ST elevation myocardial infarction secondary prevention
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| Myocardial infarction Classification and external resources | |
 | |
|---|---|
| Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA). | |
| ICD-10 | I21.-I22. |
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
| Cardiology Network |
 Discuss ST elevation myocardial infarction secondary prevention further in the WikiDoc Cardiology Network |
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Secondary prevention
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.[1]
- Beta blocker therapy such as metoprolol or carvedilol should be commenced.[1] These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia.[1] 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.[1]
- Statin therapy has been shown to reduce mortality and morbidity post-MI.[1][1] 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.[1]
- 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.[1]
- Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI.[1] 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.[1] 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.[1][1]
- Reducing excess weight and exercising regularly.[1]
- Following a diet low in cholesterol (<200 mg daily) and saturated fat.[1]
Antithrombin Therapy
Warfarin or Coumadin
Mechanism of Benefit
Clinical Trial Data, Dosing, and Side Effects
Large randomized trials have demonstrated that oral anticoagulants, when given in adequate doses, reduce the rates of adverse outcomes, at the cost of a small increase in hemorrhagic events (186–188). In the Warfarin, Aspirin, Reinfarction Study (WARIS II), warfarin without aspirin in a dose intended to achieve an INR of 2.8 to 4.2 resulted in a significant reduction in a composite end point (death, nonfatal reinfarction, or thromboembolic stroke) compared with therapy with aspirin alone (16.7% versus 20.0%)(186) Warfarin therapy resulted in a small but significant increase in major, nonfatal bleeding compared with therapy with aspirin alone (0.62% versus 0.17% per year). Chronic therapy with warfarin after STEMI presents an alternative to clopidogrel in patients with aspirin allergy.
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)
See also
- acute coronary syndrome
- angina
- Cardiac arrest
- coronary thrombosis
- Hibernating myocardium
- Stunned myocardium
- Ventricular remodeling
References
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.
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .