use status at every office visit. [2][3][4][5][6] (Level of Evidence: B) ”
“2. Every tobacco user should be advised at every visit to quit. [4][5][6][7] (Level of Evidence: A) ”
“3. The tobacco user’s willingness to quit should be assessed at every visit. (Level of Evidence: C) ”
“4. Patients should be assisted by counseling and by development of a plan for quitting that may include pharmacotherapy and/or referral to a smoking cessation program. [4][5][8][6][9][7] (Level of Evidence: A) ”
“5. Arrangement for follow up is recommended. (Level of Evidence: C) ”
“6. All patients should be advised at every office visit to avoid exposure to environmental tobacco smoke at work, home, and public places. [10][11] (Level of Evidence: B) ”

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. ↑ Rothemich SF, Woolf SH, Johnson RE; et al. (2008). “Effect on cessation counseling of documenting smoking status as a routine vital sign: an ACORN study”. Ann Fam Med. 6 (1): 60–8. doi:10.1370/afm.750. PMC 2203392. PMID 18195316.
  3. ↑ Rosser W, McDowell I, Newell C (1992). “Documenting smoking Status: Trial of three strategies”. Can Fam Physician. 38: 1623–8. PMC 2146014. PMID 21221363. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 4.2 “Systems Change: Treating Tobacco Use and Dependence”.
  5. ↑ 5.0 5.1 5.2 Cummings SR, Coates TJ, Richard RJ; et al. (1989). “Training physicians in counseling about smoking cessation. A randomized trial of the “Quit for Life” program”. Ann. Intern. Med. 110 (8): 640–7. PMID 2930094. Unknown parameter |month= ignored (help)
  6. ↑ 6.0 6.1 6.2 “www.surgeongeneral.gov”.
  7. ↑ 7.0 7.1 Anthonisen NR, Skeans MA, Wise RA, Manfreda J, Kanner RE, Connett JE (2005). “The effects of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial”. Ann. Intern. Med. 142 (4): 233–9. PMID 15710956. Unknown parameter |month= ignored (help)
  8. ↑ Cummings SR, Richard RJ, Duncan CL; et al. (1989). “Training physicians about smoking cessation: a controlled trial in private practice”. J Gen Intern Med. 4 (6): 482–9. PMID 2685206.
  9. ↑ Duncan C, Stein MJ, Cummings SR (1991). “Staff involvement and special follow-up time increase physicians’ counseling about smoking cessation: a controlled trial”. Am J Public Health. 81 (7): 899–901. PMC 1405179. PMID 2053669. Unknown parameter |month= ignored (help)
  10. ↑ The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Rockville, MD: U.S. Dept. of Health and Human Services, Public Health Service, Office of the Surgeon General. 2006. ISBN 0-16-076152-2.
  11. ↑ Institute of Medicine; Committee on Secondhand Smoke Exposure and Acute Coronary Events (2010). Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence. Washington, D.C: National Academies Press. ISBN 0-309-13839-6.


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Blood Pressure Control

Blood Pressure Control

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

Overview

If a patient’s blood pressure is greater than 120/80 mm Hg, lifestyle modifications such as weight control, alcohol moderation, salt reduction, increased physical activity, more fruits, more vegetables, and low-fat dairy diets should be initiated. If a patient’s blood pressure is greater than 140/90 mm Hg then blood pressure medications such as beta blockers and ACE inhibitors should be added as tolerated.

2006 AHA/ACC Guidelines for Secondary Prevention for Patients with Coronary and other Atherosclerotic Vascular Disease (DO NOT EDIT) [1]

Blood Pressure Management (DO NOT EDIT) [1]

Class I
“1. All patients should be counseled regarding the need for lifestyle modification: weight control; increased physical activity; alcohol moderation; sodium reduction; and emphasis on increased consumption of fresh fruits, vegetables, and low-fat dairy products. [2][3][4][5][6] (Level of Evidence: B) ”
“2. Patients with blood pressure ≥140/90 mm Hg should be treated, as tolerated, with blood pressure medication, treating initially with β-blockers and/or ACE inhibitors, with addition of other drugs as needed to achieve goal blood pressure. [2][7][8] (Level of Evidence: A)”
“ Goal: <140/90 mm Hg or <130/80 mm Hg if patient has diabetes or chronic kidney disease. ”

References

  1. ↑ 1.0 1.1 AHA. ACC. National Heart, Lung, and Blood Institute. Smith SC, Allen J, Blair SN; et al. (2006). “AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update endorsed by the National Heart, Lung, and Blood Institute”. J Am Coll Cardiol. 47 (10): 2130–9. doi:10.1016/j.jacc.2006.04.026. PMID 16697342.
  2. ↑ 2.0 2.1 Chobanian AV, Bakris GL, Black HR; et al. (2003). “Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure”. Hypertension. 42 (6): 1206–52. doi:10.1161/01.HYP.0000107251.49515.c2. PMID 14656957. Unknown parameter |month= ignored (help)
  3. ↑ Appel LJ, Moore TJ, Obarzanek E; et al. (1997). “A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group”. N. Engl. J. Med. 336 (16): 1117–24. doi:10.1056/NEJM199704173361601. PMID 9099655. Unknown parameter |month= ignored (help)
  4. ↑ Sacks FM, Svetkey LP, Vollmer WM; et al. (2001). “Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group”. N. Engl. J. Med. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. PMID 11136953. Unknown parameter |month= ignored (help)
  5. ↑ Appel LJ, Frohlich ED, Hall JE; et al. (2011). “The importance of population-wide sodium reduction as a means to prevent cardiovascular disease and stroke: a call to action from the American Heart Association”. Circulation. 123 (10): 1138–43. doi:10.1161/CIR.0b013e31820d0793. PMID 21233236. Unknown parameter |month= ignored (help)
  6. ↑ Whelton SP, Chin A, Xin X, He J (2002). “Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials”. Ann. Intern. Med. 136 (7): 493–503. PMID 11926784. Unknown parameter |month= ignored (help)
  7. ↑ “Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Final results of the Systolic Hypertension in the Elderly Program (SHEP). SHEP Cooperative Research Group”. JAMA. 265 (24): 3255–64. 1991. PMID 2046107. Unknown parameter |month= ignored (help)
  8. ↑ “Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)”. JAMA. 288 (23): 2981–97. 2002. PMID 12479763. Unknown parameter |month= ignored (help)


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Lipid Management

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]

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

  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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Physical Activity Recommendations

Physical Activity Recommendations

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]

Physical Activity (DO NOT EDIT) [1]

“ Goal: At least 30 minutes, 7 days per week (minimum 5 days per week) ”
Class I
“1. For all patients, the clinician should encourage 30 to 60 minutes of moderate-intensity aerobic activity, such as brisk walking, at least 5 days and preferably 7 days per week, supplemented by an increase in daily lifestyle activities (eg, walking breaks at work, gardening, household work) to improve cardiorespiratory fitness and move patients out of the least fit, least active high-risk cohort (bottom 20%). [2][3] (Level of Evidence: B)”
“2. For all patients, risk assessment with a physical activity history and/or an exercise test is recommended to guide prognosis and prescription. [4][5][6][7][8][9][3] (Level of Evidence: B) ”
“3. The clinician should counsel patients to report and be evaluated for symptoms related to exercise. (Level of Evidence: C) ”
Class IIb
“1. It is reasonable for the clinician to recommend complementary resistance training at least 2 days per week. [10] (Level of Evidence: C) ”

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. ↑ “2008 Physical Activity Guidelines for Americans: Contents”.
  3. ↑ 3.0 3.1 Haskell WL, Lee IM, Pate RR; et al. (2007). “Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association”. Med Sci Sports Exerc. 39 (8): 1423–34. doi:10.1249/mss.0b013e3180616b27. PMID 17762377. Unknown parameter |month= ignored (help)
  4. ↑ Balady GJ, Williams MA, Ades PA; et al. (2007). “Core components of cardiac rehabilitation/secondary prevention programs: 2007 update: a scientific statement from the American Heart Association Exercise, Cardiac Rehabilitation, and Prevention Committee, the Council on Clinical Cardiology; the Councils on Cardiovascular Nursing, Epidemiology and Prevention, and Nutrition, Physical Activity, and Metabolism; and the American Association of Cardiovascular and Pulmonary Rehabilitation”. Circulation. 115 (20): 2675–82. doi:10.1161/CIRCULATIONAHA.106.180945. PMID 17513578. Unknown parameter |month= ignored (help)
  5. ↑ Mark DB, Hlatky MA, Harrell FE, Lee KL, Califf RM, Pryor DB (1987). “Exercise treadmill score for predicting prognosis in coronary artery disease”. Ann. Intern. Med. 106 (6): 793–800. PMID 3579066. Unknown parameter |month= ignored (help)
  6. ↑ Mark DB, Shaw L, Harrell FE; et al. (1991). “Prognostic value of a treadmill exercise score in outpatients with suspected coronary artery disease”. N. Engl. J. Med. 325 (12): 849–53. doi:10.1056/NEJM199109193251204. PMID 1875969. Unknown parameter |month= ignored (help)
  7. ↑ Vanhees L, Fagard R, Thijs L, Staessen J, Amery A (1994). “Prognostic significance of peak exercise capacity in patients with coronary artery disease”. J. Am. Coll. Cardiol. 23 (2): 358–63. PMID 8294687. Unknown parameter |month= ignored (help)
  8. ↑ Kavanagh T, Mertens DJ, Hamm LF; et al. (2002). “Prediction of long-term prognosis in 12 169 men referred for cardiac rehabilitation”. Circulation. 106 (6): 666–71. PMID 12163425. Unknown parameter |month= ignored (help)
  9. ↑ Kavanagh T, Mertens DJ, Hamm LF; et al. (2003). “Peak oxygen intake and cardiac mortality in women referred for cardiac rehabilitation”. J. Am. Coll. Cardiol. 42 (12): 2139–43. PMID 14680741. Unknown parameter |month= ignored (help)
  10. ↑ Williams MA, Haskell WL, Ades PA; et al. (2007). “Resistance exercise in individuals with and without cardiovascular disease: 2007 update: a scientific statement from the American Heart Association Council on Clinical Cardiology and Council on Nutrition, Physical Activity, and Metabolism”. Circulation. 116 (5): 572–84. doi:10.1161/CIRCULATIONAHA.107.185214. PMID 17638929. Unknown parameter |month= ignored (help)


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Weight Management

Weight Management

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

Overview

If a woman’s waist has a circumference greater than 35 inches and if a man’s waist is greater than 40 inches, lifestyle changes and possible metabolic syndrome treatments should be initiated. The initial goal of weight loss therapy should be to reduce body weight by approximately 5-10 percent from the patient’s baseline weight.

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

Weight Management (DO NOT EDIT) [1]

“ Goal: Body mass index of 18.5 to 24.9 kg/m2; Waist circumference of <35 inches (<89 cm) in women and <40 inches (<102 cm) in men. ”
Class I
“1. Body mass index and/or waist circumference should be assessed at every visit, and the clinician should consistently encourage weight maintenance/reduction through an appropriate balance of lifestyle physical activity, structured exercise, caloric intake, and formal behavioral programs when indicated to maintain/achieve a body mass index between 18.5 and 24.9 kg/m2. [2][3][4][5][6][7][8][9][10] (Level of Evidence: B)”
“2. If waist circumference (measured horizontally at the iliac crest) is ≥35 inches (≥89 cm) in women and ≥40 inches (≥102 cm) in men, therapeutic lifestyle interventions should be intensified and focused on weight management. [6][7][8][9][10] (Level of Evidence: B)”
“3.The initial goal of weight loss therapy should be to reduce body weight by approximately 5% to 10% from baseline. With success, further weight loss can be attempted if indicated. (Level of Evidence: C)”

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. ↑ “Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults–The Evidence Report. National Institutes of Health”. Obes. Res. 6 Suppl 2: 51S–209S. 1998. PMID 9813653. Unknown parameter |month= ignored (help)
  3. ↑ Klein S, Burke LE, Bray GA; et al. (2004). “Clinical implications of obesity with specific focus on cardiovascular disease: a statement for professionals from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: endorsed by the American College of Cardiology Foundation”. Circulation. 110 (18): 2952–67. doi:10.1161/01.CIR.0000145546.97738.1E. PMID 15509809. Unknown parameter |month= ignored (help)
  4. ↑ Grundy SM, Cleeman JI, Daniels SR; et al. (2005). “Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement: Executive Summary”. Crit Pathw Cardiol. 4 (4): 198–203. PMID 18340209. Unknown parameter |month= ignored (help)
  5. ↑ Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW (1999). “Body-mass index and mortality in a prospective cohort of U.S. adults”. N. Engl. J. Med. 341 (15): 1097–105. doi:10.1056/NEJM199910073411501. PMID 10511607. Unknown parameter |month= ignored (help)
  6. ↑ 6.0 6.1 Jensen MK, Chiuve SE, Rimm EB; et al. (2008). “Obesity, behavioral lifestyle factors, and risk of acute coronary events”. Circulation. 117 (24): 3062–9. doi:10.1161/CIRCULATIONAHA.107.759951. PMID 18541738. Unknown parameter |month= ignored (help)
  7. ↑ 7.0 7.1 Arnlöv J, Ingelsson E, Sundström J, Lind L (2010). “Impact of body mass index and the metabolic syndrome on the risk of cardiovascular disease and death in middle-aged men”. Circulation. 121 (2): 230–6. doi:10.1161/CIRCULATIONAHA.109.887521. PMID 20038741. Unknown parameter |month= ignored (help)
  8. ↑ 8.0 8.1 Lavie CJ, Milani RV, Ventura HO (2009). “Obesity and cardiovascular disease: risk factor, paradox, and impact of weight loss”. J. Am. Coll. Cardiol. 53 (21): 1925–32. doi:10.1016/j.jacc.2008.12.068. PMID 19460605. Unknown parameter |month= ignored (help)
  9. ↑ 9.0 9.1 Gruberg L, Weissman NJ, Waksman R; et al. (2002). “The impact of obesity on the short-term and long-term outcomes after percutaneous coronary intervention: the obesity paradox?”. J. Am. Coll. Cardiol. 39 (4): 578–84. PMID 11849854. Unknown parameter |month= ignored (help)
  10. ↑ 10.0 10.1 Jacobs EJ, Newton CC, Wang Y; et al. (2010). “Waist circumference and all-cause mortality in a large US cohort”. Arch. Intern. Med. 170 (15): 1293–301. doi:10.1001/archinternmed.2010.201. PMID 20696950. Unknown parameter |month= ignored (help)


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Influenza Vaccination

Influenza Vaccination

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

Overview

It is recommended that any patient suffering from cardiovascular disease should receive an influenza vaccination every year.

Influenza Vaccination

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

Influenza Vaccination (DO NOT EDIT) [1]

Class I
“1. Patients with cardiovascular disease should have an annual influenza vaccination. [2][3][4][5] (Level of Evidence: B)”

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. ↑ Gurfinkel EP, Leon de la Fuente R, Mendiz O, Mautner B (2004). “Flu vaccination in acute coronary syndromes and planned percutaneous coronary interventions (FLUVACS) Study”. Eur. Heart J. 25 (1): 25–31. PMID 14683739. Unknown parameter |month= ignored (help)
  3. ↑ Ciszewski A, Bilinska ZT, Brydak LB; et al. (2008). “Influenza vaccination in secondary prevention from coronary ischaemic events in coronary artery disease: FLUCAD study”. Eur. Heart J. 29 (11): 1350–8. doi:10.1093/eurheartj/ehm581. PMID 18187561. Unknown parameter |month= ignored (help)
  4. ↑ Davis MM, Taubert K, Benin AL; et al. (2006). “Influenza vaccination as secondary prevention for cardiovascular disease: a science advisory from the American Heart Association/American College of Cardiology”. Circulation. 114 (14): 1549–53. doi:10.1161/CIRCULATIONAHA.106.178242. PMID 16982936. Unknown parameter |month= ignored (help)
  5. ↑ Lindsey NP, Staples JE, Lehman JA, Fischer M (2010). “Surveillance for human West Nile virus disease – United States, 1999-2008”. MMWR Surveill Summ. 59 (2): 1–17. PMID 20360671. Unknown parameter |month= ignored (help)


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Depression

Depression

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

Please help WikiDoc by adding more content here. It’s easy! Click here to learn about editing.

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

Depression (DO NOT EDIT) [1]

Class IIa

“1. For patients with recent coronary artery bypass graft surgery or myocardial infarction, it is reasonable to screen for depression if patients have access to case management, in collaboration with their primary care physician and a mental health specialist. [2][3][4][5][6] (Level of Evidence: B)”

Class IIb

“1. Treatment of depression has not been shown to improve cardiovascular disease outcomes but may be reasonable for its other clinical benefits. (Level of Evidence: C)”

Sources

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

References

  1. ↑ 1.0 1.1 1.2 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. ↑ Ziegelstein RC, Thombs BD, Coyne JC, de Jonge P (2009). “Routine screening for depression in patients with coronary heart disease never mind”. J. Am. Coll. Cardiol. 54 (10): 886–90. doi:10.1016/j.jacc.2009.01.082. PMC 2749208. PMID 19712796. Unknown parameter |month= ignored (help)
  3. ↑ Thombs BD, de Jonge P, Coyne JC; et al. (2008). “Depression screening and patient outcomes in cardiovascular care: a systematic review”. JAMA. 300 (18): 2161–71. doi:10.1001/jama.2008.667. PMID 19001627. Unknown parameter |month= ignored (help)
  4. ↑ “Screening for depression in adults: U.S. preventive services task force recommendation statement”. Ann. Intern. Med. 151 (11): 784–92. 2009. doi:10.1059/0003-4819-151-11-200912010-00006. PMID 19949144. Unknown parameter |month= ignored (help)
  5. ↑ Rollman BL, Belnap BH, LeMenager MS; et al. (2009). “Telephone-delivered collaborative care for treating post-CABG depression: a randomized controlled trial”. JAMA. 302 (19): 2095–103. doi:10.1001/jama.2009.1670. PMID 19918088. Unknown parameter |month= ignored (help)
  6. ↑ Larsen KK, Agerbo E, Christensen B, Søndergaard J, Vestergaard M (2010). “Myocardial infarction and risk of suicide: a population-based case-control study”. Circulation. 122 (23): 2388–93. doi:10.1161/CIRCULATIONAHA.110.956136. PMID 21098443. Unknown parameter |month= ignored (help)


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Beta Blockers

Beta Blockers

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]

Beta Blockers (DO NOT EDIT) [1]

Class I
“1. β-Blocker therapy should be used in all patients with left ventricular systolic dysfunction (ejection fraction ≤40%) with heart failure or prior myocardial infarction, unless contraindicated. (Use should be limited to carvedilol, metoprolol succinate, or bisoprolol, which have been shown to reduce mortality.) [2][3] (Level of Evidence: A)”
“2. β-Blocker therapy should be started and continued for 3 years in all patients with normal left ventricular function who have had myocardial infarction or ACS. [4][5] (Level of Evidence: B)”
Class IIa

“1. It is reasonable to continue β-blockers beyond 3 years as chronic therapy in all patients with normal left ventricular function who have had myocardial infarction or ACS. [4][5] (Level of Evidence: B)”

“2. It is reasonable to give β-blocker therapy in patients with left ventricular systolic dysfunction (ejection fraction ≤40%) without heart failure or prior myocardial infarction. (Level of Evidence: C)”

Class IIb

“1. β-Blockers may be considered as chronic therapy for all other patients with coronary or other vascular disease. (Level of Evidence: C)”

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. ↑ Packer M, Bristow MR, Cohn JN; et al. (1996). “The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group”. N. Engl. J. Med. 334 (21): 1349–55. doi:10.1056/NEJM199605233342101. PMID 8614419. Unknown parameter |month= ignored (help)
  3. ↑ Domanski MJ, Krause-Steinrauf H, Massie BM; et al. (2003). “A comparative analysis of the results from 4 trials of beta-blocker therapy for heart failure: BEST, CIBIS-II, MERIT-HF, and COPERNICUS”. J. Card. Fail. 9 (5): 354–63. PMID 14583895. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 Freemantle N, Cleland J, Young P, Mason J, Harrison J (1999). “beta Blockade after myocardial infarction: systematic review and meta regression analysis”. BMJ. 318 (7200): 1730–7. PMC 31101. PMID 10381708. Unknown parameter |month= ignored (help)
  5. ↑ 5.0 5.1 “Beta blockers for preventing stroke recurrence – The Cochrane Library – De Lima – Wiley Online Library”.


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Diabete Mellitus Management

Diabete Mellitus 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]

Diabetes Mellitus Management (DO NOT EDIT) [1]

Class I
“1. Care for diabetes should be coordinated with the patient’s primary care physician and/or endocrinologist. (Level of Evidence: C)”
“2. Lifestyle modifications including daily physical activity, weight management, blood pressure control, and lipid management are recommended for all patients with diabetes. [2][3][4][5][6][7][8][9][10][11][12][13] (Level of Evidence: B)”
Class IIa

“1. Metformin is an effective first-line pharmacotherapy and can be useful if not contraindicated. [12][14][15] (Level of Evidence: A)”

“2. It is reasonable to individualize the intensity of blood sugar–lowering interventions based on the individual patient’s risk of hypoglycemia during treatment. (Level of Evidence: C)”

Class IIb

“1. Initiation of pharmacotherapy interventions to achieve target HbA1c may be reasonable. [16][17][12][14][15][18][19][20][21] (Level of Evidence: A)”

“2. A target HbA1c of ≤7% may be considered. (Level of Evidence: C)”

“3. Less stringent HbA1c goals may be considered for patients with a history of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, or extensive comorbidities, or those in whom the goal is difficult to attain despite intensive therapeutic interventions. (Level of Evidence: C)”

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. ↑ 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)
  3. ↑ 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)
  4. ↑ 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)
  5. ↑ “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)
  6. ↑ Marwick TH, Hordern MD, Miller T; et al. (2009). “Exercise training for type 2 diabetes mellitus: impact on cardiovascular risk: a scientific statement from the American Heart Association”. Circulation. 119 (25): 3244–62. doi:10.1161/CIRCULATIONAHA.109.192521. PMID 19506108. Unknown parameter |month= ignored (help)
  7. ↑ Haskell WL, Lee IM, Pate RR; et al. (2007). “Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association”. Med Sci Sports Exerc. 39 (8): 1423–34. doi:10.1249/mss.0b013e3180616b27. PMID 17762377. Unknown parameter |month= ignored (help)
  8. ↑ Williams MA, Haskell WL, Ades PA; et al. (2007). “Resistance exercise in individuals with and without cardiovascular disease: 2007 update: a scientific statement from the American Heart Association Council on Clinical Cardiology and Council on Nutrition, Physical Activity, and Metabolism”. Circulation. 116 (5): 572–84. doi:10.1161/CIRCULATIONAHA.107.185214. PMID 17638929. Unknown parameter |month= ignored (help)
  9. ↑ Grundy SM, Cleeman JI, Daniels SR; et al. (2005). “Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement”. Circulation. 112 (17): 2735–52. doi:10.1161/CIRCULATIONAHA.105.169404. PMID 16157765. Unknown parameter |month= ignored (help)
  10. ↑ Jensen MK, Chiuve SE, Rimm EB; et al. (2008). “Obesity, behavioral lifestyle factors, and risk of acute coronary events”. Circulation. 117 (24): 3062–9. doi:10.1161/CIRCULATIONAHA.107.759951. PMID 18541738. Unknown parameter |month= ignored (help)
  11. ↑ “Standards of medical care in diabetes–2011”. Diabetes Care. 34 Suppl 1: S11–61. 2011. doi:10.2337/dc11-S011. PMC 3006050. PMID 21193625. Unknown parameter |month= ignored (help)
  12. ↑ 12.0 12.1 12.2 Thompson PD, Buchner D, Pina IL; et al. (2003). “Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity)”. Circulation. 107 (24): 3109–16. doi:10.1161/01.CIR.0000075572.40158.77. PMID 12821592. Unknown parameter |month= ignored (help)
  13. ↑ 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)
  14. ↑ 14.0 14.1 Selvin E, Bolen S, Yeh HC; et al. (2008). “Cardiovascular outcomes in trials of oral diabetes medications: a systematic review”. Arch. Intern. Med. 168 (19): 2070–80. doi:10.1001/archinte.168.19.2070. PMC 2765722. PMID 18955635. Unknown parameter |month= ignored (help)
  15. ↑ 15.0 15.1 “Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group”. Lancet. 352 (9131): 854–65. 1998. PMID 9742977. Unknown parameter |month= ignored (help)
  16. ↑ Skyler JS, Bergenstal R, Bonow RO; et al. (2009). “Intensive glycemic control and the prevention of cardiovascular events: implications of the ACCORD, ADVANCE, and VA diabetes trials: a position statement of the American Diabetes Association and a scientific statement of the American College of Cardiology Foundation and the American Heart Association”. Circulation. 119 (2): 351–7. doi:10.1161/CIRCULATIONAHA.108.191305. PMID 19095622. Unknown parameter |month= ignored (help)
  17. ↑ Kelly TN, Bazzano LA, Fonseca VA, Thethi TK, Reynolds K, He J (2009). “Systematic review: glucose control and cardiovascular disease in type 2 diabetes”. Ann. Intern. Med. 151 (6): 394–403. PMID 19620144. Unknown parameter |month= ignored (help)
  18. ↑ Turnbull FM, Abraira C, Anderson RJ; et al. (2009). “Intensive glucose control and macrovascular outcomes in type 2 diabetes”. Diabetologia. 52 (11): 2288–98. doi:10.1007/s00125-009-1470-0. PMID 19655124. Unknown parameter |month= ignored (help)
  19. ↑ Ray KK, Seshasai SR, Wijesuriya S; et al. (2009). “Effect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: a meta-analysis of randomised controlled trials”. Lancet. 373 (9677): 1765–72. doi:10.1016/S0140-6736(09)60697-8. PMID 19465231. Unknown parameter |month= ignored (help)
  20. ↑ Currie CJ, Peters JR, Tynan A; et al. (2010). “Survival as a function of HbA(1c) in people with type 2 diabetes: a retrospective cohort study”. Lancet. 375 (9713): 481–9. doi:10.1016/S0140-6736(09)61969-3. PMID 20110121. Unknown parameter |month= ignored (help)
  21. ↑ Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA (2008). “10-year follow-up of intensive glucose control in type 2 diabetes”. N. Engl. J. Med. 359 (15): 1577–89. doi:10.1056/NEJMoa0806470. PMID 18784090. Unknown parameter |month= ignored (help)


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Antiplatelet Agents/Anticoagulants

Antiplatelet Agents/Anticoagulants

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]

Antiplatelet Agents and Anticoagulants (DO NOT EDIT) [1]

Class I

“1. Aspirin 75–162 mg daily is recommended in all patients with coronary artery disease unless contraindicated. [2][3][4][5] (Level of Evidence: A)

  • Clopidogrel 75 mg daily is recommended as an alternative for patients who are intolerant of or allergic to aspirin. [6] (Level of Evidence: B)”

“2. A P2Y12 receptor antagonist in combination with aspirin is indicated in patients after ACS or PCI with stent placement. [7][8][9] (Level of Evidence: A)

“3. For patients undergoing coronary artery bypass grafting, aspirin should be started within 6 hours after surgery to reduce saphenous vein graft closure. Dosing regimens ranging from 100 to 325 mg daily for 1 year appear to be efficacious. [13][14][15][16] (Level of Evidence: A)”

“4. In patients with extracranial carotid or vertebral atherosclerosis who have had ischemic stroke or TIA, treatment with aspirin alone (75–325 mg daily), clopidogrel alone (75 mg daily), or the combination of aspirin plus extended-release dipyridamole (25 mg and 200 mg twice daily, respectively) should be started and continued. [17][5] (Level of Evidence: B)”

“5. For patients with symptomatic atherosclerotic peripheral artery disease of the lower extremity, antiplatelet therapy with aspirin (75–325 mg daily) or clopidogrel (75 mg daily) should be started and continued. [18][19][5][6] (Level of Evidence: A)”

“6. Antiplatelet therapy is recommended in preference to anticoagulant therapy with warfarin or other vitamin K antagonists to treat patients with atherosclerosis. [20][21][22][23] (Level of Evidence: A)

Class IIa

“1. If the risk of morbidity from bleeding outweighs the anticipated benefit afforded by thienopyridine therapy after stent implantation, earlier discontinuation (eg, <12 months) is reasonable. (Level of Evidence: C) (Note: the risk for serious cardiovascular events because of early discontinuation of thienopyridines is greater for patients with drug-eluting stents than those with bare-metal stents.)”

“2. After PCI, it is reasonable to use 81 mg of aspirin per day in preference to higher maintenance doses. [8][9][32][33][34][35][36] (Level of Evidence: B)”

“3. For patients undergoing coronary artery bypass grafting, clopidogrel (75 mg daily) is a reasonable alternative in patients who are intolerant of or allergic to aspirin. (Level of Evidence: C)”

Class IIb

“1. The benefits of aspirin in patients with asymptomatic peripheral artery disease of the lower extremities are not well established. [37][38] (Level of Evidence: B)”

“2. Combination therapy with both aspirin 75 to 162 mg daily and clopidogrel 75 mg daily may be considered in patients with stable coronary artery disease. [39] (Level of Evidence: B)”

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. ↑ Gibbons RJ, Abrams J, Chatterjee K; 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. Unknown parameter |month= ignored (help)
  3. ↑ Vandvik PO, Lincoff AM, Gore JM; et al. (2012). “Primary and secondary prevention of cardiovascular disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines”. Chest. 141 (2 Suppl): e637S–68S. doi:10.1378/chest.11-2306. PMID 22315274. Unknown parameter |month= ignored (help)
  4. ↑ Baigent C, Blackwell L, Collins R; et al. (2009). “Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials”. Lancet. 373 (9678): 1849–60. doi:10.1016/S0140-6736(09)60503-1. PMC 2715005. PMID 19482214. Unknown parameter |month= ignored (help)
  5. ↑ 5.0 5.1 5.2 “Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients”. BMJ. 324 (7329): 71–86. 2002. PMC 64503. PMID 11786451. Unknown parameter |month= ignored (help)
  6. ↑ 6.0 6.1 “A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee”. Lancet. 348 (9038): 1329–39. 1996. PMID 8918275. Unknown parameter |month= ignored (help)
  7. ↑ Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KK (2001). “Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation”. N. Engl. J. Med. 345 (7): 494–502. doi:10.1056/NEJMoa010746. PMID 11519503. Unknown parameter |month= ignored (help)
  8. ↑ 8.0 8.1 8.2 Mehta SR, Yusuf S, Peters RJ; et al. (2001). “Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study”. Lancet. 358 (9281): 527–33. PMID 11520521. Unknown parameter |month= ignored (help)
  9. ↑ 9.0 9.1 Steinhubl SR, Berger PB, Mann JT; et al. (2002). “Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial”. JAMA. 288 (19): 2411–20. PMID 12435254. Unknown parameter |month= ignored (help)
  10. ↑ Montalescot G, Wiviott SD, Braunwald E; et al. (2009). “Prasugrel compared with clopidogrel in patients undergoing percutaneous coronary intervention for ST-elevation myocardial infarction (TRITON-TIMI 38): double-blind, randomised controlled trial”. Lancet. 373 (9665): 723–31. doi:10.1016/S0140-6736(09)60441-4. PMID 19249633. Unknown parameter |month= ignored (help)
  11. ↑ Wiviott SD, Braunwald E, McCabe CH; et al. (2007). “Prasugrel versus clopidogrel in patients with acute coronary syndromes”. N. Engl. J. Med. 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. PMID 17982182. Unknown parameter |month= ignored (help)
  12. ↑ Wallentin L, Becker RC, Budaj A; et al. (2009). “Ticagrelor versus clopidogrel in patients with acute coronary syndromes”. N. Engl. J. Med. 361 (11): 1045–57. doi:10.1056/NEJMoa0904327. PMID 19717846. Unknown parameter |month= ignored (help)
  13. ↑ Chesebro JH, Fuster V, Elveback LR; et al. (1984). “Effect of dipyridamole and aspirin on late vein-graft patency after coronary bypass operations”. N. Engl. J. Med. 310 (4): 209–14. doi:10.1056/NEJM198401263100401. PMID 6361561. Unknown parameter |month= ignored (help)
  14. ↑ Lorenz RL, Schacky CV, Weber M; et al. (1984). “Improved aortocoronary bypass patency by low-dose aspirin (100 mg daily). Effects on platelet aggregation and thromboxane formation”. Lancet. 1 (8389): 1261–4. PMID 6144975. Unknown parameter |month= ignored (help)
  15. ↑ Sharma GV, Khuri SF, Josa M, Folland ED, Parisi AF (1983). “The effect of antiplatelet therapy on saphenous vein coronary artery bypass graft patency”. Circulation. 68 (3 Pt 2): II218–21. PMID 6347428. Unknown parameter |month= ignored (help)
  16. ↑ Mangano DT (2002). “Aspirin and mortality from coronary bypass surgery”. N. Engl. J. Med. 347 (17): 1309–17. doi:10.1056/NEJMoa020798. PMID 12397188. Unknown parameter |month= ignored (help)
  17. ↑ Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A (2006). “Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial”. Lancet. 367 (9523): 1665–73. doi:10.1016/S0140-6736(06)68734-5. PMID 16714187. Unknown parameter |month= ignored (help)
  18. ↑ Catalano M, Born G, Peto R (2007). “Prevention of serious vascular events by aspirin amongst patients with peripheral arterial disease: randomized, double-blind trial”. J. Intern. Med. 261 (3): 276–84. doi:10.1111/j.1365-2796.2006.01763.x. PMID 17305650. Unknown parameter |month= ignored (help)
  19. ↑ Hirsch AT, Haskal ZJ, Hertzer NR; et al. (2006). “ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation”. Circulation. 113 (11): e463–654. doi:10.1161/CIRCULATIONAHA.106.174526. PMID 16549646. Unknown parameter |month= ignored (help)
  20. ↑ Anand SS, Yusuf S (1999). “Oral anticoagulant therapy in patients with coronary artery disease: a meta-analysis”. JAMA. 282 (21): 2058–67. PMID 10591389. Unknown parameter |month= ignored (help)
  21. ↑ Hurlen M, Abdelnoor M, Smith P, Erikssen J, Arnesen H (2002). “Warfarin, aspirin, or both after myocardial infarction”. N. Engl. J. Med. 347 (13): 969–74. doi:10.1056/NEJMoa020496. PMID 12324552. Unknown parameter |month= ignored (help)
  22. ↑ Mohr JP, Thompson JL, Lazar RM; et al. (2001). “A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke”. N. Engl. J. Med. 345 (20): 1444–51. doi:10.1056/NEJMoa011258. PMID 11794192. Unknown parameter |month= ignored (help)
  23. ↑ 23.0 23.1 23.2 Anand S, Yusuf S, Xie C; et al. (2007). “Oral anticoagulant and antiplatelet therapy and peripheral arterial disease”. N. Engl. J. Med. 357 (3): 217–27. doi:10.1056/NEJMoa065959. PMID 17634457. Unknown parameter |month= ignored (help)
  24. ↑ “Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation. Analysis of pooled data from five randomized controlled trials”. Arch. Intern. Med. 154 (13): 1449–57. 1994. PMID 8018000. Unknown parameter |month= ignored (help)
  25. ↑ Turpie AG, Gent M, Laupacis A; et al. (1993). “A comparison of aspirin with placebo in patients treated with warfarin after heart-valve replacement”. N. Engl. J. Med. 329 (8): 524–9. doi:10.1056/NEJM199308193290802. PMID 8336751. Unknown parameter |month= ignored (help)
  26. ↑ Mok CK, Boey J, Wang R; et al. (1985). “Warfarin versus dipyridamole-aspirin and pentoxifylline-aspirin for the prevention of prosthetic heart valve thromboembolism: a prospective randomized clinical trial”. Circulation. 72 (5): 1059–63. PMID 3899404. Unknown parameter |month= ignored (help)
  27. ↑ “Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation: Stroke Prevention in Atrial Fibrillation III randomised clinical trial”. Lancet. 348 (9028): 633–8. 1996. PMID 8782752. Unknown parameter |month= ignored (help)
  28. ↑ Kearon C, Gent M, Hirsh J; et al. (1999). “A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism”. N. Engl. J. Med. 340 (12): 901–7. doi:10.1056/NEJM199903253401201. PMID 10089183. Unknown parameter |month= ignored (help)
  29. ↑ Becker RC, Meade TW, Berger PB; et al. (2008). “The primary and secondary prevention of coronary artery disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)”. Chest. 133 (6 Suppl): 776S–814S. doi:10.1378/chest.08-0685. PMID 18574278. Unknown parameter |month= ignored (help)
  30. ↑ Bonow RO, Carabello BA, Kanu C; et al. (2006). “ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons”. Circulation. 114 (5): e84–231. doi:10.1161/CIRCULATIONAHA.106.176857. PMID 16880336. Unknown parameter |month= ignored (help)
  31. ↑ Fiore LD, Ezekowitz MD, Brophy MT, Lu D, Sacco J, Peduzzi P (2002). “Department of Veterans Affairs Cooperative Studies Program Clinical Trial comparing combined warfarin and aspirin with aspirin alone in survivors of acute myocardial infarction: primary results of the CHAMP study”. Circulation. 105 (5): 557–63. PMID 11827919. Unknown parameter |month= ignored (help)
  32. ↑ Chen ZM, Jiang LX, Chen YP; et al. (2005). “Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial”. Lancet. 366 (9497): 1607–21. doi:10.1016/S0140-6736(05)67660-X. PMID 16271642. Unknown parameter |month= ignored (help)
  33. ↑ Brar SS, Kim J, Brar SK; et al. (2008). “Long-term outcomes by clopidogrel duration and stent type in a diabetic population with de novo coronary artery lesions”. J. Am. Coll. Cardiol. 51 (23): 2220–7. doi:10.1016/j.jacc.2008.01.063. PMID 18534267. Unknown parameter |month= ignored (help)
  34. ↑ Patrono C, Baigent C, Hirsh J, Roth G (2008). “Antiplatelet drugs: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)”. Chest. 133 (6 Suppl): 199S–233S. doi:10.1378/chest.08-0672. PMID 18574266. Unknown parameter |month= ignored (help)
  35. ↑ Steinhubl SR, Bhatt DL, Brennan DM; et al. (2009). “Aspirin to prevent cardiovascular disease: the association of aspirin dose and clopidogrel with thrombosis and bleeding”. Ann. Intern. Med. 150 (6): 379–86. PMID 19293071. Unknown parameter |month= ignored (help)
  36. ↑ Serebruany VL, Steinhubl SR, Berger PB; et al. (2005). “Analysis of risk of bleeding complications after different doses of aspirin in 192,036 patients enrolled in 31 randomized controlled trials”. Am. J. Cardiol. 95 (10): 1218–22. doi:10.1016/j.amjcard.2005.01.049. PMID 15877994. Unknown parameter |month= ignored (help)
  37. ↑ Berger JS, Krantz MJ, Kittelson JM, Hiatt WR (2009). “Aspirin for the prevention of cardiovascular events in patients with peripheral artery disease: a meta-analysis of randomized trials”. JAMA. 301 (18): 1909–19. doi:10.1001/jama.2009.623. PMID 19436018. Unknown parameter |month= ignored (help)
  38. ↑ Fowkes FG, Price JF, Stewart MC; et al. (2010). “Aspirin for prevention of cardiovascular events in a general population screened for a low ankle brachial index: a randomized controlled trial”. JAMA. 303 (9): 841–8. doi:10.1001/jama.2010.221. PMID 20197530. Unknown parameter |month= ignored (help)
  39. ↑ Bhatt DL, Flather MD, Hacke W; et al. (2007). “Patients with prior myocardial infarction, stroke, or symptomatic peripheral arterial disease in the CHARISMA trial”. J. Am. Coll. Cardiol. 49 (19): 1982–8. doi:10.1016/j.jacc.2007.03.025. PMID 17498584. Unknown parameter |month= ignored (help)


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Renin-angiotensin-aldosterone system blockers

Renin-angiotensin-aldosterone system blockers

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]

ACE Inhibitors (DO NOT EDIT) [1]

Class I
“1. ACE inhibitors should be started and continued indefinitely in all patients with left ventricular ejection fraction]] ≤40% and in those with hypertension, diabetes, or chronic kidney disease, unless contraindicated. [2][3] (Level of Evidence: A)”
Class IIa
“1. It is reasonable to use ACE inhibitors in all other patients. [4] (Level of Evidence: B)

ARBs (DO NOT EDIT) [1]

Class I
“1. The use of ARBs is recommended in patients who have heart failure or who have had a myocardial infarction with left ventricular ejection fraction ≤40% and who are ACE-inhibitor intolerant. [5][6][7] (Level of Evidence: A)”
Class IIa
“1. It is reasonable to use ARBs in other patients who are ACE-inhibitor intolerant. [8] (Level of Evidence: B)
Class IIb
“1. The use of ARBs in combination with an ACE inhibitor is not well established in those with systolic heart failure. [7][9] (Level of Evidence: A)

Aldosterone Blockade (DO NOT EDIT) [1]

Class I
“1. Use of aldosterone blockade in post–myocardial infarction patients without significant renal dysfunction# or hyperkalemia** is recommended in patients who are already receiving therapeutic doses of an ACE inhibitor and β-blocker, who have a left ventricular ejection fraction ≤40%, and who have either diabetes or heart failure. [10][11] (Level of Evidence: A)”
“ # Estimated creatinine clearance should be >30 mL/min. ”
“ ** Potassium should be <5.0 mEq/L. ”

References

  1. ↑ 1.0 1.1 1.2 1.3 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. ↑ Garg R, Yusuf S (1995). “Overview of randomized trials of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials”. JAMA. 273 (18): 1450–6. PMID 7654275. Unknown parameter |month= ignored (help)
  3. ↑ Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G (2000). “Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators”. N. Engl. J. Med. 342 (3): 145–53. doi:10.1056/NEJM200001203420301. PMID 10639539. Unknown parameter |month= ignored (help)
  4. ↑ Fox KM (2003). “Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study)”. Lancet. 362 (9386): 782–8. PMID 13678872. Unknown parameter |month= ignored (help)
  5. ↑ Pitt B, Poole-Wilson PA, Segal R; et al. (2000). “Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomised trial–the Losartan Heart Failure Survival Study ELITE II”. Lancet. 355 (9215): 1582–7. PMID 10821361. Unknown parameter |month= ignored (help)
  6. ↑ Pfeffer MA, Swedberg K, Granger CB; et al. (2003). “Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme”. Lancet. 362 (9386): 759–66. PMID 13678868. Unknown parameter |month= ignored (help)
  7. ↑ 7.0 7.1 Pfeffer MA, McMurray JJ, Velazquez EJ; et al. (2003). “Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both”. N. Engl. J. Med. 349 (20): 1893–906. doi:10.1056/NEJMoa032292. PMID 14610160. Unknown parameter |month= ignored (help)
  8. ↑ Yusuf S, Teo K, Anderson C; et al. (2008). “Effects of the angiotensin-receptor blocker telmisartan on cardiovascular events in high-risk patients intolerant to angiotensin-converting enzyme inhibitors: a randomised controlled trial”. Lancet. 372 (9644): 1174–83. doi:10.1016/S0140-6736(08)61242-8. PMID 18757085. Unknown parameter |month= ignored (help)
  9. ↑ Yusuf S, Teo KK, Pogue J; et al. (2008). “Telmisartan, ramipril, or both in patients at high risk for vascular events”. N. Engl. J. Med. 358 (15): 1547–59. doi:10.1056/NEJMoa0801317. PMID 18378520. Unknown parameter |month= ignored (help)
  10. ↑ Pitt B, Remme W, Zannad F; et al. (2003). “Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction”. N. Engl. J. Med. 348 (14): 1309–21. doi:10.1056/NEJMoa030207. PMID 12668699. Unknown parameter |month= ignored (help)
  11. ↑ Zannad F, McMurray JJ, Krum H; et al. (2011). “Eplerenone in patients with systolic heart failure and mild symptoms”. N. Engl. J. Med. 364 (1): 11–21. doi:10.1056/NEJMoa1009492. PMID 21073363. Unknown parameter |month= ignored (help)


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Cardiac Rehabilitation

Cardiac Rehabilitation

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]

Cardiac Rehabilitation (DO NOT EDIT) [1]

Class I
“1. All eligible patients with ACS or whose status is immediately post coronary artery bypass surgery or post-PCI should be referred to a comprehensive outpatient cardiovascular rehabilitation program either prior to hospital discharge or during the first follow-up office visit. [2][3][4][5] (Level of Evidence: A) ”
“2. All eligible outpatients with the diagnosis of ACS, coronary artery bypass surgery or PCI (Level of Evidence: A) [2][3][6][4], chronic angina (Level of Evidence: B) [4][5] and/or peripheral artery disease (Level of Evidence: A) [7][8] within the past year should be referred to a comprehensive outpatient cardiovascular rehabilitation program. ”
“3. A home-based cardiac rehabilitation program can be substituted for a supervised, center-based program for low-risk patients. [9][10] (Level of Evidence: A) ”
Class IIa
“1. A comprehensive exercise-based outpatient cardiac rehabilitation program can be safe and beneficial for clinically stable outpatients with a history of heart failure. [11][12][13][14] (Level of Evidence: B) ”

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. ↑ 2.0 2.1 Taylor RS, Brown A, Ebrahim S; et al. (2004). “Exercise-based rehabilitation for patients with coronary heart disease: systematic review and meta-analysis of randomized controlled trials”. Am. J. Med. 116 (10): 682–92. doi:10.1016/j.amjmed.2004.01.009. PMID 15121495. Unknown parameter |month= ignored (help)
  3. ↑ 3.0 3.1 Clark AM, Hartling L, Vandermeer B, McAlister FA (2005). “Meta-analysis: secondary prevention programs for patients with coronary artery disease”. Ann. Intern. Med. 143 (9): 659–72. PMID 16263889. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 4.2 Thomas RJ, King M, Lui K, Oldridge N, Piña IL, Spertus J (2007). “AACVPR/ACC/AHA 2007 performance measures on cardiac rehabilitation for referral to and delivery of cardiac rehabilitation/secondary prevention services”. Circulation. 116 (14): 1611–42. doi:10.1161/CIRCULATIONAHA.107.185734. PMID 17885210. Unknown parameter |month= ignored (help)
  5. ↑ 5.0 5.1 Walther C, Möbius-Winkler S, Linke A; et al. (2008). “Regular exercise training compared with percutaneous intervention leads to a reduction of inflammatory markers and cardiovascular events in patients with coronary artery disease”. Eur J Cardiovasc Prev Rehabil. 15 (1): 107–12. doi:10.1097/HJR.0b013e3282f29aa6. PMID 18277195. Unknown parameter |month= ignored (help)
  6. ↑ Hambrecht R, Walther C, Möbius-Winkler S; et al. (2004). “Percutaneous coronary angioplasty compared with exercise training in patients with stable coronary artery disease: a randomized trial”. Circulation. 109 (11): 1371–8. doi:10.1161/01.CIR.0000121360.31954.1F. PMID 15007010. Unknown parameter |month= ignored (help)
  7. ↑ McDermott MM, Ades P, Guralnik JM; et al. (2009). “Treadmill exercise and resistance training in patients with peripheral arterial disease with and without intermittent claudication: a randomized controlled trial”. JAMA. 301 (2): 165–74. doi:10.1001/jama.2008.962. PMC 3268032. PMID 19141764. Unknown parameter |month= ignored (help)
  8. ↑ Watson L, Ellis B, Leng GC (2008). “Exercise for intermittent claudication”. Cochrane Database Syst Rev (4): CD000990. doi:10.1002/14651858.CD000990.pub2. PMID 18843614.
  9. ↑ Taylor RS, Dalal H, Jolly K, Moxham T, Zawada A (2010). “Home-based versus centre-based cardiac rehabilitation”. Cochrane Database Syst Rev (1): CD007130. doi:10.1002/14651858.CD007130.pub2. PMID 20091618.
  10. ↑ Clark AM, Haykowsky M, Kryworuchko J; et al. (2010). “A meta-analysis of randomized control trials of home-based secondary prevention programs for coronary artery disease”. Eur J Cardiovasc Prev Rehabil. 17 (3): 261–70. PMID 20560165. Unknown parameter |month= ignored (help)
  11. ↑ O’Connor CM, Whellan DJ, Lee KL; et al. (2009). “Efficacy and safety of exercise training in patients with chronic heart failure: HF-ACTION randomized controlled trial”. JAMA. 301 (14): 1439–50. doi:10.1001/jama.2009.454. PMC 2916661. PMID 19351941. Unknown parameter |month= ignored (help)
  12. ↑ Belardinelli R, Georgiou D, Cianci G, Purcaro A (1999). “Randomized, controlled trial of long-term moderate exercise training in chronic heart failure: effects on functional capacity, quality of life, and clinical outcome”. Circulation. 99 (9): 1173–82. PMID 10069785. Unknown parameter |month= ignored (help)
  13. ↑ Piepoli MF, Davos C, Francis DP, Coats AJ (2004). “Exercise training meta-analysis of trials in patients with chronic heart failure (ExTraMATCH)”. BMJ. 328 (7433): 189. doi:10.1136/bmj.37938.645220.EE. PMC 318480. PMID 14729656. Unknown parameter |month= ignored (help)
  14. ↑ Passino C, Severino S, Poletti R; et al. (2006). “Aerobic training decreases B-type natriuretic peptide expression and adrenergic activation in patients with heart failure”. J. Am. Coll. Cardiol. 47 (9): 1835–9. doi:10.1016/j.jacc.2005.12.050. PMID 16682309. Unknown parameter |month= ignored (help)


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