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Myocardial infarction derivatives

A fibrate derivative or niacin should be considered in select patients with a low high-density lipoprotein (HDL) cholesterol less than 40 mg/dL (1.04 mmol/L) and/or a high triglyceride level greater than 200 mg/dL (2.26 mmol/L). In a large randomized trial in men with established CAD and low levels of HDL cholesterol, the use of gemfibrozil (600 mg twice daily) significantly decreased the risk of non-fatal myocardial infarction or death from coronary causes.78... [Pg.104]

Excessive doses of thyroid hormone may lead to heart failure, angina pectoris, and myocardial infarction. Allergic or idiosyncratic reactions can occur with the natural animal-derived products such as desiccated thyroid and thyroglobulin, but they are extremely rare with the synthetic products used today. Excess exogenous thyroid hormone may reduce bone density and increase the risk of fracture. [Pg.250]

Amiodarone (11), a benzofuran derivative, was initially developed as a coronary vasodilator in the early 1960 s [11,12]. Several years later, the efficacy of the compound as an antiarrhythmic agent began to be exploited. The first clinical trials with amiodarone were reported in 1974 [13]. Amiodarone was effective in controlling the tachyarrhythmias of eleven patients with Wolff-Parkinson-White syndrome. Since that time the compound has been studied extensively [14,15]. Recently, in the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT), amiodarone was shown to reduce mortality during a mean 18 month period following myocardial infarction (13.8% deaths in placebo group vs. 2.1 % deaths in the treatment group) [16]. [Pg.71]

Using plasma procainamide levels as a guide to therapy, it has been demonstrated (K13), contrary to evidence derived from uncontrolled trials (E2), that procainamide is valuable for preventing as well as controlling ventricular arrhythmias which develop in the immediate post-myocardial infarct period and are one of the main causes of death at this time. [Pg.85]

Although much of the data regarding the frequency of conduction abnormalities during acute myocardial infarction were derived from studies prior to the era of rapid reperfusion [14 17], data from more recent trials suggest that the incidence of intraventricular conduction defects has changed very little. [Pg.50]

In the Transplantation of Progenitor Cells and Regeneration Enhancement in Acute Myocardial Infarction (TOPCARE-AMI) trial, patients were randomized to receive either bone marrow-derived... [Pg.112]

Herreros J, Prosper F, Perez A, et al. Autologous intra-myocardial injection of cultured skeletal muscle-derived stem cells in patients with non-acute myocardial infarction. Eur Heart J. Nov 2003 24(22) 2012-2020. [Pg.141]

Alemtuzumab is a recombinant DNA-derived humanized monoclonal antibody used in the treatment of chronic lymphocytic leukemia and T-cell lymphoma. It targets CD52, a protein present on the surface of mature lymphocytes. Alemtuzumab has been associated with infusion-related events including hypotension, rigors, fever, shortness of breath, bron-chospasm, chills, and/or rash. Also reported were syncope, pulmonary infiltrates, cardiac arrhythmias, myocardial infarction and cardiac arrest. [Pg.461]

ACE inhibitors are widely prescribed for patients with atherosclerosis, hypertension, or diabetes, and after myocardial infarction, because of proven beneficial effects in each of these groups. In light of the results in the setting of stent restenosis, whether a patient with hypertension or some other target disorder who carries the DD genotype derives less benefit from ACE inhibitor therapy warrants consideration. [Pg.394]

Aspirin (acetylsalicylic acid, Figure 7.9) is a derivative of salicyclic acid, which was first used in 1875 as an antipyretic and antirheumatic. The usual dose for mild pain is 300-600 mg orally. In the treatment of rheumatic diseases, larger doses, 5-8 g daily, are often required. Aspirin is rapidly hydrolysed in the plasma, liver and eiythrocytes to salicylate, which is responsible for some, but not all, of the analgesic activity. Both aspirin and salicylate are excreted in the urine. Excretion is facilitated by alkalinisation of the urine. Metabolism is normally very rapid, but the liver enzymes responsible for metabolism are easily saturated and after multiple doses the terminal half-life may increase from the normal 2-3 h to 10 h. A soluble salt, lysine acetylsalicylic acid, with similar pharmacological properties to aspirin, has been used by parenteral administration for postoperative pain. Aspirin in low doses (80-160 mg daily) is widely used in patients with cardiovascular disease to reduce the incidence of myocardial infarction and strokes. The prophylaxis against thromboembolic disease by low-dose aspirin is due to inhibition of COX-1-generated thromboxane A2 production. Because platelets do not form new enzymes, and COX-1 is irreversibly inhibited by aspirin, inhibition of platelet function lasts for the lifetime of a platelet (8-10 days). [Pg.136]

Dopamine agonists are contraindicated in patients with a history of psychotic illness or recent myocardial infarction, or with active peptic ulceration. The ergot-derived agonists are best avoided in patients with peripheral vascular disease. [Pg.609]

Schachinger VES, Elsasser A, Haberbosch W, et al. Intracoronary infusion of bone marrow-derived progenitor cells in acute myocardial infarction a randomized, doubleblind, placebo-controlled muticenter trial (REPAIR-AMI), In Scientific Sessions of the American Heart Association 2005, Internet communication, 2005. [Pg.434]

Janssens SDC, Bogaert J, Theunissen K, et al. Autologous bone marrow-derived stem-cell transfer in patients with ST-segment elevation myocardial infarction double-blind, randomised controlled trial. Lancet 2006 367 1 13-121. [Pg.437]


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See also in sourсe #XX -- [ Pg.682 ]




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Infarct

Infarct, myocardial

Infarction

Myocardial infarction

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