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.

Transcriptomic analysis by microarray technology demonstrated differential expression during a 48 h time course suggesting a potential use of some of these genes as biomarkers for very early stages of ACS, as well as for monitoring early cardiac ischemic recovery.

objective: Describe clinical characteristics of patients (P) admitted to hospital with suspected acute coronary syndrome (ACS), identifying medical treatment and in-hospital mortality.Methods: Evaluated were 860 patients with ACS from January through December, 2003. We evaluated baseline characteristics, ACS mode of presentation, medication during hospital stay, indication for clinical treatment or myocardial revascularization (MR) and in-hospital mortality.Results: Five hundred and three (58.3%) were male, mean age 62.6 years (± 11.9). Seventy-eight (9.1%) were discharged with the diagnosis of acute ST-elevation myocardial infarction (STEMI), 238 (27.7%) with non-ST-elevation myocardial infarction (non-STEMI), 516 (60%) with unstable angina (UA), two (0.2%) with atypical manifestations of ACS and 26 (3%) with noncardiac chest pain. During hospitalization, 87.9% of patients were given a beta-blocker, 95.9% acetylsalicylic acid, 89.9% anti-thrombin therapy, 86.2% intravenous nitroglycerin, 6.4% glycoprotein (GP) IIb/IIIa receptor inhibitor, 35.9% clopidogrel, 77.9% angiotensin-converting enzyme inhibitor, and 70,9% statin drugs. Coronary arteriography was performed in 72 patients (92.3%) with STEMI, and in 452 (59.8%) with non-STEMI ACS (p< 0.0001). Myocardial revascularization (MR) surgery was indicated for 12.9% and percutaneous coronary intervention for 26.6%. In-hospital mortality was 4.8%, and no difference was recorded between the proportion of deaths among patients with STEMI and non-STEMI ACS (6.4% versus 4.8%; p = 0.578). Conclusion:In this registry, we provide a description of ACS patient, which allows the evaluation of the demographic characteristics, medical treatment prescribed, and in-hospital mortality. A greater awareness of our reality may help the medical community to adhere more strictly to the procedures set by guidelines.key words: Acute coronary syndrome, registry, chest pain, unstable angina, acute myocardial infarction.

BackgroundThe classification or index of heart failure severity in patients with acute myocardial infarction (AMI) was proposed by Killip and Kimball aiming at assessing the risk of in-hospital death and the potential benefit of specific management of care provided in Coronary Care Units (CCU) during the decade of 60.ObjectiveTo validate the risk stratification of Killip classification in the long-term mortality and compare the prognostic value in patients with non-ST-segment elevation MI (NSTEMI) relative to patients with ST-segment elevation MI (STEMI), in the era of reperfusion and modern antithrombotic therapies.MethodsWe evaluated 1906 patients with documented AMI and admitted to the CCU, from 1995 to 2011, with a mean follow-up of 05 years to assess total mortality. Kaplan-Meier (KM) curves were developed for comparison between survival distributions according to Killip class and NSTEMI versus STEMI. Cox proportional regression models were developed to determine the independent association between Killip class and mortality, with sensitivity analyses based on type of AMI. Results: The proportions of deaths and the KM survival distributions were significantly different across Killip class >1 (p <0.001) and with a similar pattern between patients with NSTEMI and STEMI. Cox models identified the Killip classification as a significant, sustained, consistent predictor and independent of relevant covariables (Wald χ2 16.5 [p = 0.001], NSTEMI) and (Wald χ2 11.9 [p = 0.008], STEMI).ConclusionThe Killip and Kimball classification performs relevant prognostic role in mortality at mean follow-up of 05 years post-AMI, with a similar pattern between NSTEMI and STEMI patients.