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Heart attack myocardial infarction

EXAMPLE 14.3 Aspartate aminotransferase and alanine aminotransferase are released into the blood when tissues are damaged. For example, they are used as diagnostic tools when heart or liver damage has occurred, such as after a heart attack (myocardial infarct) or in hepatitis, respectively. Following tissue damage and ceU death, these enzymes (and others) are released into the blood. Damage to heart muscle is further characterized by the presence of creatine kinase (Sec. 13.12) in the plasma. [Pg.435]

The plaques of Alzheimer s disease and the fibrous state of the prions of mad cow disease (both with resulting brain destruction), the thrombi of stroke (cerebral thrombosis) and of heart attack (myocardial infarction), and the familiar manifestation of death (rigor mortis) represent excursions too far in the direction of protein insolubility. The favorable actions of antioxidants keep proteins from becoming so soluble (unfolded) that protein function disappears and proteolytic degradation ensues. Of course, the lack of blood clotting, hemophilia (the lack of clotting proteins to become insoluble by association of oil-like domains), results in death. Such devastations result from loss of proper balance between solubility and insolubility. They represent excursions too far from the cusp of insolubility, that is, too far from the boundary between insolubility and solubility. [Pg.3]

Cardiovascular disease Cardiomyopathy Congestive heart failure Myocardial infarction (heart attack)... [Pg.44]

Recombinant human erythropoietin (rHuEpo) may increase the risk of thrombosis (201). It has been reported that patients with carcinoma of the cervix who received chemotherapy and rHuEpo have an increased risk of symptomatic venous thrombosis (201). In clinical trials where the maintenance hematocrit was 3% on PROCRIT clotting of the arteriovenous shunts occurred at an annual rate of about 0.25 events per patient per year. However, other thrombotic conditions such as cerebrovascular events, transient ischemic attacks, myocardial infarction, or pulmonary embolism occurred at a rate of 0,04 events per patient per year (202). In a separate study of I, I I I untreated patients on hemodialysis, clotting of arteriovenous shunts occurred at a rate of 0.5 events per patient per year. In patients with chronic renal failure on hemodialysis who also had congestive heart failure, ischemic heart disease and venous thrombosis were increased in patients who were treated with PROCRIT targeted to a hematocrit level of 42 3% compared to those targeted to 30 3% (202). It has also been reported... [Pg.16]

Clinically, hypertension is a common (up to 34 %) cardiovascular event associated with bevacizumab treatment (Avastin PI 2013). Other cardiovascular events that may be associated with bevacizumab treatment include congestive cardiac failure, supraventricular tachycardia, and arterial thromboembolic events including cerebral infarction, transient ischemic attacks, myocardial infarction, angina, and hemorrhage (Nazer et al. 2011). The congestive heart failure may, in some cases, be associated with prior or concomitant use of anthacyclines. [Pg.423]

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. [Pg.180]

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). [Pg.131]

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. [Pg.309]

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... [Pg.531]

MI myocardial infarction (heart attack) RF rheumatoid factor... [Pg.648]

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. [Pg.210]

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). [Pg.395]

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. [Pg.126]

Deliver Reliable, Evidence-Based Care for Acute Myocardial Infarction... to prevent deaths from heart attack... [Pg.94]

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. [Pg.165]

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. [Pg.62]


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Heart Myocardial infarction

Heart attack infarction

Heart infarct

Infarct

Infarct, myocardial

Infarction

Myocardial infarction

Myocardial infarction attack

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