CARLOS JOSE DORNAS GONCALVES BARBOSA
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
4 resultados
Resultados de Busca
Agora exibindo 1 - 4 de 4
- Do Diabetic Patients with Acute Coronary Syndromes Have a Higher Threshold for Ischemic Pain?(2014) NICOLAU, Jose Carlos; BARBOSA, Carlos Jose Dornas Goncalves; FRANCI, Andre; BARACIOLI, Luciano Moreira; FRANKEN, Marcelo; LIMA, Felipe Gallego; GIRALDEZ, Roberto Rocha; KALIL FILHO, Roberto; RAMIRES, Jose Antonio Franchini; GIUGLIANO, Robert P.Background: Data from over 4 decades have reported a higher incidence of silent infarction among patients with diabetes mellitus (DM), but recent publications have shown conflicting results regarding the correlation between DM and presence of pain in patients with acute coronary syndromes (ACS). Objective: Our primary objective was to analyze the association between DM and precordial pain at hospital arrival. Secondary analyses evaluated the association between hyperglycemia and precordial pain at presentation, and the subgroup of patients presenting within 6 hours of symptom onset. Methods: We analyzed a prospectively designed registry of 3,544 patients with ACS admitted to a Coronary Care Unit of a tertiary hospital. We developed multivariable models to adjust for potential confounders. Results: Patients with precordial pain were less likely to have DM (30.3%) than those without pain (34.0%; unadjusted p = 0.029), but this difference was not significant after multivariable adjustment, for the global population (p = 0.84), and for subset of patients that presented within 6 hours from symptom onset (p = 0.51). In contrast, precordial pain was more likely among patients with hyperglycemia (41.2% vs 37.0% without hyperglycemia, p = 0.035) in the overall population and also among those who presented within 6 hours (41.6% vs. 32.3%, p = 0.001). Adjusted models showed an independent association between hyperglycemia and pain at presentation, especially among patients who presented within 6 hours (OR = 1.41, p = 0.008). Conclusion: In this non-selected ACS population, there was no correlation between DM and hospital presentation without precordial pain. Moreover, hyperglycemia correlated significantly with pain at presentation, especially in the population that arrived within 6 hours from symptom onset.
- Relation of High Lipoprotein (a) Concentrations to Platelet Reactivity in Individuals with and Without Coronary Artery Disease(2020) SALSOSO, Rocio; DALCOQUIO, Talia F.; FURTADO, Remo H. M.; FRANCI, Andre; BARBOSA, Carlos J. D. G.; GENESTRETI, Paulo R. R.; STRUNZ, Celia M. C.; LIMA, Viviane; BARACIOLI, Luciano M.; GIUGLIANO, Robert P.; GOODMAN, Shaun G.; GURBEL, Paul A.; MARANHAO, Raul C.; NICOLAU, Jose C.Introduction Lipoprotein (a) [Lp(a)] is a risk factor for coronary artery disease (CAD). To the best of our knowledge, this is the first study addressing the relationship between Lp(a) and platelet reactivity in primary and secondary prevention. Methods Lp(a) was evaluated in 396 individuals with (82.3%) and without (17.7%) obstructive CAD. The population was divided into two groups according to Lp(a) concentrations with a cutoff value of 50 mg/dL. The primary objective was to evaluate the association between Lp(a) and adenosine diphosphate (ADP)-induced platelet reactivity using the VerifyNow (TM) P2Y(12)assay. Platelet reactivity was also induced by arachidonic acid and collagen-epinephrine (C-EPI) and assessed by Multiplate (TM), platelet function analyzer (TM) 100 (PFA-100), and light transmission aggregometry (LTA) assays. Secondary objectives included the assessment of the primary endpoint in individuals with or without CAD. Results Overall, 294 (74.2%) individuals had Lp(a) < 50 mg/dL [median (IQR) 13.2 (5.8-27.9) mg/dL] and 102 (25.8%) had Lp(a) >= 50 mg/dL [82.5 (67.6-114.5) mg/dL],P < 0.001. Univariate analysis in the entire population revealed no differences in ADP-induced platelet reactivity between individuals with Lp(a) >= 50 mg/dL (249.4 +/- 43.8 PRU) versus Lp(a) < 50 mg/dL (243.1 +/- 52.2 PRU),P = 0.277. Similar findings were present in individuals with (P = 0.228) and without (P = 0.669) CAD, and regardless of the agonist used or method of analysis (allP > 0.05). Finally, multivariable analysis did not show a significant association between ADP-induced platelet reactivity and Lp(a) >= 50 mg/dL [adjusted OR = 1.00 [(95% CI 0.99-1.01),P = 0.590]. Conclusion In individuals with or without CAD, Lp(a) >= 50 mg/dL was not associated with higher platelet reactivity.
- 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.