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Abstract Aims Mortality risk after hospitalization for heart failure (HF) is high, especially in the first 90 days. This study aimed to construct a model automatically predicting 90 day post-discharge mortality using electronic health record (EHR) data 48 h after admission and artificial intelligence. Methods All HF-related admissions from 2015 to 2020 in a single hospital were included in the model training. Comprehensive EHR data were collected 48 h after admission. Natural language processing was applied to textual information. Deaths were identified from the French national database. After variable selection with least absolute shrinkage and selection operator, a logistic regression model was trained. Model performance [area under the receiver operating characteristic curve (AUC)] was tested in two independent cohorts of patients admitted to two hospitals between March and December 2021. Results The derivation cohort included 2257 admissions (248 deaths after hospitalization). The evaluation cohorts included 348 and 388 admissions (34 and 38 deaths, respectively). Forty-two independent variables were selected. The model performed well in the derivation cohort [AUC: 0.817; 95% confidence interval (CI) (0.789–0.845)] and in both evaluation cohorts [AUC: 0.750; 95% CI (0.672–0.829) and AUC: 0.723; 95% CI (0.644–0.803]), with better performance than previous models in the literature. Calibration was good: ‘low-risk’ (predicted mortality ≤8%), ‘intermediate-risk’ (8–12.5%) and ‘high-risk’ (>12.5%) patients had an observed 90 day mortality rate of 3.8%, 8.4% and 19.4%, respectively. Conclusions The study proposed a robust model for the automatic prediction of 90 day mortality risk 48 h after hospitalization for decompensated HF. This could be used to identify high-risk patients for intensification of therapeutic management.

Abstract Aims In the Tri.FR trial, tricuspid transcatheter edge-to-edge repair (T-TEER) reduced severity of tricuspid regurgitation (TR) and improved the composite clinical score, driven by patient-reported outcomes. The purpose of this study was to describe the longitudinal impact of T-TEER on different dimensions and items of quality of life compared with guideline-directed medical treatment (OMT) alone. Methods and results Patients were randomized to T-TEER +OMT (n = 152) or OMT alone (n = 148). Health status was assessed at baseline, 6 weeks, 6 months, and 1 year using the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the Minnesota Living with Heart Failure (MLHF) Questionnaire. Mixed effects linear regression analysed changes over time. Patients receiving T-TEER + OMT experienced a significant increase in KCCQ overall summary score (KCCQ-OS) at all time points: +17.0 points (95% confidence interval [CI] 13.1–21.5) at 6 weeks, +15.9 points (95% CI 11.2–20.6) at 6 months, and +18.7 points (95% CI 13.8–23.6) at 1 year. The mean between-group difference in KCCQ-OS was +10.3 points (95% CI 5.6–15.0) in favour of T-TEER + OMT, evident at 6 weeks and sustained for 1 year. Similarly, MLHF total scores improved significantly in the T-TEER group (mean between-group difference −8.61 points, 95% CI –12.6 to −4.6), including physical (−3.9, 95% CI –5.9 to −1.9) and emotional (−2.2, 95% CI –3.4 to −1.0) subscales. Conclusions Compared with OMT alone, T-TEER resulted in substantial, multidimensional, and sustained improvements in patient-reported quality of life. These findings reinforce the value of T-TEER in managing severe symptomatic TR. This study is one of the first randomised trials to demonstrate that transcatheter tricuspid valve repair (T-TEER) yields substantial and sustained improvements in quality of life across multiple domains, beyond clinical and echocardiographic outcomes. Using both the Kansas City Cardiomyopathy Questionnaire and the Minnesota Living with Heart Failure questionnaire, the Tri.FR trial robustly quantifies patient-perceived benefits-particularly in physical and emotional well-being-following T-TEER. The findings position T-TEER as a pivotal, patient-centred strategy for managing severe symptomatic tricuspid regurgitation, especially in elderly, high-risk patients with heart failure with preserved ejection fraction.

Dilated cardiomyopathy (DCM) is a structural heart disease with strong genetic background. Monogenic forms of DCM are observed in families with mutations located mostly in genes encoding structural and sarcomeric proteins. However, strong evidence suggests that genetic factors also affect the susceptibility to idiopathic DCM. To identify risk alleles for non-familial forms of DCM, we carried out a case-control association study, genotyping 664 DCM cases and 1,874 population-based healthy controls from Germany using a 50K human cardiovascular disease bead chip covering more than 2,000 genes pre-selected for cardiovascular relevance. After quality control, 30,920 single nucleotide polymorphisms (SNP) were tested for association with the disease by logistic regression adjusted for gender, and results were genomic-control corrected. The analysis revealed a significant association between a SNP in HSPB7 gene (rs1739843, minor allele frequency 39%) and idiopathic DCM (p = 1.06 × 10⁻⁶, OR  = 0.67 [95% CI 0.57-0.79] for the minor allele T). Three more SNPs showed p < 2.21 × 10⁻⁵. De novo genotyping of these four SNPs was done in three independent case-control studies of idiopathic DCM. Association between SNP rs1739843 and DCM was significant in all replication samples: Germany (n =564, n = 981 controls, p = 2.07 × 10⁻³, OR = 0.79 [95% CI 0.67-0.92]), France 1 (n = 433 cases, n = 395 controls, p =3.73 × 10⁻³, OR  = 0.74 [95% CI 0.60-0.91]), and France 2 (n = 249 cases, n = 380 controls, p = 2.26 × 10⁻⁴, OR  = 0.63 [95% CI 0.50-0.81]). The combined analysis of all four studies including a total of n = 1,910 cases and n = 3,630 controls showed highly significant evidence for association between rs1739843 and idiopathic DCM (p = 5.28 × 10⁻¹³, OR= 0.72 [95% CI 0.65-0.78]). None of the other three SNPs showed significant results in the replication stage.This finding of the HSPB7 gene from a genetic search for idiopathic DCM using a large SNP panel underscores the influence of common polymorphisms on DCM susceptibility.

Aims Major bleeding events in heart failure (HF) patients are poorly described. We sought to investigate the importance of major bleeding and its impact on outcomes in HF patients. Methods and results We analysed incident bleeding and ischaemic events during a 3 year follow‐up in 2910 HF outpatients included in a prospective multicentre registry. Major bleeding was defined as a Type ≥3 bleed using the Bleeding Academic Research Consortium definition. Ischaemic event was a composite of ischaemic stroke and myocardial infarction. Events were adjudicated by a blinded committee. At inclusion, most patients (89%) received at least one antithrombotic: anticoagulation (53.9%) and/or antiplatelet therapy (46.2%). Bleeding occurred in 111 patients 3 year cumulative incidence: 3.6% [95% confidence interval (CI) 3.0–4.3] and ischaemic events in 102 patients [3 year cumulative incidence: 3.3% (95% CI 2.7–4.0)]. Most bleedings were Bleeding Academic Research Consortium 3a (32.5%) or 3b (31.5%). Most frequent sites of bleeding were gastrointestinal (40.6%) and intracranial (27.9%). Variables associated with bleeding were atrial fibrillation [hazard ratio (HR) = 2.63 (95% CI 1.66–4.19), P < 0.0001], diabetes [HR = 1.62 (95% CI 1.11–2.38), P = 0.012], and older age [HR = 1.19 per 10 year increase (95% CI 1.00–1.41), P = 0.049]. Anticoagulation use was associated with a two‐fold increase in the bleeding risk. Bleeding events as well as ischaemic events were strongly associated with subsequent mortality [adjusted HRs: 5.67 (4.41–7.29), P < 0.0001 and 4.29 (3.18–5.78), P < 0.0001, respectively]. Conclusions In HF outpatients, antithrombotics are widely used. Bleeding occurs at a stable rate of 1.2% annually (as frequent as ischaemic events) and is associated with a dramatic increase in mortality (at least as severe as ischaemic events). Most events occurred in patients receiving anticoagulation. Knowledge of these findings may help physicians to manage antithrombotics in HF patients.

Aims Chronic heart failure reduces quality and quantity of life and is expensive for healthcare systems. Medical treatment relies on guideline‐directed therapy, but clinical follow‐up and remote management is highly variable and poorly effective. New remote management strategies are needed to maintain clinical stability and avoid hospitalizations for acute decompensation. Methods and results The CardioMEMS Post‐Market Study is a prospective, international, single‐arm, multicentre, open‐label study (NCT02954341) designed to examine the feasibility of haemodynamic guided heart failure management using a small pressure sensor permanently implanted in the pulmonary artery (PA). Daily uploaded PA pressures will be reviewed weekly to remotely guide medical management of patients with persistent NYHA Class III symptoms at baseline and a hospitalization in the prior 12 months. The study will enrol up to 800 patients from 85 sites across the United Kingdom, Europe, and Australia. The primary safety endpoint will assess device or system‐related complications or sensor failures after 2 years of follow‐up. Efficacy will be estimated after 1 year of follow‐up comparing HF hospitalization rates before and after sensor implantation. Observational endpoints will include mortality, patient, and investigator monitoring compliance, PA pressure changes, quality of life, and several pre‐defined subgroup analyses. Conclusions The CardioMEMS Post‐Market Study will investigate the generalizability of remote haemodynamic guided HF management in a number of national settings. The results may support the more widespread implementation of this novel clinical management approach.

Dilated cardiomyopathy (DCM) is a structural heart disease with strong genetic background. Monogenic forms of DCM are observed in families with mutations located mostly in genes encoding structural and sarcomeric proteins. However, strong evidence suggests that genetic factors also affect the susceptibility to idiopathic DCM. To identify risk alleles for non-familial forms of DCM, we carried out a case-control association study, genotyping 664 DCM cases and 1,874 population-based healthy controls from Germany using a 50K human cardiovascular disease bead chip covering more than 2,000 genes pre-selected for cardiovascular relevance. After quality control, 30,920 single nucleotide polymorphisms (SNP) were tested for association with the disease by logistic regression adjusted for gender, and results were genomic-control corrected. The analysis revealed a significant association between a SNP in HSPB7 gene (rs1739843, minor allele frequency 39%) and idiopathic DCM (p = 1.06×10-6, OR = 0.67 [95% CI 0.57-0.79] for the minor allele T). Three more SNPs showed p < 2.21×10-5. De novo genotyping of these four SNPs was done in three independent case-control studies of idiopathic DCM. Association between SNP rs1739843 and DCM was significant in all replication samples: Germany (n = 564, n = 981 controls, p = 2.07×10-3, OR = 0.79 [95% CI 0.67-0.92]), France 1 (n = 433 cases, n = 395 controls, p = 3.73×10-3, OR = 0.74 [95% CI 0.60-0.91]), and France 2 (n = 249 cases, n = 380 controls, p = 2.26×10-4, OR = 0.63 [95% CI 0.50-0.81]). The combined analysis of all four studies including a total of n = 1,910 cases and n = 3,630 controls showed highly significant evidence for association between rs1739843 and idiopathic DCM (p = 5.28×10-13, OR = 0.72 [95% CI 0.65-0.78]). None of the other three SNPs showed significant results in the replication stage. This finding of the HSPB7 gene from a genetic search for idiopathic DCM using a large SNP panel underscores the influence of common polymorphisms on DCM susceptibility.

We present the results of the largest genome wide association study (GWAS) performed so far in dilated cardiomyopathy (DCM), a leading cause of systolic heart failure and cardiovascular death, with 2,719 cases and 4,440 controls in the discovery population. We identified and replicated two new DCM-associated loci, one on chromosome 3p25.1 (lead SNP rs62232870, p = 8.7 × 10−11 and 7.7 × 10−4 in the discovery and replication step, respectively) and the second on chromosome 22q11.23 (lead SNP rs7284877, p = 3.3 × 10−8 and 1.4 × 10−3 in the discovery and replication step, respectively) while confirming two previously identified DCM loci on chromosome 10 and 1, BAG3 and HSPB7. The genetic risk score constructed from the number of lead risk-alleles at these four DCM loci revealed that individuals with 8 risk-alleles were at a 27% increased risk of DCM compared to individuals with 5 risk alleles (median of the referral population). We estimated the genome wide heritability at 31% ± 8%. In silico annotation and functional 4C-sequencing analysis on iPSC-derived cardiomyocytes strongly suggest SLC6A6 as the most likely DCM gene at the 3p25.1 locus. This gene encodes a taurine and beta-alanine transporter whose involvement in myocardial dysfunction and DCM is supported by recent observations in humans and mice. Although less easy to discriminate the better candidate at the 22q11.23 locus, SMARCB1 appears as the strongest one. This study provides both a better understanding of the genetic architecture of DCM and new knowledge on novel biological pathways underlying heart failure, with the potential for a therapeutic perspective.

Objective The purpose of this paper is to describe a study protocol of a clinical trial exploring the effectiveness of the new mobile application MyDéfi proposing personalized feedback, on both alcohol consumption and quality of life, as well as the blood alcohol exposure biomarker phosphatidylethanol, in university students displaying binge drinking behavior. Methods This prospective national multicentric randomized, two‐arm (1:1), double‐blind controlled trial will recruit 628 students (aged 18–25 years) with binge drinking behavior. Participants will be randomized in the “intervention” group (personalized feedback) or the “control” group (generic feedback) and will undergo four monthly visits. Monthly dried blood spot sample for measuring phosphatidylethanol concentration and online questionnaires will be collected. Our primary objective is to assess the reduction weekly standard drinks, through self‐report gathered via MyDéfi. Secondary objectives will evaluate the application's impact on the dosage of phosphatidylethanol blood concentration and on quality of life”. Results Recruitment started in March 2024 and will end in March 2026. Conclusion This study aims to determine the effectiveness of two versions of the same mobile application (generic vs. personalized feedback) on alcohol consumption in students displaying binge drinking behavior. The effectiveness of the application will be measured, with a secondary objective of quantifying phosphatidylethanol. Our study will open new perspectives on the use of digital interventions for students who do not actively seek treatment. Trial Registration Trial registration number (NCT06084832), the date of registration (10th October 2023) and when this was done (16th October 2023). https://clinicaltrials.gov/study/NCT06084832

On the one hand the heterogeneity of the circulatory system requires the use of different models in its different compartments, featuring different assumptions on the spatial degrees of freedom. On the other hand, the mutual interactions between its compartments imply that these models should preferably not be considered separately. These requirements have led to the concept of geometrical multiscale modeling , where the main idea is to couple 3D models with reduced 1D and/or 0D models. As such detailed information on the flow field in a specific region of interest can be obtained while accounting for the global circulation. However, the combination of models with different mathematical features gives rise to many difficulties such as the assignment of boundary conditions at the interface between two models and the development of robust coupling algorithms, as the subproblems are usually solved in a partitioned way. This review aims to give an overview of the most important aspects concerning 3D–1D–0D coupled models. In addition, some applications are presented in order to illustrate the potentialities of these coupled models.

Abstract Background As the epidemiology of encephalitis varies from one country to another, international travel may be an important clue for the diagnostic workout of this puzzling disease. Methods We performed an ancillary study using the ENCEIF prospective cohort conducted in 62 clinical sites in France from 2016 to 2019. All cases of encephalitis in adults that fulfilled a case definition derived from the International Encephalitis Consortium were included. Travellers were defined as patients who spent at least one night in a foreign country within the last six months. Results Of the 494 encephalitis patients enrolled, 69 (14%) were travellers. As compared to non-travellers, they were younger (median age, 48 years [interquartile range, 36–69] vs 66 [49–76], P < 0.001), less likely to be immunocompromised: 2/69 (3%) vs 56/425 (13%), P = 0.02, and reported more arthralgia: 7/69 (10%) vs 11/425 (3%), P = 0.007. The risk of poor outcome at hospital discharge (Glasgow outcome scale ≤3), was similar for travellers and for non-travellers after adjustment (aOR 0.80 [0.36–1.80], P = 0.594). Arboviruses were the main causes of encephalitis in travellers: 15/69 (22%) vs 20/425 (5%) in non-travellers, P < 0.001, and Herpes simplex virus (HSV) was the second (9/69, 13%). Of note, in 19% (13/69) of cases, the risk of encephalitis in travellers may have been decreased with a vaccine. Conclusion The two primary causes of encephalitis in travellers are arboviruses and HSV. Empirical treatment of encephalitis in travellers must include acyclovir. Pre-travel advice and vaccination may decrease the risk of encephalitis in travellers.