Myocardial infarction therapy

Replacement therapy of hypothyroidism. Whether primary, i.e caused by thyroid disease, or secondary, i.e resulting from TSH deficiency, hypothyroidism is treated by oral administration of T4. Since too rapid activation of metabolism entails the hazard of cardiac overload (angina pectoris, myocardial infarction), therapy is usually started with low doses and gradually increased. The final maintenance dose required to restore a euthyroid state depends on individual needs (approx. 

It is indicated in pulmonary hypertension, prophylaxis of angina pectoris, post myocardial infarction therapy, CHF and acute LVF. It is not recommended for acute attacks of angina. 

Central nervous system toxicity is rarely observed with catecholamines or drugs such as phenylephrine. In moderate doses, amphetamines commonly cause restlessness, tremor, insomnia, and anxiety in high doses, a paranoid state may be induced. Cocaine may precipitate convulsions, cerebral hemorrhage, arrhythmias, or myocardial infarction. Therapy is discussed in Chapter 59 Management of the Poisoned Patient. 

Like p-blockers, ACE inhibitors are most effective in hypertensive patients who are white and young. However, when used in combination with a diuretic, the effectiveness of ACE inhibitors is similar in white and black hypertensive patients. Unlike p-blockers, ACE inhibitors are effective in the management of patients with chronic congestive heart failure (see p. 156). ACE inhibitors are now a standard in the care of a patient following a myocardial infarction. Therapy is started 24 hours after the end of the infarction. 

DNLM 1. Myocardial infarction-therapy. 2. Angioplasty, Transluminal, Percutaneous Coronary. 3. Combined Modality Therapy. 4. Thrombolytic Therapy. WG 300 P536 2005] RC685.I6P48 2005 616.1 237061-dc22... 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

Other Cardiovascular Agents Effecting Atherosclerosis. A large amount of clinical data is available concerning semm Upid profiles in patients subjected to dmg therapy for other cardiovascular diseases. Atheroma, for example, may be the underlying cause of hypertension and myocardial infarction. There are on the order of 1.5 million heart attacks pet year in the United States (155). 

A third study (85) enrolled 7825 hypertensive patients (55% males and 45% females) having diastoHc blood pressures (DBP) of 99—104 mm Hg (13—14 Pa) there were no placebo controls. Forty-six percent of the patients were assigned to SC antihypertensive dmg therapy, ie, step 1, chlorthaUdone step 2, reserpine [50-55-5] or methyldopa [555-30-6], and step 3, hydralazine [86-54-4]. Fifty-four percent of the patients were assigned to the usual care (UC) sources in the community. Significant reductions in DBP and in cardiovascular and noncardiovascular deaths were noted in both groups. In the SC group, deaths from ischemic heart disease increased 9%, and deaths from coronary heart disease (CHD) and acute myocardial infarctions were reduced 20 and 46%, respectively. 

Thrombolytic Enzymes. Although atherosclerosis and the accompanying vascular wall defects are ultimately responsible for such diseases as acute pulmonary embolism, arterial occlusion, and myocardial infarction, the lack of blood flow caused by a fibrin clot directly results in tissue injury and in the clinical symptoms of these devastating diseases (54). Thrombolytic enzyme therapy removes the fibrin clot by dissolution, and has shown promise in the treatment of a number of thrombo-occlusive diseases (60). 

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

Antiplatetelet Trialists Collaboration (2002) Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 324 71-86... 

Therapeutically t-PA and urokinase are the most important drugs for fibrinolytic therapy (myocardial infarction, stroke, massive pulmonary embolism). This treatment is associated with an enhanced risk of bleeding complications. 

Krumholz HM, Pasternak RC, Weinstein MC, et al. Cost effectiveness of thrombolytic therapy with streptokinase in elderly patients with suspected acute myocardial infarction. N Engl J Med 1992 327 7-13. 

Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to improve vascular outcomes due to their cholesterol-lowering effects as well as multiple pleiotropic effects. In high-risk populations, statin therapy is known to reduce the risk of vascular events such as myocardial infarction and stroke. A meta-analysis of 10 trials involving 79,494 subjects showed that statin therapy reduced the incidence of stroke by 18%, major coronary events by 27%, and all-cause mortality by 15%. The SPARCL trial recently showed that high-dose HMG-CoA reductase inhibitors prevent recurrent stroke and transient ischemic attacks. ... 

Antiplatelet Trialist Collaboration. Collaborative overview of randomised trials of antiplatelet treatment. Part I prevention of death, myocardial infarction and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ 1994 308 81-106. 

Contraindications to Fibrinolytic Therapy in Patients With ST-Elevation Myocardial Infarction... 

Antiplatelet therapy with aspirin should be considered for all patients without contraindications, particularly in patients with a history of myocardial infarction. Clopidogrel may be considered in patients with allergies or intolerance to aspirin. In some patients, combination antiplatelet therapy with aspirin and clopidogrel may be used. 

To control risk factors and prevent major adverse cardiac events, statin therapy should be considered in all patients with ischemic heart disease, particularly in those with elevated low-density lipoprotein cholesterol. In the absence of contraindications, angiotensin-converting enzyme inhibitors should be considered in ischemic heart disease patients who also have diabetes melli-tus, left ventricular dysfunction, history of myocardial infarction, or any combination of these. Angiotensin receptor blockers... 

Treatment of sinus bradycardia is only necessary in patients who become symptomatic. If the patient is taking any med-ication(s) that may cause sinus bradycardia, the drug(s) should be discontinued whenever possible. If the patient remains in sinus bradycardia after discontinuation of the drug(s) and after five half-lives of the drug(s) have elapsed, then the drugs(s) can usually be excluded as the etiology of the arrhythmia. In certain circumstances, however, discontinuation of the medication(s) may be undesirable, even if it may be the cause of symptomatic sinus bradycardia. For example, if the patient has a history of myocardial infarction or HF, discontinuation of a (3-blocker is undesirable, because (3-blockers have been shown to reduce mortality and prolong life in patients with those diseases, and the benefits of therapy with... 

Randomized trials have been completed assessing the role of antiplatelet therapy with aspirin for primary stroke prevention. The use of aspirin in patients with no history of stroke or ischemic heart disease reduced the incidence of non-fatal myocardial infarction (MI) but not of stroke. A meta-analysis of eight trials found that the risk of stroke was slightly increased with aspirin use, especially hemorrhagic stroke. Major bleeding risk was also increased with aspirin use.4 Aspirin is beneficial in the primary prevention of MI, but not for primary stroke prevention. 

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... 

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