ST elevation myocardial infarction secondary prevention
Revision as of 15:18, 5 October 2012 by Michael Maddaleni(talk | contribs)(/* ACC / AHA Guidelines- Recommendations for Smoking (DO NOT EDIT){{cite journal |author=Antman EM, Hand M, Armstrong PW, et al |title=2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial I...)
Patients are usually treated with several long-term medications following a ST elevation myocardial infarction with the goal of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:[1]
Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased.[2]
Beta blocker therapy such as metoprolol or carvedilol should be commenced.[3] These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia.[4] β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.[5]
Statin therapy has been shown to reduce mortality and morbidity post-MI.[6][7] The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.[8] A study by AJC by Herbert D. Aranow, et al. indicates that, for patients who underwent lipid-lowering therapy prior to having an acute myocardial infarction (AMI), infarct size was significantly less than for patients who had not received this earlier treatment. Data from 10,548 patients were collected from both the Global Use of Streptokinase or t-PA for Occluded Coronary Arteries (GUSTO) IIb (n=6,414) and the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Supression Using Integrilin Therapy (PURSUIT) (n=4,134) studies, with infarct size measured by patients' peak creatine kinase (CK) -MB levels. Patients who had lipid-lowering therapy had a median peak CK-MB of 4.2 times the upper limit of normal (ULN) compared to 5.2 times the ULN for those who were not pre-treated (p<0.0001). These results suggest a potential benefit of lipid-lowering therapy for patients at risk for an AMI. Noted limitations of the study include: the observational study design (both the potential effects of confounding variables and the "healthy-user bias" ); the lack of documented information differentiating between statin and nonstatin therapies; and the exclusion from analysis of patients who died during the index hospitalization.
The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above.[9]
Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI.[10] While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of ventricular fibrillation.[11] However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids.[12][13]
Reducing excess weight and exercising regularly.
Keeping BP and diabetes under check.
Following a diet low in cholesterol (<200 mg daily) and saturated fat.
Increasing HDL- Patients with low HDL [A lipoprotein that transports cholesterol in the blood; composed of a high proportion of protein and relatively little cholesterol] (<35 mg/dl) are encouraged to exercise regularly and to take medications to increase HDL levels.
ACC / AHA Guidelines- Recommendations for Secondary Prevention (DO NOT EDIT)[14]
ACC / AHA Guidelines- Recommendations for Smoking (DO NOT EDIT)[14]
2007 Goal
Complete cessation, no exposure to environmental tobacco smoke
ACC / AHA Guidelines- Recommendations for Blood Pressure Control (DO NOT EDIT)[14]
“
2007 Goal
Less than 140/90 mm Hg or less than 130/80 if patient has diabetes or chronic kidney disease
For all patients:
Class I
1. For patients with blood pressure greater than or equal to 140/90 mm Hg (or greater than or equal to 130/80 mm Hg for patients with diabetes or chronic kidney disease), it is recommended to initiate or maintain 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. (Level of Evidence: B)
ACC / AHA Guidelines- Recommendations for Lipid Management (DO NOT EDIT)[14]
“
2007 Goal
LDL-C substantially less than 100 mg per dL (If triglycerides are greater than or equal to 200 mg per dL, non–HDL-C should be less than 130 mg per dL.)
Recommendations
1. Starting dietary therapy is recommended for all patients. Reduce intake of saturated fats (to less than 7% of total calories), trans fatty acids, and cholesterol (to less than 200 mg per day). (Class I Recommendation; Level of Evidence: B)
2. Adding plant stanol/sterols (2 g per day) and/or viscous fiber (greater than 10 g per day) is reasonable to further lower LDL-C. (Class IIa Recommendation; Level of Evidence: A)
3. Promotion of daily physical activity and weight management is recommended. (Class I Recommendation; Level of Evidence: B)
4. It may be reasonable to encourage increased consumption of omega-3 fatty acids in the form of fish or in capsules (1 g per day) for risk reduction. For treatment of elevated triglycerides, higher doses are usually necessary for risk reduction. (Class IIb Recommendation; Level of Evidence: B)
5. A fasting lipid profile should be assessed in all patients and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. (Class I Recommendation; Level of Evidence: A) For hospitalized patients, initiation of lipid-lowering medication is indicated as recommended below before discharge according to the following schedule:
LDL-C should be less than 100 mg per dL. (Class I Recommendation; Level of Evidence: A)
Further reduction of LDL-C to less than 70 mg per dL is reasonable. (Class IIa Recommendation; Level of Evidence: A)
If baseline LDL-C is greater than or equal to 100 mg per dL, LDL-lowering drug therapy should be initiated. (Class I Recommendation; Level of Evidence: A)
If on-treatment LDL-C is greater than or equal to 100 mg per dL, intensifying LDL-lowering drug therapy (may require LDL-lowering drug combination) is recommended. (Class I Recommendation; Level of Evidence: A)
If baseline LDL-C is 70 to 100 mg per dL, it is reasonable to treat to LDL-C less than 70 mg per dL. (Class IIa Recommendation; Level of Evidence: B)
If triglycerides are greater than or equal to 150 mg per dL or HDL-C is less than 40 mg per dL, weight management, physical activity, and smoking cessation should be emphasized. (Class I Recommendation; Level of Evidence: B)
If triglycerides are 200 to 499 mg per dL, non–HDL-C target should be less than 130 mg per dL. (Class I Recommendation; Level of Evidence: B)
If triglycerides are 200 to 499 mg per dL, further reduction of non–HDL-C to less than 100 mg per dL is reasonable. (Class IIa Recommendation; Level of Evidence: B)
6. Therapeutic options to reduce non–HDL-C include:
More intense LDL-C–lowering therapy is indicated. (Class I Recommendation; Level of Evidence: B)
2. For all patients, it is recommended that risk be assessed with a physical activity history and/or an exercise test to guide prescription. (Level of Evidence: B)
3. For all patients, encouraging 30 to 60 minutes of moderate-intensity aerobic activity is recommended, such as brisk walking on most—preferably all—days of the week, supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, and household work). (Level of Evidence: B)
Class IIb
1. Encouraging resistance training 2 days per week may be reasonable. (Level of Evidence: C)
”
ACC / AHA Guidelines- Recommendations for Weight Management (DO NOT EDIT)[14]
Waist circumference: Men less than 40 inches (102 cm), women less than 35 inches (89 cm)
Class I
1. It is useful to assess BMI and/or waist circumference on each visit and consistently encourage weight maintenance/reduction through an appropriate balance of physical activity, caloric intake, and formal behavioral programs when indicated to maintain/achieve a BMI between 18.5 and 24.9 kg/m2. (Level of Evidence: B)
2. The initial goal of weight loss therapy should be to reduce body weight by approximately 10% from baseline. With success, further weight loss can be attempted if indicated through further assessment. (Level of Evidence: B)
3. If waist circumference (measured horizontally at the iliac crest) is 35 inches (89 cm) or greater in women and 40 inches (102 cm) or greater in men, it is useful to initiate lifestyle changes and consider treatment strategies for metabolic syndrome as indicated. (Level of Evidence: B)
”
ACC / AHA Guidelines- Recommendations for Diabetes Management (DO NOT EDIT)[14]
1. It is recommended to initiate lifestyle and pharmacotherapy to achieve near-normal HbA1c. (Level of Evidence: B)
2. Beginning vigorous modification of other risk factors (e.g., physical activity, weight management, blood pressure control, and cholesterol management as recommended above) is beneficial. (Level of Evidence: B)
ACC / AHA Guidelines- Recommendations for Antiplatelet Agents/Anticoagulants: Aspirin (DO NOT EDIT)[14]
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Class I
1. For all post-PCISTEMIstented patients without aspirin resistance, allergy, or increased risk of bleeding, aspirin 162 mg to 325 mg daily should be given for at least 1 month after BMS implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation, after which long-term aspirin use should be continued indefinitely at a dose of 75 mg to 162 mg daily. (Level of Evidence: B)
Class IIa
1. In patients for whom the physician is concerned about risk of bleeding lower-dose 75 mg to 162 mg of aspirin is reasonable during the initial period after stent implantation. (Level of Evidence: C)
”
ACC / AHA Guidelines- Recommendations for Antiplatelet Agents/Anticoagulants: Clopidogrel (DO NOT EDIT)[14]
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Class I
1. For all post-PCI patients who receive a DES, clopidogrel 75 mg daily should be given for at least 12 months if patients are not at high risk of bleeding. For post-PCI patients receiving a BMS, clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks). (Level of Evidence: B)
2. For all STEMI patients not undergoing stenting (medical therapy alone or PTCA without stenting), treatment with clopidogrel should continue for at least 14 days. (Level of Evidence: B)
Class IIa
1. Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) is reasonable in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. (Level of Evidence: C)
”
ACC / AHA Guidelines- Recommendations for Antiplatelet Agents/Anticoagulants: Warfarin (DO NOT EDIT)[14]
2. 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)
3. In patients requiring warfarin, clopidogrel, and aspirin therapy, an INR of 2.0 to 2.5 is recommended with low dose aspirin (75 mg to 81 mg) and a 75 mg dose of clopidogrel. (Level of Evidence: C)
”
ACC / AHA Guidelines- Recommendations for Renin-Angiotensin-Aldosterone System Blockers: ACE Inhibitors (DO NOT EDIT)[14]
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Class I
1. ACE inhibitors should be started and continued indefinitely in all patients recovering from STEMI with LVEF less than or equal to 40% and for those with hypertension, diabetes, or chronic kidney disease, unless contraindicated. (Level of Evidence: A)
2. ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI who are not lower risk (lower risk defined as those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed), unless contraindicated. (Level of Evidence: B)
Class IIa
1. Among lower risk patients recovering from STEMI (i.e., those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed) use of ACE inhibitors is reasonable. (Level of Evidence: B)
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ACC / AHA Guidelines- Recommendations for Renin-Angiotensin-Aldosterone System Blockers: Angiotensin Receptor Blockers (DO NOT EDIT)[14]
The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction [15]
The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction [14]
References
↑Smith A, Aylward P, Campbell T, et al. Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513
↑Peters RJ, Mehta SR, Fox KA; et al. (2003). "Effects of aspirin dose when used alone or in combination with clopidogrel in patients with acute coronary syndromes: observations from the Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) study". Circulation. 108 (14): 1682–7. doi:10.1161/01.CIR.0000091201.39590.CB. PMID14504182. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Yusuf S, Peto R, Lewis J, Collins R, Sleight P (1985). "Beta blockade during and after myocardial infarction: an overview of the randomized trials". Prog Cardiovasc Dis. 27 (5): 335–71. PMID2858114.CS1 maint: Multiple names: authors list (link)
↑Pfeffer MA, Braunwald E, Moyé LA; et al. (1992). "Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators". N. Engl. J. Med. 327 (10): 669–77. PMID1386652. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Ray KK, Cannon CP (2005). "The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes". J. Am. Coll. Cardiol. 46 (8): 1425–33. doi:10.1016/j.jacc.2005.05.086. PMID16226165. Unknown parameter |month= ignored (help)
↑Keating GM, Plosker GL (2004). "Eplerenone : a review of its use in left ventricular systolic dysfunction and heart failure after acute myocardial infarction". Drugs. 64 (23): 2689–707. PMID15537370.
↑Leaf A, Albert CM, Josephson M; et al. (2005). "Prevention of fatal arrhythmias in high-risk subjects by fish oil n-3 fatty acid intake". Circulation. 112 (18): 2762–8. doi:10.1161/CIRCULATIONAHA.105.549527. PMID16267249. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Brouwer IA, Zock PL, Camm AJ; et al. (2006). "Effect of fish oil on ventricular tachyarrhythmia and death in patients with implantable cardioverter defibrillators: the Study on Omega-3 Fatty Acids and Ventricular Arrhythmia (SOFA) randomized trial". JAMA. 295 (22): 2613–9. doi:10.1001/jama.295.22.2613. PMID16772624. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Raitt MH, Connor WE, Morris C; et al. (2005). "Fish oil supplementation and risk of ventricular tachycardia and ventricular fibrillation in patients with implantable defibrillators: a randomized controlled trial". JAMA. 293 (23): 2884–91. doi:10.1001/jama.293.23.2884. PMID15956633. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑ 14.0014.0114.0214.0314.0414.0514.0614.0714.0814.0914.1014.1114.1214.1314.1414.15Antman EM, Hand M, Armstrong PW; et al. (2008). "2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee". Circulation. 117 (2): 296–329. doi:10.1161/CIRCULATIONAHA.107.188209. PMID18071078. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)