ST elevation myocardial infarction secondary prevention: Difference between revisions
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=== Warfarin or Coumadin === | === Warfarin or Coumadin === | ||
'''Mechanism of Benefit''' | '''Mechanism of Benefit''' | ||
'''Guidelines (Do not Edit)''' | '''Guidelines (Do not Edit)''' | ||
Revision as of 19:53, 30 April 2009
| Myocardial infarction | |
| ICD-10 | I21-I22 |
|---|---|
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
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 Discuss ST elevation myocardial infarction secondary prevention further in the WikiDoc Cardiology Network |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor: Cafer Zorkun, M.D., Ph.D. [2]
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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.
Antithrombin Therapy
Warfarin or Coumadin
Mechanism of Benefit
Guidelines (Do not Edit)
Class I
- 1. Warfarin should be given to aspirin-allergic post-STEMI patients with indications for anticoagulation as follows:
- a. Without stent implanted (INR 2.5 to 3.5). (Level of Evidence: B)
- b. With stent implanted and clopidogrel 75 mg/d administered concurrently (INR 2.0 to 3.0). (Level of Evidence: C)
- 2. Warfarin (INR 2.5 to 3.5) is a useful alternative to clopidogrel in aspirin-allergic patients after STEMI who do not have a stent implanted. (Level of Evidence: B)
- 3. Warfarin (INR 2.0 to 3.0) should be prescribed for post-STEMI patients with either persistent or paroxysmal atrial fibrillation. (Level of Evidence: A)
- 4. In post-STEMI patients with LV thrombus noted on an imaging study, warfarin should be prescribed for at least 3 months (Level of Evidence: B) and indefinitely in patients without an increased risk of bleeding (Level of Evidence: C).
- 5. Warfarin alone (INR 2.5 to 3.5) or warfarin (INR 2.0 to 3.0) in combination with aspirin (75 to 162 mg) should be prescribed in post-STEMI patients who have no stent implanted and who have indications for anticoagulation. (Level of Evidence: B)
- 6. STEMI patients with acute ischemic stroke and persistent atrial fibrillation should receive lifelong moderate intensity (international normalized ratio [INR] 2 to 3) warfarin therapy. (Level of Evidence: A)
- 7. STEMI patients with or without acute ischemic stroke who have a cardiac source of embolism (atrial fibrillation, mural thrombus, or akinetic segment) should receive moderate-intensity (INR 2 to 3) warfarin therapy (in addition to aspirin). The duration of warfarin therapy should be dictated by clinical circumstances (eg, at least 3 months for patients with an LV mural thrombus or akinetic segment and indefinitely in patients with persistent atrial fibrillation). The patient should receive LMWH or UFH until adequately anticoagulated with warfarin. (Level of Evidence: B)
- 8. DVT or pulmonary embolism after STEMI should be treated with full-dose LMWH for a minimum of 5 days and until the patient is adequately anticoagulated with warfarin. Start warfarin concurrently with LMWH and titrate to INR of 2 to 3. (Level of Evidence: A)
- 9. If true aspirin allergy is present, warfarin therapy with a target INR of 2.5 to 3.5 is a useful alternative to clopidogrel in patients less than 75 years of age who are at low risk for bleeding and who can be monitored adequately for dose adjustment to maintain a target INR range. (Level of Evidence: C)
Class IIa
- 1. In post-STEMI patients less than 75 years of age without specific indications for anticoagulation who can have their level of anticoagulation monitored reliably, warfarin alone (INR 2.5 to 3.5) or warfarin (INR 2.0 to 3.0) in combination with aspirin (75 to 162 mg) can be useful for secondary prevention. (Level of Evidence: B)
- 2. It is reasonable to prescribe warfarin to post-STEMI patients with LV dysfunction and extensive regional wall-motion abnormalities. (Level of Evidence: A)
Class IIb
- 1. Warfarin may be considered in patients with severe LV dysfunction, with or without CHF. (Level of Evidence: C)
Recommendations for Secondary Prevention
Source: National Guideline Clearinghouse
Smoking
Goal: Complete cessation. No exposure to environmental tobacco smoke.
- Ask about tobacco use status at every visit. Level of Evidence I (B)
- Advise every tobacco user to quit. Level of Evidence I (B)
- Assess the tobacco user's willingness to quit. Level of Evidence I (B)
- Assist by counseling and developing a plan for quitting. Level of Evidence I (B)
- Arrange follow-up, referral to special programs, or pharmacotherapy (including nicotine replacement and bupropion). Level of Evidence I (B)
- Urge avoidance of exposure to environmental tobacco smoke at work and home. Level of Evidence I (B)
Blood Pressure Control
Goal: <140/90 mm Hg or <130/80 mm Hg if patient has diabetes or chronic kidney disease
For all patients:
- 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 I (B) [14]
For patients with blood pressure >140/90 mm Hg (or >130/80 mm Hg for individuals with chronic kidney disease or diabetes):
- As tolerated, add blood pressure medication, treating initially with beta-blockers and/or angiotensin-converting enzyme (ACE) inhibitors, with addition of other drugs such as thiazides as needed to achieve goal blood pressure. Level of Evidence I (A) [14]
Lipid Management
Goal: Low-density lipoprotein cholesterol (LDL-C) < 100 mg/dL. If triglycerides are >200 mg/dL non-high-density lipoprotein cholesterol (HDL-C) should be <130 mg/dL.[14]
For all patients:
- Start dietary therapy. Reduce intake of saturated fats (to <7% of total calories), trans-fatty acids, and cholesterol (to <200 mg/dL). I (B)[14]
- Adding plant stanol/sterols (2 g/day) and viscous fiber (>10 g/day) will further lower LDL-C
- Promote daily physical activity and weight management. I (B) [14]
- Encourage increased consumption of omega-3 fatty acids in the form of fishb or in capsule form (1 g/day) for risk reduction. For treatment of elevated triglycerides, higher doses are usually necessary for risk reduction. IIb (B) [14]
For lipid management:
Assess fasting lipid profile in all patients, and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. For hospitalized patients, initiate lipid-lowering medication as recommended below before discharge according to the following schedule:
- LDL-C should be <100 mg/dL I (A)[14], and
- Further reduction of LDL-C to <70 mg/dL is reasonable. IIa (A)[14]
- If baseline LDL-C is >100 mg/dL, initiate LDL-lowering drug therapy.c I (A)[14]
- If on-treatment LDL-C >100 mg/dL, intensify low-density lipoprotein (LDL)-lowering therapy (may require LDL-lowering drug combinationd). I (A)
- If baseline LDL-C is 70 to 100 mg/dL, it is reasonable to treat to LDL-C <70 mg/dL. IIa (B)[14]
- If triglycerides are 200 to 499 mg/dL, non-HDL-C should be <130 mg/dL. I (B) [14], and
- Further reduction of non-HDL-C to <100 mg/dL is reasonable. IIa (B)[14]
- Therapeutic options to reduce non-HDL-C are:
If triglycerides are >500 mg/dL, therapeutic options to prevent pancreatitis are fibratef or niacinf before LDL-lowering therapy; and treat LDL-C to goal after triglyceride-lowering therapy. Achieve non-HDL-C <130 mg/dL if possible. I (C)[14]
Physical Activity
Goal: 30 minutes, 7 days per week (minimum 5 days per week)
- For all patients, assess risk with a physical activity history and/or an exercise test, to guide prescription. I (B)[14]
- For all patients, encourage 30 to 60 minutes of moderate-intensity aerobic activity, 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, household work). I (B)[14]
- Encourage resistance training 2 days per week. IIb (C)[14]
- Advise medically supervised programs for high-risk patients (e.g., recent acute coronary syndrome or revascularization, heart failure). I (B)[14]
Weight Management
Goal: Body mass index: 18.5 to 24.9 kg/m2. Waist circumference: men <40 inches, women <35 inches.
- Assess body mass index 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 body mass index between 18.5 and 24.9 kg/m2. I (B)[14]
- If waist circumference (measured horizontally at the iliac crest) is >35 inches in women and >40 inches in men, initiate lifestyle changes and consider treatment strategies for metabolic syndrome as indicated. I (B)[14]
- 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. I (B)[14]
Diabetes Management
Goal: Glycosylated hemoglobin (HbA1c) <7%
- Initiate lifestyle and pharmacotherapy to achieve near-normal HbA1c. I (B)[14]
- Begin vigorous modification of other risk factors (e.g., physical activity, weight management, blood pressure control, and cholesterol management as recommended above). I (B)[14]
- Coordinate diabetic care with patient's primary care physician or endocrinologist. I (C)[14]
Antiplatelet Agents / Anticoagulants
- Start aspirin 75 to 162 mg/day and continue indefinitely in all patients unless contraindicated. I (A)[14]
- For patients undergoing coronary artery bypass grafting, aspirin should be started within 48 hours after surgery to reduce saphenous vein graft closure. Dosing regimens ranging from 100 to 325 mg/day appear to be efficacious. Doses higher than 162 mg/day can be continued for up to 1 year. I (B)[14]
- Start and continue clopidogrel 75 mg/day in combination with aspirin for up to 12 months in patients after acute coronary syndrome or percutaneous coronary intervention with stent placement (>1 month for bare metal stent, >3 months for sirolimus-eluting stent, and >6 months for paclitaxel-eluting stent). I (B)[14]
- Patients who have undergone percutaneous coronary intervention with stent placement should initially receive higher-dose aspirin at 325 mg/day for 1 month for bare metal stent, 3 months for sirolimus-eluting stent, and 6 months for paclitaxel-eluting stent. I (B)[14]
- Manage warfarin to international normalized ratio=2.0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter, and in post–myocardial infarction patients when clinically indicated (e.g., atrial fibrillation, left ventricular thrombus). I (A)[14]
- Use of warfarin in conjunction with aspirin and/or clopidogrel is associated with increased risk of bleeding and should be monitored closely. I (B)[14]
Renin-Angiotensin-Aldosterone System Blockers
Angiotensin-converting enzyme (ACE) inhibitors:
- Start and continue indefinitely in all patients with left ventricular ejection fraction <40% and in those with hypertension, diabetes, or chronic kidney disease, unless contraindicated. I (A)[14]
- Consider for all other patients. I (B)[14]
- Among lower-risk patients with normal left ventricular ejection fraction in whom cardiovascular risk factors are well controlled and revascularization has been performed, use of ACE inhibitors may be considered optional. IIa (B)[14]
Angiotensin receptor blockers:
- Use in patients who are intolerant of ACE inhibitors and have heart failure or have had a myocardial infarction with left ventricular ejection fraction <40%. I (A)[14]
- Consider in other patients who are ACE inhibitor intolerant. I (B)[14]
- Consider use in combination with ACE inhibitors in systolic-dysfunction heart failure. IIb (B)[14]
Aldosterone blockade:
- Use in post-myocardial infarction patients, without significant renal dysfunctiong or hyperkalemiah, who are already receiving therapeutic doses of an ACE inhibitor and beta-blocker, have a left ventricular ejection fraction <40%, and have either diabetes or heart failure. I (A)[14]
Beta-Blockers
- Start and continue indefinitely in all patients who have had myocardial infarction, acute coronary syndrome, or left ventricular dysfunction with or without heart failure symptoms, unless contraindicated. I (A)[14]
- Consider chronic therapy for all other patients with coronary or other vascular disease or diabetes unless contraindicated. IIa (C)[14]
Influenza Vaccination
Patients with cardiovascular disease should have an influenza vaccination. I (B)[14]
See also
- acute coronary syndrome
- angina
- Cardiac arrest
- coronary thrombosis
- Hibernating myocardium
- Stunned myocardium
- Ventricular remodeling
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. PMID 14504182. Unknown parameter
|month=ignored (help) - ↑ 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. PMID 2858114.
- ↑ Dargie HJ (2001). "Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial". Lancet. 357 (9266): 1385–90. PMID 11356434. Unknown parameter
|month=ignored (help) - ↑ 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. PMID 1386652. Unknown parameter
|month=ignored (help) - ↑ Sacks FM, Pfeffer MA, Moye LA; et al. (1996). "The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators". N. Engl. J. Med. 335 (14): 1001–9. PMID 8801446. Unknown parameter
|month=ignored (help) - ↑ Sacks FM, Moyé LA, Davis BR; et al. (1998). "Relationship between plasma LDL concentrations during treatment with pravastatin and recurrent coronary events in the Cholesterol and Recurrent Events trial". Circulation. 97 (15): 1446–52. PMID 9576424. Unknown parameter
|month=ignored (help) - ↑ 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. PMID 16226165. 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. PMID 15537370.
- ↑ "Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico". Lancet. 354 (9177): 447–55. 1999. PMID 10465168. Unknown parameter
|month=ignored (help) - ↑ 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. PMID 16267249. Unknown parameter
|month=ignored (help) - ↑ 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. PMID 16772624. Unknown parameter
|month=ignored (help) - ↑ 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. PMID 15956633. Unknown parameter
|month=ignored (help) - ↑ 14.00 14.01 14.02 14.03 14.04 14.05 14.06 14.07 14.08 14.09 14.10 14.11 14.12 14.13 14.14 14.15 14.16 14.17 14.18 14.19 14.20 14.21 14.22 14.23 14.24 14.25 14.26 14.27 14.28 14.29 14.30 14.31 14.32 14.33 14.34 14.35 14.36 14.37 14.38 14.39 14.40 14.41 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". Circulation. 113 (19): 2363–72. doi:10.1161/CIRCULATIONAHA.106.174516. PMID 16702489. Unknown parameter
|month=ignored (help)
External links
- Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study, from the United States National Heart, Lung and Blood Institute
- Heart Attack - overview of resources from MedlinePlus.
- Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada
- Regional PCI for STEMI Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI
- STEMI Systems - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
- American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.
- American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack.