Aims The EURO-ENDO registry aimed to study the management and outcomes of patients with infective endocarditis (IE). Methods and results Prospective cohort of 3116 adult patients (2470 from Europe, 646 from non-ESC countries), admitted to 156 hospitals in 40 countries between January 2016 and March 2018 with a diagnosis of IE based on ESC 2015 diagnostic criteria. Clinical, biological, microbiological, and imaging [echocardiography, computed tomography (CT) scan, 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT)] data were collected. Infective endocarditis was native (NVE) in 1764 (56.6%) patients, prosthetic (PVIE) in 939 (30.1%), and device-related (CDRIE) in 308 (9.9%). Infective endocarditis was community-acquired in 2046 (65.66%) patients. Microorganisms involved were staphylococci in 1085 (44.1%) patients, oral streptococci in 304 (12.3%), enterococci in 390 (15.8%), and Streptococcus gallolyticus in 162 (6.6%). 18F-fluorodeoxyglucose positron emission tomography/computed tomography was performed in 518 (16.6%) patients and presented with cardiac uptake (major criterion) in 222 (42.9%) patients, with a better sensitivity in PVIE (66.8%) than in NVE (28.0%) and CDRIE (16.3%). Embolic events occurred in 20.6% of patients, and were significantly associated with tricuspid or pulmonary IE, presence of a vegetation and Staphylococcus aureus IE. According to ESC guidelines, cardiac surgery was indicated in 2160 (69.3%) patients, but finally performed in only 1596 (73.9%) of them. In-hospital death occurred in 532 (17.1%) patients and was more frequent in PVIE. Independent predictors of mortality were Charlson index, creatinine > 2 mg/dL, congestive heart failure, vegetation length > 10 mm, cerebral complications, abscess, and failure to undertake surgery when indicated. Conclusion Infective endocarditis is still a life-threatening disease with frequent lethal outcome despite profound changes in its clinical, microbiological, imaging, and therapeutic profiles.
Patients receiving aCRT had a reduced risk of AF compared with those receiving convCRT. Most of the reduction in AF occurred in subgroups with prolonged AV conduction at baseline and with significant left atrial reverse remodeling.
Background: Although atrial fibrillation (AF) is associated with exacerbation of heart failure with preserved ejection fraction (HFpEF), the relationships between maintenance of sinus rhythm (SR) and clinical outcomes in HFpEF is unknown. We investigated whether maintenance of SR was associated with better prognosis compared with rate control in patients with concomitant HFpEF and AF. Methods: We conducted a retrospective, observational study of 283 patients with HFpEF and AF. Of these, 107 patients achieved maintenance of SR by catheter ablation and/or antiarrhythmic drugs (rhythm control) and 176 were treated with rate control. The propensity score (PS) for each patient in both treatment groups was estimated, resulting in selectively matched subgroups of 79 patients each. All-cause death and a composite of cardiovascular death or hospitalization for heart failure (HF) were analyzed. Results: During a median follow-up period of 24 months, all-cause mortality was comparable between groups; however, maintenance of SR was significantly associated with a lower incidence of the composite endpoint [adjusted hazard ratio (HR), 0.30; 95% confidence interval, 0.18-0.98; p = 0.04] in the PSmatched cohort. The PS-adjusted multivariable analysis based on 283 pre-matched patients also revealed that rhythm control was associated with a lower rate of the composite endpoint (adjusted HR, 0.27; 95% CI, 0.12-0.61; p = 0.002). Subgroup analyses suggested that rhythm control was consistently related to the composite endpoint across a wide spectrum of HFpEF patients. Conclusions: Maintenance of SR was associated with a lower risk of composite of cardiovascular death or hospitalization for HF in patients with HFpEF and AF. A randomized trial is necessary to confirm this result.
Herein we describe the structure–property relationships of three biazulene isomers (2,6′-biazulene (BAz1), 2,2′-biazulene (BAz2), and 6,6′-biazulene (BAz3)). The unimolecular planarities of these molecules follow the order BAz2 > BAz1 > BAz3, which is ascribable to the planar five-membered and the twisted seven-membered biaryl rings. This order is the same as the conjugation-expansion order, and the intramolecular reorganization energies show a similar trend. Hole mobility follows the order BAz2 > BAz3 > BAz1, where the lowest mobility of BAz1 is attributable to its asymmetric molecular orbital distribution. 2,2′-Binaphthalene (BNp), a structural isomer of biazulene, shows no field-effect transistor characteristics. Transfer integrals clearly support the observed superiority and inferiority of these hole-transport properties. This study demonstrates the crucial importance of both molecular structure and molecular orbital symmetries for charge transfer. The dimer approach involving the 2,6-positions of azulene generates linear structures due to the structural features of its five-membered and seven-membered rings. Hence, azulenes, which are relatively asymmetric from an aromatic perspective, exhibit high symmetries as their biazulene isomers. This is in contrast to the loss of symmetry when naphthalene is dimerized through its 2-position.
Neutrophils are recruited into the heart at an early stage following a myocardial infarction (MI). These secrete several proteases, one of them being neutrophil elastase (NE), which promotes inflammatory responses in several disease models. It has been shown that there is an increase in NE activity in patients with MI; however, the role of NE in MI remains unclear. Therefore, the present study aimed to investigate the role of NE in the pathogenesis of MI in mice. NE expression peaked on day 1 in the infarcted hearts. In addition, NE deficiency improved survival and cardiac function post-MI, limiting fibrosis in the noninfarcted myocardium. Sivelestat, an NE inhibitor, also improved survival and cardiac function post-MI. Flow cytometric analysis showed that the numbers of heart-infiltrating neutrophils and inflammatory macrophages (CD11b+F4/80+CD206low cells) were significantly lower in NE-deficient mice than in wild-type (WT) mice. At the border zone between intact and necrotic areas, the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive apoptotic cells was lower in NE-deficient mice than in WT mice. Western blot analyses revealed that the expression levels of insulin receptor substrate 1 and phosphorylation of Akt were significantly upregulated in NE-knockout mouse hearts, indicating that NE deficiency might improve cardiac survival by upregulating insulin/Akt signaling post-MI. Thus, NE may enhance myocardial injury by inducing an excessive inflammatory response and suppressing Akt signaling in cardiomyocytes. Inhibition of NE might serve as a novel therapeutic target in the treatment of MI.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.