REMO HOLANDA DE MENDONCA FURTADO
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
6 resultados
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- Long-term ticagrelor for secondary prevention in patients with prior myocardial infarction and no history of coronary stenting: insights from PEGASUS-TIMI 54(2020) FURTADO, Remo H. M.; NICOLAU, Jose C.; MAGNANI, Giulia; IM, Kyungah; BHATT, Deepak L.; STOREY, Robert F.; STEG, P. Gabriel; SPINAR, Jindrich; BUDAJ, Andrzej; KONTNY, Frederic; CORBALAN, Ramon; KISS, Robert G.; ABOLA, Maria Teresa; JOHANSON, Per; JENSEN, Eva C.; BRAUNWALD, Eugene; SABATINE, Marc S.; BONACA, Marc P.Aims PEGASUS-TIMI 54 demonstrated that long-term dual antiplatelet therapy (DAPT) with aspirin and ticagrelor reduced the risk of major adverse cardiovascular events (MACE), with an acceptable increase in bleeding, in patients with prior myocardial infarction (MI). While much of the discussion around prolonged DAPT has been focused on stented patients, patients with prior MI without prior coronary stenting comprise a clinically important subgroup. Methods and results This was a pre-specified analysis from PEGASUS-TIMI 54, which randomized 21 162 patients with prior MI (1-3years) and additional high-risk features to ticagrelor 60 mg, 90 mg, or placebo twice daily in addition to aspirin. A total of 4199 patients had no history of coronary stenting at baseline. The primary efficacy outcome (MACE) was the composite of cardiovascular death, MI, or stroke. Patients without history of coronary stenting had higher baseline risk of MACE [13.2% vs. 8.0%, adjusted hazard ratio (HR) 1.41, 95% confidence interval (CI) 1.15-1.73, in the placebo arm]. The relative risk reduction in MACE with ticagrelor (pooled doses) was similar in patients without (HR 0.82, 95% CI 0.68-0.99) and with prior stenting (HR 0.85, 95% CI 0.75-0.96; P for interaction = 0.76). Conclusion Long-term ticagrelor reduces thrombotic events in patients with prior MI regardless of whether they had prior coronary stenting. These data highlight the benefits of DAPT in prevention of spontaneous atherothrombotic events and indicate that long-term ticagrelor may be considered in high-risk patients with prior MI even if they have not been treated with stenting.
- Morphine and Cardiovascular Outcomes Among Patients With Non-ST-Segment Elevation Acute Coronary Syndromes Undergoing Coronary Angiography(2020) FURTADO, Remo H. M.; NICOLAU, Jose C.; GUO, Jianping; IM, Kyungah; WHITE, Jennifer A.; SABATINE, Marc S.; NEWBY, L. Kristin; GIUGLIANO, Robert P.BACKGROUND Mechanistic studies have shown that morphine blunts the antiplatelet effects of oral adenosine diphosphate receptor blockers. However, the clinical relevance of this interaction is controversial. OBJECTIVES This study sought to explore the association between morphine and ischemic events in 5,438 patients treated with concomitant clopidogrel presenting with non-ST-segment elevation acute coronary syndromes (NSTEACS) in the EARLY ACS (Early Glycoprotein IIb/IIIa Inhibition in Patients With Non-ST-Segment Elevation Acute Coronary Syndrome) trial. Patients not treated with clopidogrel (n = 3,462) were used as negative controls. METHODS Endpoints were the composite of death, myocardial infarction (MI), recurrent ischemia, or thrombotic bailout at 96 h (4-way endpoint) and the composite of death or MI at 30 days. RESULTS In patients treated with clopidogrel, morphine use was associated with higher rates of the 4-way endpoint at 96 h (adjusted odds ratio [OR]: 1.40; 95% confidence interval [CI]: 1.04 to 1.87; p = 0.026). There was a trend for higher rates of death or MI at 30 days (adjusted OR: 1.29; 95% CI: 0.98 to 1.70; p = 0.072), driven by events in the first 48 h (adjusted hazard ratio: 1.54; 95% CI: 1.07 to 2.23; p = 0.021). In patients not treated with clopidogrel, morphine was not associated with either the 4-way endpoint at 96 h (adjusted OR: 1.05; 95% CI: 0.74 to 1.49; p = 0.79; p(interaction) = 0.36) or death or MI at 30 days (adjusted OR: 1.07; 95% CI: 0.77 to 1.48; p = 0.70; p(interaction) = 0.46). CONCLUSIONS When used concomitantly with clopidogrel pre-treatment, morphine was associated with higher rates of ischemic events in patients with NSTEACS. (C) 2020 by the American College of Cardiology Foundation.
- Caffeinated Beverage Intake, Dyspnea With Ticagrelor, and Cardiovascular Outcomes: Insights From the PEGASUS-TIMI 54 Trial(2020) FURTADO, Remo H. M.; VENKATESWARAN, Ramkumar V.; NICOLAU, Jose C.; GURMU, Yared; BHATT, Deepak L.; STOREY, Robert F.; STEG, P. Gabriel; MAGNANI, Giuglia; GOTO, Shinya; DELLBORG, Mikael; KAMENSKY, Gabriel; ISAZA, Daniel; AYLWARD, Philip; JOHANSON, Per; BONACA, Marc P.BACKGROUND: A proposed cause of dyspnea induced by ticagrelor is an increase in adenosine blood levels. Because caffeine is an adenosine antagonist, it can potentially improve drug tolerability with regard to dyspnea. Furthermore, association between caffeine and cardiovascular events is of clinical interest. METHODS AND RESULTS: This prespecified analysis used data from the PEGASUS TIMI 54 (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54) trial, which randomized 21 162 patients with prior myocardial infarction to ticagrelor 60 mg or 90 mg or matching placebo (twice daily). Baseline caffeine intake in cups per week was prospectively collected for 9694 patients. Outcomes of interest included dyspnea, major adverse cardiovascular events (ie, the composite of cardiovascular death, myocardial infarction, or stroke), and arrhythmias. Dyspnea analyses considered the pooled ticagrelor group, whereas cardiovascular outcome analyses included patients from the 3 randomized arms. After adjustment, caffeine intake, compared with no intake, was not associated with lower rates of dyspnea in patients taking ticagrelor (adjusted hazard ratio (HR), 0.91; 95% CI, 0.76-1.10; P= 0.34). There was no excess risk with caffeine for major adverse cardiovascular events (adjusted HR, 0.78; 95% CI, 0.63-0.98; P=0.031), sudden cardiac death (adjusted HR, 0.98; 95% CI, 0.57-1.70; P=0.95), or atrial fibrillation (adjusted odds ratio, 1.07; 95% CI, 0.56-2.04; P=0.84). CONCLUSIONS: In patients taking ticagrelor for secondary prevention after myocardial infarction, caffeine intake at baseline was not associated with lower rates of dyspnea compared with no intake. Otherwise, caffeine appeared to be safe in this population, with no apparent increase in atherothrombotic events or clinically significant arrhythmias.
- Platelet function, coagulation and fibrinolysis in patients with previous coronary and cerebrovascular ischemic events(2019) BARBOSA, Carlos Jose Dornas Goncalves; BARREIROS, Renata de Souza; FRANCI, Andre; ARANTES, Flavia Bittar Brito; FURTADO, Remo Holanda de Mendonca; STRUNZ, Celia Maria Cassaro; ROCHA, Tania Rubia Flores da; BARACIOLI, Luciano Moreira; RAMIRES, Jose Antonio Franchini; KALIL-FILHO, Roberto; NICOLAU, Jose CarlosOBJECTIVES: Ischemic stroke (IS) or transient ischemic attack (TIA) history is present in 4-17% of patients with coronary artery disease (CAD). This subgroup of patients is at high risk for both ischemic and bleeding events. The aim of this study was to determine the role of platelet aggregability, coagulation and endogenous fibrinolysis in patients with CAD and previous IS or TIA. METHODS: A prospective case-control study that included 140 stable CAD patients divided into two groups: the CASE group (those with a previous IS/TIA, n=70) and the CONTROL group (those without a previous IS/TIA, n=70). Platelet aggregability (VerifyNow Aspirin (R) and VerifyNow P2Y12 (R)), coagulation (fibrinogen and thromboelastography by Reorox (R)) and endogenous fibrinolysis (D dimer and plasminogen activator inhibitor-1) were evaluated. RESULTS: Patients in the CASE group presented significantly higher systolic blood pressure levels (135.84 +/- 16.09 vs 123.68 +/- 16.11, p <0.01), significantly more previous CABG (25.71% vs 10%, p=0.015) and significantly higher calcium channel blocker usage (42.86% vs 24.29%, p=0.02) than those in the control group. In the adjusted models, low triglyceride values, low hemoglobin values and higher systolic blood pressure were significantly associated with previous IS/TIA (CASE group). Most importantly, platelet aggregability, coagulation and fibrinolysis tests were not independently associated with previous cerebrovascular ischemic events (CASE group). CONCLUSION: Platelet aggregability, coagulation and endogenous fibrinolysis showed similar results among CAD patients with and without previous IS/TIA. Therefore, it remains necessary to identify other targets to explain the higher bleeding risk presented by these patients.
- 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.
- Effects of exercise on platelet reactivity after myocardial infarction: a randomized clinical trial(2023) DALCOQUIO, Talia Falcao; SANTOS, Mayara Alves dos; ALVES, Leandro Silva; ARANTES, Flavia Bittar Brito; FERREIRA-SANTOS, Larissa; RONDON, Maria Urbana Pinto Brandao; FURTADO, Remo Holanda M.; FERRARI, Aline Gehlen; RIZZO, Paulo Roberto Genestreti; SALSOSO, Rocio; FRANCI, Andre; BARACIOLI, Luciano Moreira; ALVES, Maria Janieire de Nazare Nunes; NEGRAO, Carlos Eduardo; NICOLAU, Jose CarlosExercise training (ET) can lower platelet reactivity in patients with cardiovascular risk factors. However, the effects of ET on platelet reactivity in higher-risk patients is unknown. The aim of this study was to evaluate the effects of ET on platelet reactivity in patients with recent myocardial infarction (MI). Ninety patients were randomly assigned 1 month post-MI to the intervention (patients submitted to a supervised ET program) or control group. All patients were on dual antiplatelet therapy (DAPT). Platelet reactivity by VerifyNow-P2Y(12) (measured by P2Y(12) reaction units - PRU5) test was determined at baseline and at the end of 14 +/- 2 weeks of follow-up at rest (primary endpoint), and multiplate electrode aggregometry (MEA) adenosine diphosphate (ADP) and aspirin (ASPI) tests were performed immediately before and after the maximal cardiopulmonary exercise test (CPET) at the same time points (secondary endpoints). Sixty-five patients (mean age 58.9 +/- 10 years; 73.8% men; 60% ST elevation MI) completed follow-up (control group, n = 31; intervention group, n = 34). At the end of the follow-up, the mean platelet reactivity was 172.8 +/- 68.9 PRU5 and 166.9 +/- 65.1 PRU5 for the control and intervention groups, respectively (p = .72). Platelet reactivity was significantly increased after the CPET compared to rest at the beginning and at the end of the 14-week follow-up (among the intervention groups) by the MEA-ADP and MEA-ASPI tests (p < .01 for all analyses). In post-MI patients on DAPT, 14 weeks of supervised ET did not reduce platelet reactivity.