Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

No abstract

The CREATE-ECLA Randomized Controlled TrialThe CREATE-ECLA Trial Group Investigators* See also pp 427 and 489.

To assess the contribution of Factor IX/IXa, to intravascular thrombosis, a canine coronary thrombosis model was studied. Thrombus formation was initiated by applying current to a needle in the circumflex coronary artery. When 50% occlusion of the vessel developed, the current was stopped and animals received an intravenous bolus of either saline, bovine glutamylglycyl-arginyl-Factor IXa (IXai), a competitive inhibitor of Factor IXa assembly into the intrinsic Factor X activation complex, bovine Factor IX, or heparin. Animals receiving saline or Factor IX developed coronary occlusion due to a fibrin/platelet thrombus in 70±11 min. In contrast, infusion of IXai prevented thrombus formation completely (> 180 min) at doses of 460 and 300 ,ug/kg, and partially blocked thrombus formation at 150 ,g/kg. IXai attenuated the accumulation of 1'I-fibrinogen/ fibrin at the site of the thrombus by -67% (P < 0.001) and resulted in -26% decrease in serotonin release from platelets in coronary sinus (P < 0.05). Hemostatic variables in animals receiving IXai, remained within normal limits. Animals given heparin in a concentration sufficient to prevent occlusive thrombosis had markedly increased bleeding, whereas heparin levels that maintained extravascular hemostasis did not prevent intracoronary thrombosis. This suggests that Factor IX/IXa can contribute to thrombus formation, and that inhibition of IXa participation in the clotting mechanism blocks intravascular thrombosis without impairing extravascular hemostasis. (J.

Classe I: evidência ou concordância geral de que o tratamento é benéfico, útil e eficaz.Classe II: evidência conflitante e/ou divergência de opinião quanto à utilidade e à eficácia do tratamento.Classe IIa: forças das evidências/opiniões em favor da utilidade e da eficácia.Classe IIb: forças das evidências/opiniões menos bem estabelecidas quanto à utilidade e à eficácia.Classe III: evidência ou concordância geral de que o tratamento não é útil/eficaz e em alguns casos pode ser prejudicial. Nível de evidência A: presença de múltiplos estudos clínicos randomizados.Nível de evidência B: presença de um único estudo clínico randomizado ou de estudos não-randomizados.Nível de evidência C: consenso de especialistas.O nível de evidência será apresentado apenas para os tratamentos do infarto do miocárdio, não se aplicando aos procedimentos diagnósticos. Todos os métodos complementares deverão ser realizados por profissionais experientes, segundo as recomendações específicas de cada especialidade.