Myocardial infarction attacks

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. 

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). 

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. 

Defined as worsening (in intensity or frequency) angina attacks, sudden-onset angina at rest, and angina lasting more than 15 min. As these may herald myocardial infarction, they require urgent medical attention. 

These drugp are contraindicated in patients with known hypersensitivity to the drug or to any constituents of the drug, after a recent myocardial infarction (heart attack), or in patients with thyrotoxicosis. When hypothyroidism is a cause or contributing factor to a myocardial infarction or heart disease, the physician may prescribe small doses of thyroid hormone... 

MI myocardial infarction (heart attack) RF rheumatoid factor... 

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. ... 

Another vasoactive substance produced by the endothelium is thromboxane A2 (TxA2). Normally, small amounts of TxA2 are released continuously however, increased synthesis appears to be associated with some cardiac diseases. Synthesized from arachidonic acid, a plasma membrane phospholipid, TxA2 is a potent vasoconstrictor. Furthermore, this substance stimulates platelet aggregation, suggesting that it plays a role in thrombotic events such as myocardial infarction (heart attack). Nonsteroidal anti-inflammatory drugs such as aspirin and ibuprofen block formation of TxA2 and reduce formation of blood clots. 

Various antibody preparations have been developed that facilitate imaging of vascular-related conditions, including myocardial infarction, deep vein thrombosis and atherosclerosis. Anti-myosin monoclonal antibody fragments (Fab) labelled with mIn, for example, have been used for imaging purposes in conjunction with a planar gamma camera. The antibody displays specificity for intracellular cardiac myosin, which is exposed only upon death of heart muscle tissue induced by a myocardial infarction (heart attack). 

The response-to-injury hypothesis states that risk factors such as oxidized LDL, mechanical injury to the endothelium, excessive homocysteine, immunologic attack, or infection-induced changes in endothelial and intimal function lead to endothelial dysfunction and a series of cellular interactions that culminate in atherosclerosis. The eventual clinical outcomes may include angina, myocardial infarction, arrhythmias, stroke, peripheral arterial disease, abdominal aortic aneurysm, and sudden death. 

Goal BP values are <140/90 for most patients, but <130/80 for patients with diabetes mellitus, significant chronic kidney disease, known coronary artery disease (myocardial infarction [MI], angina), noncoronary atherosclerotic vascular disease (ischemic stroke, transient ischemic attack, peripheral arterial disease [PAD], abdominal aortic aneurysm), or a 10% or greater Framingham 10-year risk of fatal coronary heart disease or nonfatal MI. Patients with LV dysfunction have a BP goal of <120/80 mm Hg. 

Deliver Reliable, Evidence-Based Care for Acute Myocardial Infarction... to prevent deaths from heart attack... 

Cardiovascular disease Cardiomyopathy Congestive heart failure Myocardial infarction (heart attack)... 

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. 

Goldberg RJ, Zevallos JC, Yarzebski J, et al. Prognosis of acute myocardial infarction complicated by complete heart block (the Worcester Heart Attack Study). Am. J. Cardiol. 1992 69 1135-41. 

The salicylates are also potent antipyretic agents, with the exception of diflunisal, which is only weakly active. Aspirin acts at two distinct but related sites. It decreases prostaglandin-induced fever in response to pyrogens and induces a decrease in interleukin-1 modulation of the hypothalamic control of body temperature. Thus, the hypothalamic control of body temperature returns, vasodilation occurs, heat dissipates, and fever decreases. Other uses of aspirin include inhibition of platelet aggregation via inhibition of thromboxanes, which has been shown to decrease the incidence of blood clots, myocardial infarction, and transient ischemic attacks. 

Acetaminophen is similar to salicylates in that it is a useful analgesic for mild to moderate pain, with equal efficacy to aspirin, and like aspirin, it is antipyretic. However, acetaminophen exerts little if any effects on platelet aggregation and is not antiinflammatory. Thus, it is not useful for patients with arthritis or other inflammatory diseases. It is also not useful as an antithrombotic agent in the prevention of myocardial infarction or transient ischemic attacks. Acetaminophen does not produce the gastric ulceration that can occur with aspirin and is useful in patients who are salicylate sensitive or who have a history of ulcers or other gastric ulcerations. 

Adverse reactions associated with their administration include hypertension, headache, and possible seizures. Nausea, vomiting, chest pains, difficulties in breathing, and leg cramps also have been reported. These alkaloids should not be used in cases of threatened spontaneous abortion or in patients with known allergies to the drugs. Contraindications generally include angina pectoris, myocardial infarction, pregnancy, and a history of a cerebrovascular accident, transient ischemic attack, or hypertension. 

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