Identifying and, when present, treating category I risk factors can be an optimal secondary prevention strategy in patients with STEMI. You can read more about general coronary heart disease secondary prevention HERE
Long-term Medical Therapy and 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:
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 EKG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.
Statin therapy has been shown to reduce mortality and morbidity post-MI. 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. 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.
Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI. 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. 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.
Reducing excess weight and exercising regularly.
Keeping blood pressure 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.
2007 Update of 2004 ACC / AHA Guidelines for the management of ST Segment Elevation Myocardial Infarction - Recommendations for Secondary Prevention (DO NOT EDIT)
"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.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)"
The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction 
The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction 
↑Smith A, Aylward P, Campbell T, et al. Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513
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↑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)
↑ 14.014.114.214.314.414.514.614.714.814.9Antman 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)