Bloqueia a produção de prostaglandinas pela inibição da ciclo-oxigenase (prostaglandina H sintase), com maior seletividade para a isoforma COX-1. O efeito antitrombótico se deve à inibição de COX-1 nas plaquetas que bloqueiam a produção de tromboxano e a agregação de plaquetas. Atividade quimiopreventiva contra tumores colorretais e outros tumores sólidos.
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Journal of the American College of Cardiology, 66(7), 777-787 (2015-08-14)
Bleeding limits anticoagulant treatment in patients with acute coronary syndromes (ACS). We investigated whether background concomitant antiplatelet therapy influences the effects of apixaban after ACS. This study examined high-risk ACS patients who were treated with aspirin or aspirin plus clopidogrel
The American journal of cardiology, 115(9), 1185-1193 (2015-03-24)
The optimal antiaggregant therapy after coronary stenting in patients receiving oral anticoagulants (OACs) is currently debated. MEDLINE and Cochrane Library were searched for studies reporting outcomes of patients who underwent PCI and who were on triple therapy (TT) or dual-antiplatelet
Journal of thrombosis and haemostasis : JTH, 3(10), 2340-2345 (2005-09-10)
Aspirin (acetylsalicylic acid) irreversibly inhibits platelet cyclooxygenase (COX)-1, the enzyme that converts arachidonic acid (AA) to the potent platelet agonist thromboxane (TX) A2. Despite clear benefit from aspirin in patients with cardiovascular disease (CAD), evidence of heterogeneity in the way
Journal of the American College of Cardiology, 46(7), 1258-1263 (2005-10-04)
We investigated whether use of low-dose enteric-coated (EC) aspirin for secondary prevention of cardiovascular events has sufficient bioavailability to achieve complete platelet cyclooxygenase (COX) inhibition in all individuals. Aspirin reduces cardiovascular morbidity and mortality in patients with pre-existing vascular disease;
The relation between platelet reactivity and stent thrombosis, major bleeding, and other adverse events after coronary artery implantation of drug-eluting stents has been incompletely characterised. We aimed to determine the relation between platelet reactivity during dual therapy with aspirin and
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