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Background There is a lack of evidence regarding the benefits of β-blocker treatment after invasively managed acute myocardial infarction (MI) without reduced left ventricular ejection fraction (LVEF). Methods and results TREatment with Beta-blockers after myOcardial infarction withOut reduced ejection fraction (REBOOT) trial is a pragmatic, controlled, prospective, randomized, open-label blinded endpoint (PROBE design) clinical trial testing the benefits of β-blocker maintenance therapy in patients discharged after MI with or without ST-segment elevation. Patients eligible for participation are those managed invasively during index hospitalization (coronary angiography), with LVEF >40%, and no history of heart failure (HF). At discharge, patients will be randomized 1:1 to β-blocker therapy (agent and dose according to treating physician) or no β-blocker therapy. The primary endpoint is a composite of all-cause death, nonfatal reinfarction, or HF hospitalization over a median follow-up period of 2.75 years (minimum 2 years, maximum 3 years). Key secondary endpoints include the incidence of the individual components of the primary composite endpoint, the incidence of cardiac death, and incidence of malignant ventricular arrhythmias or resuscitated cardiac arrest. The primary endpoint will be analyzed according to the intention-to-treat principle. Conclusion The REBOOT trial will provide robust evidence to guide the prescription of β-blockers to patients discharged after MI without reduced LVEF.

Background Previous studies have shown that left ventricular (LV) global longitudinal strain (GLS) is a feasible and reliable predictor for outcomes in heart failure (HF) patients with greater accuracy than LV ejection fraction (LVEF). However, these studies rarely included stable or asymptomatic patients. Purpose To assess the predictive value of GLS, as compared to LVEF, in asymptomatic stable HF patients. Methods This is a retrospective study, including patients with HF with reduced and mid-range ejection fraction (HFrEF: LVEF<40%; HFmrEF: LVEF 40–49%) in NYHA I with no history of decompensation within the previous 6 months. All patients underwent comprehensive baseline echocardiographic assessment. The primary endpoint was the composite of cardiovascular death, hospitalization and need for intensification of HF treatment within a 12 month follow-up period. Results Out of 837 patients with LVEF <50% that underwent follow-up in our HF unit between January 2016 and December 2017, 153 patients were included in the study. The mean age was 74 (±10.2) years and 82% were male. The cumulative incidence of HF progression was 17.8%, with a median time to event of 193 days. Death and hospitalization due to HF accounted for three-quarters of the events. The mean LVEF was 40.9% (± 6.96),without significant differences between patients with and without clinical progression (39.5% vs 43%, p=0.093). We did not find significant differences between the two groups, concerning LV and atrial dimensions, as well as mitral inflow, PSAP and tricuspid annular systolic plane excursion (TAPSE). LV GLS was significantly lower (i.e. less negative) in patients that presented clinical progression, that in patients without disease progression (−7.7 vs −12.2, p<0.001). Receiver operating characteristic curve and univariate Cox regression analysis identified GLS as the most accurate predictor for clinical progression among all continuous variables (AUC: 0.809, cut-off: −8.5%, sensitivity: 74.1%, specificity: 89%, HR: 14.78 (95% CI: 6.2–35.1), p<0.001). LVEF predicted HF progression less precisely (AUC: 0.654, cut-off: 42%, sensitivity: 70.4%, specificity: 54%, HR: 2.38 (95% CI: 1.1–5.2), p=0.03). Conclusion In asymptomatic stable HF patients (in NYHA I), LV GLS showed to be a more accurate predictor of clinical disease progression than LVEF. Funding Acknowledgement Type of funding sources: None. Global longitudinal strain (GLS)Receiver operating characteristic (ROC)

Resumo Objetivo: Apresentar uma revisão da literatura a respeito da displasia broncopulmonar. Métodos: Foram selecionados, através do Medline, os artigos mais significativos publicados na literatura sobre displasia bronco-pulmonar. Resultados: A presente revisão analisa os diferentes conceitos, a patogenia, a clínica, o tratamento e as medidas preventivas da displasia broncopulmonar. Conclusões: Displasia broncopulmonar é uma doença freqüen-te em recém-nascidos de muito baixo peso que desenvolvem doença de membrana hialina e necessitam ventilação mecânica. Os fatores patogênicos são prematuridade, oxigenioterapia, ventilação mecâ-nica, edema pulmonar e infecção. O tratamento consiste em manter uma boa oxigenação, controle hídrico, cuidados nutricionais, diuré-ticos, betamiméticos, xantinas e corticosteróides. A prevenção cons-ta de controle da prematuridade, uso de esteróide pré-natal, superó-xido desmutase e corticosteróides pós-natal. J. pediatr. (Rio J.). 1998; 74 (Supl.1): S95-S98: displasia broncopulmonar, oxigênio, ventilação mecânica, prematuridade. Abstract Objective: To review the literature on bronchopulmonary dys-plasia. Methods: The most important articles on bronchopulmonary dysplasia were selected through MEDLINE. Results: The present review analyzes the different concepts, pathogenesis, clinical presentation, treatment and prophylaxis of bronchopulmonary dysplasia. Conclusions: bronchopulmonary dysplasia is a frequent condition of very low birth weight infants with hyaline membrane disease who require mechanical ventilation. The pathogenic factors are prematurity, oxygen therapy, mechanical ventilation, pulmonary edema, and infection. Treatment is based on good oxygenation, fluid restriction, nutritional support, diuretics, betamimetic drugs, xanthines, and steroids. Prophylaxis includes avoiding prematurity and using pre-natal steroids, superoxide dismutase, and post-natal steroids. J. pediatr. (Rio J.). 1998; 74 (Supl.1): S95-S98: bronchopulmo-nary dysplasia, oxygen, mechanical ventilation, prematurity. Introdução Displasia broncopulmonar (DBP) foi descrita pela pri-meira vez em 1967 por Northway e colaboradores 1. Todos os recém-nascidos descritos eram prematuros, tinham tido do-ença de membrana hialina, foram ventilados com pressão positiva intermitente e receberam altas concentrações de oxigênio inspirado. A doença, inicialmente, foi descrita em quatro estágios clínico-radiológicos distintos. Os estágios I e II eram indistinguíveis da doença de membrana hialina e ocorriam nos primeiros dez dias de vida. Os estágios III e IV caracterizavam a sua cronicidade, sendo, o quarto estágio, o mais severo, podendo persistir por mais de 28 dias. A incidência de DBP varia de 30% a 60 % em crianças com peso de nascimento abaixo de 1500 gramas e que necessitaram de ventilação mecânica 2,3. Definição A definição inicial de DBP baseava-se nos achados radiológicos de um paciente que necessitasse cronicamente de ventilação mecânica. Posteriormente, Bancalari e colaboradores sugeriram que o diagnóstico de DBP f...