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Heparins death/myocardial infarction

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]

Effects of recombinant hirudin (lepirudin) compared with heparin on death, myocardial infarction, refractory angina, and revascularisation procedures in patients with acute myocardial ischaemia without ST elevation A randomised trial. Organisation to Assess Strategies for Ischemic Syndromes (OASIS-2) Investigators. Lancet 1999 353(9151) 429-38. [Pg.41]

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]

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]

Oler A, Whooley MA, Oler J, et al, Adding heparin to aspirin reduces the incidence of myocardial infarction and death in patients with unstable angina. A meta-analysis. JAMA 1996 276 81 1-815. [Pg.125]

The RISC Group. Risk of myocardial infarction and death during treatment with low dose aspirin and intravenous heparin in men with unstable coronary artery disease. Lancet 1990 336(8719) 827-30. [Pg.27]

In a meta-analysis of individual patients data from 11 randomized comparisons of direct thrombin inhibitors (hirudin, bivalirudin, argatroban, efegatran, or inogatran) with heparin, 35 970 patients were treated for up to 7 days and followed for at least 30 days (1). Compared with heparin, the direct thrombin inhibitors were associated with a lower risk of death or myocardial infarction at the end of treatment (OR = 0.85 95% Cl = 0.77, 0.94) and at 30 days (OR = 0.91 Cl = 0.84, 0.99). There was no excess of intracranial hemorrhages with the direct thrombin inhibitors. [Pg.1142]

Abciximab (ReoPro) is the Fab fragment of a humanized monoclonal antibody directed against the a bp3 receptor. It also binds to the vitronectin receptor on platelets, vascular endothelial cells, and smooth-muscle cells. The antibody is used in conjunction with percutaneous angioplasty for coronary thromboses, and when used in conjunction with aspirin and heparin, has been shown to be quite effective in preventing restenosis, recurrent myocardial infarction, and death. [Pg.35]

Tirofiban Tiroflban (Aggrastat), a nonpeptide, small-molecule inhibitor of anePs, appears to have a similar mechanism of action as eptifibatide. Tiroflban has a short duration of action and has efficacy in non-Q-wave myocardial infarction and unstable angina. Reductions in death and myocardial infarction have been about 20% compared to placebo, results similar to those with eptifibatide. Side effects also are similar to those of eptifibatide. The agent is specific to anePs and does not react with the vitronectin receptor. Metaanalysis of trials using anePs inhibitors suggests that their value in antiplatelet therapy after acute myocardial infarction is limited. Tiroflban is administered intravenously at an initial rate of 0.4 pg/kg per minute for 30 minutes, and then continued at 0.1 mg/kg per minute for 12 to 24 hours after angioplasty or atherectomy. It is used in conjunction with heparin. [Pg.235]

The comprehensive review by Douglas provides a recent discussion of the clinically useful anticoagulants. Recent studies have shown heparin to be clearly effective in clinical states In which disseminated Intravascular coagulation was Indicated to be a pathologic factor.75 xhe most commonly employed oral anticoagulants are of the coumarin type such as warfarin and nicoumalone. The oral anticoagulants appear to be of value in the prevention of thromboembolic complications after myocardial infarction.9 76 However, anticoagulation therapy has been found to have no effect on death-rate in these patients.77 Warfarin has been shown to be effective in the prevention of postoperative venous thrombosis. [Pg.84]


See other pages where Heparins death/myocardial infarction is mentioned: [Pg.215]    [Pg.101]    [Pg.571]    [Pg.73]    [Pg.75]    [Pg.604]    [Pg.521]    [Pg.304]    [Pg.373]    [Pg.264]    [Pg.283]    [Pg.2]    [Pg.88]    [Pg.89]    [Pg.127]    [Pg.132]    [Pg.604]    [Pg.486]    [Pg.583]    [Pg.239]    [Pg.33]    [Pg.235]    [Pg.960]    [Pg.963]    [Pg.963]    [Pg.963]    [Pg.82]   


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Death heparins

Heparins myocardial infarction

Infarct

Infarct, myocardial

Infarction

Myocardial infarction

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