CARLOS JOSE DORNAS GONCALVES BARBOSA
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
5 resultados
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- Influence of Direct Thrombin Inhibitor and Low Molecular Weight Heparin on Platelet Function in Patients with Coronary Artery Disease: A Prospective Interventional Trial(2020) ARANTES, Flavia B. B.; MENEZES, Fernando R.; FRANCI, Andre; BARBOSA, Carlos J. D. G.; DALCOQUIO, Talia F.; NAKASHIMA, Carlos A. K.; BARACIOLI, Luciano M.; FURTADO, Remo H. M.; NOMELINI, Quintiliano S. S.; RAMIRES, Jose A. F.; KALIL FILHO, Roberto; NICOLAU, Jose C.Introduction The interaction between anticoagulants and platelet function is complex. Previous publications showed mixed results regarding the role of heparins in platelet aggregation. On the other hand, the direct thrombin inhibitor (DTI) dabigatran might enhance the risk of myocardial infarction in patients with atrial fibrillation, which could be related to increased platelet aggregability. Methods This was a prospective, interventional study of patients with chronic coronary artery disease (CAD) taking low-dose aspirin. The objective of the current study was to compare the effects of dabigatran versus enoxaparin on platelet aggregability. Subjects initially were on orally administered dabigatran for 5 days followed by subcutaneously administered enoxaparin after a 30-day washout period. Platelet function was assessed at baseline and after each intervention by multiple electrode aggregometry (MEA-ASPI) (primary endpoint), serum thromboxane B2 (TXB2), VerifyNow Aspirin (TM), and coagulation tests (secondary endpoints). Results Compared to baseline MEA-ASPI values, dabigatran increased platelet aggregation while enoxaparin decreased platelet aggregation (+ 5 U +/- 24.1 vs - 6 U +/- 22.2, respectively, p = 0.012). The TXB2 assay showed the same pattern (+ 2 pg/ml for dabigatran vs - 13 pg/ml for enoxaparin, p = 0.011). None of the additional tests showed significant differences between the groups. Individually, compared to baseline TXB2 results, enoxaparin significantly decreased platelet activation [33 (16.5-95) pg/mL vs 20 (10-52) pg/mL, respectively, p = 0.026], but no significant differences were observed with dabigatran. Conclusions DTI and anti-Xa drugs exert opposite effects on platelet function. A significant decrease in platelet activation through COX1 (also known as prostaglandin G/H synthase 1) was observed with enoxaparin, but no significant differences in platelet function were observed with dabigatran.
- Lipid transfer to high-density lipoproteins in coronary artery disease patients with and without previous cerebrovascular ischemic events(2019) BARBOSA, Carlos J. D. G.; MARANHAO, Raul C.; BARREIROS, Renata S.; FREITAS, Fatima R.; FRANCI, Andre; STRUNZ, Celia M. C.; ARANTES, Flavia B. B.; TAVONI, Thauany M.; RAMIRES, Jose A. F.; KALIL FILHO, Roberto; NICOLAU, Jose C.Background Patients with coronary artery disease (CAD) and previous ischemic cerebrovascular events (ICVE, ischemic stroke, or transitory ischemic attack) constitute a high-risk subgroup for cardiovascular outcomes. High-density lipoprotein cholesterol (HDL-C) levels are correlated with cardiovascular events. Lipid transfer to HDL affects structure size and HDL subclass profile. Impairment of this transfer could influence ischemic risk seen in patients with CAD + ICVE. The objective was to evaluate the HDL ability to receive the lipids in patients with CAD with or without ICVE. Methods Patients with CAD + ICVE (n = 60) and patients with CAD only (n = 60) were matched by age, sex, acute coronary syndromes (ACS) event type, and time elapsed between the ACS event and inclusion in the study. Lipid transfer to HDL was evaluated by incubating donor lipid nanoparticles labeled with radioactive unesterified cholesterol (UC) and esterified cholesterol (EC), phospholipid (PL), and triglyceride (TG) with whole plasma. After the chemical precipitation of non-HDL fractions and nanoparticles, the supernatant was counted for HDL radioactivity. Results CAD + ICVE group presented with impaired lipid transfer to HDL for PL (CAD + ICVE: 21.14 +/- 2.7% vs CAD: 21.67 +/- 3.1%, P = .03), TG (CAD + ICVE: 4.88 +/- 0.97% vs CAD: 5.63 +/- 0.92%, P = .002), and UC (CAD + ICVE: 5.55 +/- 1.19% vs CAD: 6.16 +/- 1.14%, P = .009). Lipid transfer to HDL was similar in both groups for EC. Adjusted models showed similar results. Conclusion Patients with CAD and ICVE have reduced lipid transfer to HDL compared to those with CAD only. Dysfunctional HDL may account for the higher incidence of ischemic outcomes observed in this population.
conferenceObject DRUG INTERACTION BETWEEN CLOPIDOGREL AND RANITIDINE OR OMEPRAZOLE IN PATIENTS WITH CORONARY HEART DISEASE: A DOUBLE-BLIND, DOUBLE-DUMMY, RANDOMIZED COMPARATIVE STUDY(2014) FURTADO, Remo Holanda de Mendonca; FREIRE, Beatriz Tonon; STRUNZ, Celia; BARBOSA, Carlos J. D. G.; FRANCI, Andre; ARANTES, Flavia B. B.; FILHO, Cyrillo C.; MENEZES, Fernando R.; D'AMICO, Elbio A.; NICOLAU, Jose- Influence of proven oral therapies in the very old with acute coronary syndromes: A 15 year experience(2015) NICOLAU, Jose C.; FRANCI, Andre; BARBOSA, Carlos Jose D. G.; BARACIOLI, Luciano M.; FRANKEN, Marcelo; FURTADO, Remo H. M.; GIRALDEZ, Roberto R. C. V.; GANEM, Fernando; LIMA, Felipe G.; MENEZES, Fernando R.; ARANTES, Flavia B. B.; RAMIRES, Jose A. F.; KALIL FILHO, Roberto; GIUGLIANO, Robert P.
- Increased bodyweight and inadequate response to aspirin in individuals with coronary artery disease(2019) FURTADO, Remo H. M.; GIUGLIANO, Robert P.; DALCOQUIO, Talia F.; ARANTES, Flavia B. B.; BARBOSA, Carlos J. D. G.; GENESTRETI, Paulo R. R.; FRANCI, Andre; MENEZES, Fernando R.; NAKASHIMA, Carlos A. K.; SCANAVINI FILHO, Marco A.; FERRARI, Aline G.; SALSOSO, Rocio; BARACIOLI, Luciano M.; NICOLAU, Jose C.Recent reports have suggested that aspirin effect might be influenced by bodyweight, with decreased efficacy in heavier individuals. We investigated the influence of bodyweight on aspirin pharmacodynamics in two independent datasets of patients taking non-enteric coated aspirin 100mg QD for coronary artery disease (CAD). In the first dataset, 368 patients had their platelet aggregation assessed using VerifyNow Aspirin and measured in Aspirin Reaction Units (ARU). In the second dataset, 70 patients had serum thromboxane B2 (TXB2) dosage assessed by an ELISA assay and measured in pg/mL. Platelet aggregation was independently associated with bodyweight, with 8.41 (95% CI 1.86-14.97; adjusted p-value=0.012) increase in ARU for every 10kg. Furthermore, the rate of non-response to aspirin (defined as ARU550) was significantly associated with increased bodyweight (adjusted p-value=0.007), with OR=1.23 (95% CI 1.06-1.42) for every 10kg. Similar results were found considering body mass index (in kg/m(2)), with 15.5 (95% CI 5.0 to 25.9; adjusted p-value=0.004) increase in ARU for every 10kg and non-response OR=1.43 (95% CI 1.13 to 1.81, adjusted p-value=0.003) for every 5kg/m(2). Moreover, serum TXB2 was higher in patients weighting more than 70kg (222.6 +/- 62.9 versus 194.9 +/- 61.9pg/mL; adjusted p-value=0.018). In two different datasets of patients with CAD on non-enteric coated aspirin 100mg QD, increased bodyweight was independently associated with impaired response to aspirin.