REMO HOLANDA DE MENDONCA FURTADO
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
4 resultados
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- 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 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.
- Platelet Reactivity and Coagulation Markers in Patients with COVID-19(2021) BERTOLIN, Adriadne J.; DALCOQUIO, Talia F.; SALSOSO, Rocio; FURTADO, Remo H. de M.; KALIL-FILHO, Roberto; HAJJAR, Ludhmila A.; SICILIANO, Rinaldo F.; KALLAS, Esper G.; BARACIOLI, Luciano M.; LIMA, Felipe G.; GIRALDEZ, Roberto R.; CAVALHEIRO-FILHO, Cyrillo; VIEIRA, Alexandra; STRUNZ, Celia M. C.; GIUGLIANO, Robert P.; TANTRY, Udaya S.; GURBEL, Paul A.; NICOLAU, Jose C.Introdution COVID-19 is associated with an increased risk of thrombotic events. However, the contribution of platelet reactivity (PR) to the aetiology of the increased thrombotic risk associated with COVID-19 remains unclear. Our aim was to evaluate PR in stable patients diagnosed with COVID-19 and hospitalized with respiratory symptoms (mainly dyspnoea and dry cough), in comparison with a control group comprised of non-hospitalized healthy controls. Methods Observational, case control study that included patients with confirmed COVID-19 (COVID-19 group, n = 60) and healthy individuals matched by age and sex (control group, n = 60). Multiplate electrode aggregometry (MEA) tests were used to assess PR with adenosine diphosphate (MEA-ADP, low PR defined as < 53 AUC), arachidonic acid (MEA-ASPI, low PR < 86 AUC) and thrombin receptor-activating peptide 6 (MEA-TRAP, low PR < 97 AUC) in both groups. Results The rates of low PR with MEA-ADP were 27.5% in the COVID-19 group and 21.7% in the control group (OR = 1.60, p = 0.20); with MEA-ASPI, the rates were, respectively, 37.5% and 22.5% (OR = 3.67, p < 0.001); and with MEA-TRAP, the incidences were 48.5% and 18.8%, respectively (OR = 9.58, p < 0.001). Levels of d-dimer, fibrinogen, and plasminogen activator inhibitor 1 (PAI-1) were higher in the COVID-19 group in comparison with the control group (all p < 0.05). Thromboelastometry was utilized in a subgroup of patients and showed a hypercoagulable state in the COVID-19 group. Conclusion Patients hospitalized with non-severe COVID-19 had lower PR compared to healthy controls, despite having higher levels of d-dimer, fibrinogen, and PAI-1, and hypercoagulability by thromboelastometry.
- Effects of Ticagrelor and Clopidogrel on Coronary Microcirculation in Patients with Acute Myocardial Infarction(2022) SCANAVINI-FILHO, Marco Antonio; BERWANGER, Otavio; MATTHIAS, Wilson; AGUIAR, Miguel O.; CHIANG, Hsu P.; AZEVEDO, Luciene; BARACIOLI, Luciano M.; LIMA, Felipe G.; FURTADO, Remo H. M.; DALCOQUIO, Talia F.; MENEZES, Fernando R.; FERRARI, Aline G.; LUCA, Fabio de; GIUGLIANO, Robert P.; GOODMAN, Shaun; NICOLAU, Jose C.Introduction Clopidogrel has been demonstrated to be effective in improving coronary microcirculation (CM) among patients with ST-elevation myocardial infarction (STEMI) treated with fibrinolytics. Ticagrelor is a more potent adenosine diphosphate (ADP) receptor blocker proven to be superior to clopidogrel among patients with acute coronary syndromes. The present study aimed to compare the effects of ticagrelor and clopidogrel on CM in patients with STEMI treated with fibrinolytics. Methods The present study prospectively included 48 patients participating in the TREAT trial, which randomly assigned patients with STEMI undergoing fibrinolysis to ticagrelor versus clopidogrel. The primary endpoint of this study was the evaluation of the CM using the global myocardial perfusion score index (global MPSI) obtained by myocardial contrast echocardiography (MCE). Platelet aggregation to ADP was evaluated by Multiplate (R) and expressed as area under the curve (AUC). Results The global MPSI demonstrated no differences between the groups [mean 1.4 (1.2-1.5) in the ticagrelor group and 1.2 (1.2-1.5) in the clopidogrel group (p = 0.41)]. Platelet aggregability was lower in the ticagrelor group (18.1 +/- 9.7 AUC), compared to the clopidogrel group (26.1 +/- 12.5 AUC, p = 0.01). Conclusion We found no improvement in coronary microcirculation with ticagrelor compared to clopidogrel among patients with STEMI treated with fibrinolytics, despite the fact that platelet aggregation to ADP was lower with ticagrelor.