Myocardial infarction secondary prevention

Metoprolol is nsed in moderate hypertension, serions conditions of myocardial infarction, for preventing death of cardiovascular tissue, in angina, tachycardia, extrasystole, and for secondary prophylaxis after a heart attack. The most common synonyms are lopresor, betaloc, and others. 

Ticlopidine inhibits the P2Yj2 platelet ADP receptor, thus inhibiting ADP-dependent activation of the GP Ilb/IIIa receptor. It has a slow onset of action and takes 3-7 days to reach its maximal antiplatelet effect. It is inactive in vitro and must undergo activation by the hepatic cytochrome p450 enzyme system. Secondary prevention trials have found that ticlopidine-treated patients have an estimated RRR of 33% for the composite endpoint of stroke, myocardial infarction, or vascular death after ischemic stroke. Significant adverse effects include bone marrow depression, rash, diarrhea, and thrombotic thrombocytopenic purpura. No clinical trials have studied ticlopidine for the treatment of stroke in the acute phase. 

Devise a pharmacotherapy and risk-factor modification treatment plan for secondary prevention of coronary heart disease events in a patient following myocardial infarction. 

As of 1995, almost 38% of all women 50 to 75 years of age were using HRT.1 It was in 1996 that the United States Preventive Services Task Force (USPSTF) first published its recommendations that not all postmenopausal women should be prescribed HRT, but rather, therapy should be individualized based on risk factors. This recommendation was further supported with publication of the Heart and Estrogen/Progestin Replacement Study (HERS) in 1998, which demonstrated that women who had established CHD were at an increased risk of experiencing a myocardial infarction within the first year of HRT use compared with a similar group of women without CHD risk factors. As a result, the authors concluded that HRT is not recommended for the secondary prevention of CHD.2 Then, in 2002, the Women s Health Initiative (WHI) report was published. This trial demonstrated that HRT was not protective against CHD but... 

The AHA/ASA guidelines recommend that antiplatelet therapy as the cornerstone of antithrombotic therapy for the secondary prevention of ischemic stroke and should be used in noncardioembolic strokes. Aspirin, dopidogrel, and extended-release dipyridamole plus aspirin are all considered first-line antiplatelet agents (see Table 13-1). The combination of aspirin and clopido-grel can only be recommended in patients with ischemic stroke and a recent history of myocardial infarction or coronary stent placement and then only with ultra-low-dose aspirin to minimize bleeding risk. 

Lipid modifying drugs (statins) have shown secondary cardio-vascular preventive effects (myocardial infarction) in a very large number of patients. Only one study (Shepherd et al. 2002) has been conducted in the elderly and showed similar results. However there was a significant increased cancer risk (25%). 

European Secondary Prevention Study Group. Translation of clinical trials into practice a European population-based study of the use of thrombolysis for acute myocardial infarction. Lancet 1996 347(9010) 1203-7. 

Blockers are used as therapeutics in the treatment of hypertension, myocardial ischaemia (angina pectoris), tachyarrhythmias, and in the secondary prevention following myocardial infarction. More recently the cautious use of /3-blockers has been found to be of potential benefit in the treatment of congestive heart failure (NYHA stages II and III). 

ACE-inhibitors are known to cause regression of left ventricular and vascular hypertrophy. This phenomenon is important in the long-term treatment of hypertension, where cardiac hypertrophy is known to be an important, virtually independent risk factor. Data that are beginning to emerge, which indicate that ACE-inhibitors may be beneficial as secondary prevention in postinfarct patients, especially if signs of heart failure occur. This favourable influence of the ACE-inhibitors may be the result of haemodynamic effects, a favourable effect on neuroendocrine mechanisms, and also a beneficial influence on the process of remodeling of the heart, secondary to a myocardial infarction. 

Arterial thrombi (white thrombi) are formed initially from both platelets and fibrin in medium-sized arteries on the basis of atherosclerosis. These thrombi can lead to symptoms of, among others, myocardial ischemia and myocardial infarction. The treatment is primarily aimed at prevention of thrombus formation with platelet aggregation inhibitors. For the treatment of myocardial infarction thrombolytic agents are used and for secondary prevention both oral anticoagulants and anti-platelet drugs are employed. 

Sulfinpyrazone is a uricosuric and also inhibits platelet functions, probably mainly as a result of some inhibition of prostaglandin synthesis. However clinical efficacy in secondary prevention of myocardial infarction is inconsistent at the most. 

Beta-adrenoceptor antagonists are used to treat hypertension, angina pectoris, arrhythmias and secondary myocardial infarct prevention following primary infarction (timolol, metoprolol and propranolol). 

The FDA has approved the use of 325 mg/d for primary prophylaxis of myocardial infarction but urges caution in this use of aspirin by the general population except when prescribed as an adjunct to risk factor management by smoking cessation and lowering of blood cholesterol and blood pressure. Meta-analysis of many published trials of aspirin and other antiplatelet agents confirms the value of this intervention in the secondary prevention of vascular events among patients with a history of vascular events. 

People with diabetes have a much worse outcome after acute myocardial infarction, with a mortality rate at least twice that in non-diabetics. However, tight control of blood glucose, with immediate intensive insulin treatment during the peri-infarct period followed by intensive subcutaneous insulin treatment, was associated with a 30% reduction in mortality at 1 year, as reported in the DIGAMI study. In addition, the use of beta-blockers in this group of patients had an independent secondary preventive effect (198). The use of beta-blockers in diabetics with ischemic heart disease should be encouraged (199). 

MacDonald TM, Butler R, Newton RW, Morris AD. Which drugs benefit diabetic patients for secondary prevention of myocardial infarction DARTS/MEMO Collaboration. Diabet Med 1998 15(4) 282-9. 

In view of the perceived benefit of aspirin in the secondary prevention of stroke and myocardial infarction, two large trials involving physicians as subjects were initiated to study the effect of aspirin in the primary prevention of arterial thrombosis. In the American study, 22,000 volunteers (age 40 to 84 years) were randomly assigned to take 325 mg of aspirin every other day or placebo. The trial was halted early, after a mean follow-up of 5 years, when a 45% reduction in the incidence of myocardial infarction and a 72% reduction in the incidence of fatal myocardial infarction were noted with aspirin treatment. However, total mortality was reduced only 4% in the aspirin group, a difference that was not statistically significant, and there was a trend for a greater risk of hemorrhagic stroke with aspirin. Thus, the prophylactic use of aspirin in an apparently healthy population is not recommended at this time, unless there are risk factors for cardiovascular disease. 

Pedersen TR, Faergeman O, KasteleinJJ, etal, High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction the IDEAL study a randomized controlled trial. JAMA 2005 294 2437-2445,... 

The antiplatelet/antithrombotic activity of dipyridamole has been demonstrated in laboratory and in animal models, and has been shown to inhibit platelet aggregation and vessel-wall thrombogenesis [9-11]. Dipyridamole has been given either alone or with aspirin in the management of myocardial infarction and stroke. For the secondary prevention of stroke or transient ischemic attack, the drug may be given as a modified-release preparation in a dose of 200 mg twice daily. Dipyridamole administered intravenously results in a marked coronary vasodilation and is used in stress testing in patients with ischemic heart disease [5]. 

What classes of drugs should be initiated as standard secondary prevention treatment following acute myocardial infarction in this patient ... 

NICE (National Institute for Health and Clinical Excellence) (2007) Secondary prevention in primary and secondary care for patients following a myocardial infarction. Available at http //www.nice.org.uk/nicemedia/pdf/CG48NICEGuidance.pdf [Accessed 10 April 2008],... 

There is strong evidence that beta-blockers can reduce mortality by up to 23% post myocardial infarction. Beta-blockers should be used to reduce the risk of further cardiovascular disease events irrespective of whether the blood pressure is raised or not. There is no evidence that any beta-blocker is more effective than another in secondary prevention, hence a beta-blocker which is well tolerated and that can be taken once or twice daily should be used. Atenolol, bisoprolol or metoprolol are suitable agents. These agents are not specifically licensed post myocardial infarction but all are licensed for angina and the doses for this indication should be used i.e. 

The NICE clinical guidelines on secondary prevention of myocardial infarction (2007) now recommend that ACE inhibitors should be used in all patients post myocardial infarction with or without LVSD (i.e. ejection fraction <40%). 

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