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Heparin infarction

Camerlingo M, Salvi P, Belloni G, Gamba T, Mario Cesana B, Mamoli A. Intravenous heparin started within the first 3 hours after onset of symptoms as a treatment for acute nonlacunar hemispheric cerebral infarctions. Stroke 2005 36 2415-2420. [Pg.157]

A specific immunoassay for measuring two-chain factor VIIa levels in plasma has been developed to identify activation of factor VII in patients with acute coronary syndromes suchs as myocardial infarction and unstable angina (12). Because regulation of factor VIIa is believed to be mediated by tissue factor pathway inhibitor (TFPI), its measurement is also useful in assessing thombotic and cardio-vasular disorders. Because TFPI is released by heparin, its measurement is also useful in assessing the efficacy of heparin and endothelial cell function (93). [Pg.155]

J Heparin-induced thrombocytopenia (HIT) is a serious immune-mediated problem that requires immediate intervention. For patients receiving therapeutic UFH doses, a baseline platelet count should be obtained before therapy is initiated and then every-other-day for 14 days or until therapy is stopped, whichever occurs first. HIT should be suspected if a patient develops a thromboembolic event (e.g., DVT, PE, stroke, myocardial infarction, limb artery occlusion) during or soon after receiving UFH. The platelet... [Pg.181]

The CURE study involved 12,562 patients randomized to receive Plavix (300 mg loading dose followed by 75 mg daily) or placebo and were treated for up to a year. Patients also received aspirin or other standard treatment such as heparin. The results showed that Plavix had a 20% relative risk reduction compared with placebo (582 cases of cardiovascular death, myocardial infarction, or stroke) versus 719 cases for placebo. [Pg.201]

ISIS-3. ISIS-3 a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin alone among 41299 cases of suspected acute myocardial infarction. Lancet 1992 339 753-70. [Pg.448]

It is believed that heparin acts by neutralizing a number of active blood coagulation factors, thus disrupting the transformation of prothrombin into thrombin. Heparin is used to prevent thrombo-formation in myocardial infarctions, thrombosis, and embolism, for maintaining liquid conditions in the blood in artificial blood drcnlation and hemodialysis. Synonyms of this drug are arteven, hepalen, leparan, Uquemin, panheprin, vetren, and many others. [Pg.325]

Collen, D. (1998). Staphylokinase a potent, uniquely fibrin-selective thrombolytic agent. Nature Med. 4(3), 279-284. Collins, R. et al. (1997). Drug therapy—aspirin, heparin and fibrinolytic therapy in suspected acute myocardial infarction. N. Engl. J. Med. 336(12), 847-860. [Pg.401]

Drug therapy of acute coronary syndromes including unstable angina and non-Q-wave myocardial infarction includes use of aspirin, heparin and anti-ischaemic drugs and is similar in older patients to other age groups. Activation of platelet thromboxane production in the coronary circulation has been demonstrated in unstable angina. The risk of myocardial infarction or death is reduced by approximately 50% by early aspirin therapy in recommended doses of 160-325 mg per day and continued... [Pg.214]

Krumholz HM, Hennen J, Ridker PM, Murillo JE, Wang Y, Vaccarino V et al. Use and effectiveness of intravenous heparin therapy for treatment of acute myocardial infarction in the elderly. J Am Coll Cardiol 1998 31(5) 973-9. [Pg.222]

Tirofiban is a synthetic, nonpeptide inhibitor of glycoprotein-(GP)-receptors. Tirofiban has a rapid onset and short duration of action after intravenous administration. Coagulation parameters turn to normal 4-8 hours after the drug is withdrawn. Tirofiban in combination with heparin and aspirin is indicated in the management of patients with unstable angina or non-Q-wave myocardial infarction. [Pg.373]

Randomized comparison of direct thrombin inhibition versus heparin in conjunction with fibrinolytic therapy for acute myocardial infarction results from the GUSTO-lib Trial. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO-lib) Investigators. J Am Coll Cardiol, 1998.31(7) 1493-8. [Pg.255]

Jin, K., Sun, Y., Xie, L., Childs, J., , X.O., Greenberg, D.A. (2004). Post-ischemic administration of heparin-binding epidermal growth factor-like growth factor (HB-EGF) reduces infarct size and modifies neurogenesis after focal cerebral ischemia in the rat. J... [Pg.29]

In present times, because of early mobilization and shorter stays in hospital, venous thrombosis in the legs and resulting pulmonary embolism has declined to a large degree. In persons with acute myocardial infarction, prophylactic low-dose heparin has reduced the incidence of venous thrombosis in the legs. It is considered as a reasonable alternative to warfarin in selected patients. Preventive anlicoagulalion may be indicated in some cases to prevent strokes due to left ventricular mitral thrombi embolizing in tire brain. [Pg.133]

Small subcutaneous closes of heparin have been found to be effective in high-nsk post-surgical patients and in patients with acute myocardial infarction. The preventive treatment is commenced a few hours before an operative procedure and continued postoperatively for 4 to 5 days. As the result of a study in 1975. low-dose heparin prophylaxis in high-nsk patients who undergo abdomina-thoracic surgery has become a widely accepted practice, However, preventive anticoagulant therapy, to date, has been unsatisfactory and controversial in the instances of hip surgery or prostatectomy. [Pg.134]

Heparin has a strong clearing action on postprandial lipidemia by activating lipoprotein lipase. This has been thought to be associated with an increase in free fatty acid-induced dysrhythmias and death in patients with myocardial infarction. [Pg.606]

Heparin and antiplatelet drugs are therefore used in various forms of angina to help prevent infarction. When administered with the traditional anti-anginal medications, these anticoagulants can help decrease morbidity and mortality in people with ischemic heart disease. For more details on the effects of anticoagulant medications, please refer to Chapter 25. [Pg.313]


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See also in sourсe #XX -- [ Pg.24 , Pg.25 ]




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