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Zusammenfassung. Die akute Rechtsherzinsuffizenz ist ein kritischer Zustand, der anhand der klinischen Präsentation kombiniert mit Echokardiografie diagnostiziert wird. Zusatzdiagnostik inkl. Labor, EKG, Rechtsherzkatheter und weitere bildgebende Verfahren werden zur Ursachenabklärung benötigt. Therapeutisch spielen die Identifikation und Behandlung der zu Grunde liegenden Pathologie, die Reduktion der rechtsventrikulären Nachlast (sofern möglich), eine Optimierung der Vorlast (häufig Diuretika, selten Volumen) und eine Kreislaufunterstützung mittels Vasopressoren und/oder Inodilatatoren eine zentrale Rolle. In schweren Fällen kommen spezielle Therapien und mechanische Kreislaufunterstützungssysteme ins Spiel.

The current European Society of Cardiology (ESC) Heart Failure Guidelines are the most comprehensive ESC document covering heart failure to date; however, the section focused on acute heart failure remains relatively too concise. Although several topics are more extensively covered than in previous versions, including some specific therapies, monitoring and disposition in the hospital, and the management of cardiogenic shock, the lack of high-quality evidence in acute, emergency, and critical care scenarios, poses a challenge for providing evidence-based recommendations, in particular when by comparison the data for chronic heart failure is so extensive. The paucity of evidence and specific recommendations for the general approach and management of acute heart failure in the emergency department is particularly relevant, because this is the setting where most acute heart failure patients are initially diagnosed and stabilized. The clinical phenotypes proposed are comprehensive, clinically relevant and with minimal overlap, whilst providing additional opportunity for discussion around respiratory failure and hypoperfusion. F.P. has received research grants from Abbott, Becton Dickenson, Brainbox, Calcimedica, CSL Behring, Cue, Ortho Clinical Diagnostics, Relypsa, Roche, Salix, Siemens. Consultant: Abbott, Astra-Zeneca, Beckman, Bosch, Fast Biomedical, Forrest Devices, Ischemia Care, Dx, Instrument Labs, Janssen, Nabriva, Ortho Clinical Diagnostics, Osler, Relypsa, Roche, Quidel, Salix, Siemens, Upstream and has stock/ownership interests in AseptiScope Inc, Brainbox Inc, Braincheck Inc, Coagulo Inc, Comprehensive Research Associates LLC, Comprehensive Research Management Inc, Emergencies in Medicine LLC, Fast Inc, Forrest Devices, Ischemia DX LLC, Lucia Inc, Prevencio Inc, ScPharma, Trivirum Inc, Upstream Inc. E.P.’ employer has received support from Novartis for consulting work and she has consulted for scPharmaceuticals outside of the submitted work. She has received research support from the NIH (R01HL148439). Sí

Background and aims STRONG-HF showed that rapid up-titration of guideline-recommended medical therapy (GRMT), in a high intensity care (HIC) strategy, was associated with better outcomes compared to usual care (UC). The aim of this study was to assess the role of N-terminal pro-B-type natriuretic peptide (NT-proBNP) at baseline and its changes early during up-titration. Methods A total of 1077 patients hospitalized for acute heart failure (HF) and with a >10% NT-proBNP decrease from screening (i.e. admission) to randomization (i.e. pre-discharge), were included. Patients in HIC were stratified by further NT-proBNP changes from randomization to 1 week later as decreased (≥30% decrease), stable (10% increase). The primary endpoint was 180-day HF readmission or death. Results The effect of HIC vs. UC was independent of baseline NT-proBNP. Patients in the HIC group with stable or increased NT-proBNP were older, with more severe acute HF and worse renal and liver function. Per protocol, patients with increased NT-proBNP received more diuretics and were up-titrated more slowly during the first weeks after discharge. However, by 6 months they reached 70.4% optimal GRMT doses, compared with 80.3% for those with NT-proBNP decrease. As a result, the primary endpoint at 60 and 90 days occurred in 8.3% and 11.1% of patients with increased NT-proBNP vs 2.2% and 4.0% in those with decreased NT-proBNP (p=0.039 and p=0.045, respectively). However, no difference in outcome was found at 180 days (13.5% vs. 13.2%; p=0.93). Conclusions Among patients with acute HF enrolled in STRONG-HF, HIC reduced 180-day HF readmission or death regardless of baseline NT-proBNP. GRMT up-titration early post-discharge utilizing increased NT-proBNP as guidance to increase diuretic therapy and reduce the GRMT up-titration rate resulted in the same 180-day outcomes regardless of early post-discharge NT-proBNP change.

ObjectivesTo evaluate the potential of soluble cluster of differentiation 146 (sCD146) in the detection and grading of congestion in patients with acute dyspnoea.DesignSubanalysis of the prospective observational Lithuanian Echocardiography Study of Dyspnoea in Acute Settings (LEDA) cohort.SettingTwo Lithuanian university centres.ParticipantsAdult patients with acute dyspnoea admitted to the emergency department.MethodsCongestion was assessed using clinical and sonographic parameters. All patients underwent sCD146 and N-terminal pro-B-type natriuretic peptide (NT-proBNP) testing.ResultsThe median value of sCD146 concentration in the study cohort (n=437) was 405 (IQR 315–509) ng/mL. sCD146 was higher in patients with peripheral oedema than in those without (median (IQR) 472 (373–535) vs 400 (304–501) ng/mL, p=0.009) and with pulmonary rales than in those without (439 (335–528) vs 394 (296–484) ng/mL, p=0.001). We found a parallel increase of estimated right atrial pressure (eRAP) and sCD146 concentration: sCD146 was 337 (300–425), 404 (290–489) and 477 (363–572) ng/mL in patients with normal, moderately elevated and high eRAP, respectively (p=0.001). In patients with low NT-proBNP, high sCD146 distinguished a subgroup with a higher prevalence of oedema as compared with patients with low levels of both biomarkers (76.0% vs 41.0%, p=0.010). Moreover, high sCD146 indicated a higher prevalence of elevated eRAP, irrespective of NT-proBNP concentration (pConclusionsCD146 concentration reflects the degree of intravascular and tissue congestion assessed by clinical and echocardiographic indices, with this association maintained in patients with low NT-proBNP. Our data support the notion that NT-proBNP might represent heart stretch while sCD146 rather represents peripheral venous congestion.

Heart transplantation (HTx) is the treatment of choice in patients with late-stage advanced heart failure (Advanced HF). Survival rates 1, 5, and 10 years after transplantation are 87%, 77%, and 57%, respectively, and the average life expectancy is 9.16 years. However, because of the donor organ shortage, waiting times often exceed life expectancy, resulting in a waiting list mortality of around 20%. This review aims to provide an overview of current standard, recent advances, and future developments in the treatment of Advanced HF with a focus on long-term mechanical circulatory support and HTx.

Background Improved understanding and assessment of the complex physiology of volume regulation in haemodialysis (HD) patients are required to improve patient care and reduce mortality associated with fluid overload (FO). Methods We searched for FO-related biomarkers among 184 peptides associated with cardiovascular disease in a cohort of 30 HD patients. First, we assessed the direct impact of HD on the peptides of interest by comparing plasma concentrations before and after treatment. Then, we compared cardiovascular peptide profiles between patients with and without FO as defined by bioimpedance analysis (BIA). The plasma concentration of selected candidate biomarkers for FO was determined by enzyme-linked immunosorbent assay (ELISA) and correlated with previously described FO-related clinical and laboratory parameters. For validation, results were confirmed in an independent cohort of 144 HD patients. Results We found seven peptides positively [NT-proBNP, B-type natriuretic peptide (BNP), vascular endothelial growth factor D (VEGFD), tumour necrosis factor-related apoptosis-inducing ligand receptor 2, growth differentiation factor 15, tumour necrosis factor ligand superfamily member 13B, chitinase-3-like protein 1] and five negatively (leptin, renin, epidermal growth factor receptor, interleukin-1 receptor antagonist, myeloblastin) correlated to FO. In addition to natriuretic peptides, VEGFD emerged as third peptide highly correlated with BIA (ρ = 0.619, P Conclusion VEGFD is a novel FO-related biomarker with unique diagnostic and prognostic properties.

Heart transplantation (HTx) is the treatment of choice in patients with late-stage advanced heart failure (Advanced HF). Survival rates 1, 5, and 10 years after transplantation are 87%, 77%, and 57%, respectively, and the average life expectancy is 9.16 years. However, because of the donor organ shortage, waiting times often exceed life expectancy, resulting in a waiting list mortality of around 20%. This review aims to provide an overview of current standard, recent advances, and future developments in the treatment of Advanced HF with a focus on long-term mechanical circulatory support and HTx.

The prognostic significance of the right ventricle (RV) has recently been recognised in several conditions, primarily those involving the left ventricle, the lungs and their vascular bed, or the right-sided chambers. Recent advances in imaging techniques have created new opportunities to study RV anatomy, physiology and pathophysiology, and contemporary research efforts have opened the doors to new treatment possibilities. Nevertheless, the treatment of RV failure remains challenging. Optimal management should consider the anatomical and physiological particularities of the RV and include appropriate imaging techniques to understand the underlying pathophysiological mechanisms. Treatment should include rapid optimisation of volume status, restoration of perfusion pressure and improvement of myocardial contractility and rhythm, and, in case of refractory RV failure, mechanical circulatory support.

Aim This study aimed at evaluating the effects of sacubitril/valsartan on neprilysin (NEP), and the metabolism of natriuretic peptides in heart failure (HF) and providing additional mechanistic information on the mode of action of the drug. Methods and results We enrolled 73 chronic HF patients who were switched from angiotensin-converting enzyme inhibitor or angiotensin receptor blocker to sacubitril/valsartan. In addition to clinical and echocardiographic assessment, plasma biomarkers were measured at baseline, day 30 and day 90 after initiation of treatment. Sacubitril/valsartan led to decrease in New York Heart Association class and improvement of echocardiographic parameters, as well as a dose-dependent decrease in soluble NEP (sNEP) activity, while sNEP concentration remained unchanged. Neprilysin inhibition translated into an increase in its substrates such as atrial natriuretic peptide (ANP), substance P, and glucagon-like peptide 1, the latter translating into a decrease in fructosamine. Cardiac troponin and soluble ST2 levels, biomarkers of HF severity unrelated to NEP metabolism also decreased. While there was a ∼4-fold increase in ANP, we observed no change in plasma brain natriuretic peptide (BNP) and plasma BNP activity, and a mild decrease in N-terminal proBNP (NT-proBNP) concentrations. Finally, we found a progressive increase in the relationship between BNP and NT-proBNP, which strongly correlated with an increase in T71 proBNP glycosylation (R2 = 0.94). Conclusion Sacubitril/valsartan rapidly and strongly reduced sNEP activity, leading to an increase in levels of NEP substrates. These data suggest a pleiotropic favourable impact of sacubitril/valsartan on the metabolism of HF patients with ANP rather than BNP as major effectors amongst natriuretic peptides.

Acute heart failure and acute pulmonary embolism share many features, including epidemiological aspects, clinical presentation, risk factors and pathobiological mechanisms. As such, it is not surprising that diagnosis and management of these common conditions might be challenging for the treating physician, in particular when both are concomitantly present. While helpful guidelines have been elaborated for both acute heart failure and pulmonary embolism, not many studies have been published on the coexistence of these diseases. With a special focus on diagnostic tools and therapeutic options, the authors review the available literature and, when evidence is lacking, present their own approach to the management of dyspnoeic patients with acute heart failure and pulmonary embolism.

Acute myocardial infarction complicated by cardiogenic shock (AMICS) is a critical syndrome with a high risk of morbidity and mortality. Current management consists of coronary revascularisation, vasoactive drugs, and circulatory and ventilatory support, which are tailored to patients mainly on the basis of clinicians' experience rather than evidence-based recommendations. For many therapeutic interventions in AMICS, randomised clinical trials have not shown a meaningful survival benefit, and a disproportionately high rate of neutral and negative results has been reported. In this context, an accurate definition of the AMICS syndrome for appropriate patient selection and optimisation of study design are warranted to achieve meaningful results and pave the way for new, evidence-based therapeutic options. In this Position Paper, we provide a statement of priorities and recommendations agreed by a multidisciplinary group of experts at the Critical Care Clinical Trialists Workshop in February, 2020, for the optimisation and harmonisation of clinical trials in AMICS. Implementation of proposed criteria to define the AMICS population-moving beyond a cardio-centric definition to that of a systemic disease-and steps to improve the design of clinical trials could lead to improved outcomes for patients with this life-threatening syndrome.

Accurate diagnosis and timely treatment initiation are crucial to optimize outcome of women affected by acute PPCM. Therapeutic interventions—in particular in pregnant women—may be limited, since they always need to consider both the health of the mother and the fetus. Particularly challenging are severe forms of acute PPCM leading to cardiopulmonary instability, as the mortality of these women is particularly high. Interdisciplinary approaches of cardiologists, intensivists, obstetricians, neonatologists, anesthetists, and cardiac surgeons are necessary in case of acute PPCM. As evidence from large randomized clinical trials is lacking, this chapter provides practical recommendations for the acute treatment of PPCM causing acute heart failure based on recent data and clinical experience.

Little is known about the evolution of diaphragmatic function in the early post-cardiac surgery period. The main purpose of this work is to describe its evolution using ultrasound measurements of muscular excursion and thickening fraction (TF). Single-center prospective study of 79 consecutive uncomplicated elective cardiac surgery patients, using motion-mode during quiet unassisted breathing. Excursion and TF were measured sequentially for each patient [pre-operative (D1), 1 day (D2) and 5 days (D3) after surgery]. Pre-operative median for right and left hemidiaphragmatic excursions were 1.8 (IQR 1.6 to 2.1) cm and 1.7 (1.4 to 2.0) cm, respectively. Pre-operative median right and left thickening fractions were 28 (19 to 36) % and 33 (22 to 51) %, respectively. At D2, there was a reduction in both excursion (right: 1.5 (1.1 to 1.8) cm, p

© 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology. This is an open access article under the terms of the Creative Commons Attribution-Non Commercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes., Aims: Changes in echocardiographic parameters and biomarkers of cardiac and venous pressures or estimated plasma volume during hospitalization associated with decongestive treatments in acute heart failure (AHF) patients with either preserved left ventricular ejection fraction (LVEF) (HFPEF) or reduced LVEF (HFREF) are poorly assessed. Methods and results: From the metabolic road to diastolic heart failure: diastolic heart failure (MEDIA‐DHF) study, 111 patients were included in this substudy: 77 AHF (43 HFPEF and 34 HFREF) and 34 non‐cardiac dyspnea patients. Echocardiographic measurements and blood samples were obtained within 4 h of presentation at the emergency department and before hospital discharge. In AHF patients, echocardiographic indices of cardiac and venous pressures, including inferior vena cava diameter [from 22 (16–24) mm to 13 (11–18) mm, P = 0.009], its respiratory variability [from 32 (8–44) % to 43 (29–70) %, P = 0.04], medial E/e' [from 21.1 (15.8–29.6) to 16.6 (11.7–24.3), P = 0.004], and E wave deceleration time [from 129 (105–156) ms to 166 (128–203) ms, P = 0.003], improved during hospitalization, similarly in HFPEF and HFREF patients. By contrast, no changes were seen in non‐cardiac dyspnea patients. In AHF patients, all plasma biomarkers of cardiac and venous pressures, namely B‐type natriuretic peptide [from 935 (514–2037) pg/mL to 308 (183–609) pg/mL, P < 0.001], mid‐regional pro‐atrial natriuretic peptide [from 449 (274–653) pmol/L to 366 (242–549) pmol/L, P < 0.001], and soluble CD‐146 levels [from 528 (406–654) ng/mL to 450 (374–529) ng/mL, P = 0.003], significantly decreased during hospitalization, similarly in HFPEF and HFREF patients. Echocardiographic parameters of cardiac chamber dimensions [left ventricular end‐diastolic volume: from 120 (76–140) mL to 118 (95–176) mL, P = 0.23] and cardiac index [from 2.1 (1.6–2.6) mL/min/m2 to 1.9 (1.4–2.4) mL/min/m2, P = 0.55] were unchanged in AHF patients, except tricuspid annular plane systolic excursion (TAPSE) that improved during hospitalization [from 16 (15–19) mm to 19 (17–21) mm, P = 0.04]. Estimated plasma volume increased in both AHF [from 4.8 (4.2–5.6) to 5.1 (4.4–5.8), P = 0.03] and non‐cardiac dyspnea patients (P = 0.01). Serum creatinine [from 1.18 (0.90–1.53) to 1.19 (0.86–1.70) mg/dL, P = 0.89] and creatinine‐based estimated glomerular filtration rate [from 59 (40–75) mL/min/1.73m2 to 56 (38–73) mL/min/1.73m2, P = 0.09] were similar, while plasma cystatin C [from 1.50 (1.20–2.27) mg/L to 1.78 (1.33–2.59) mg/L, P < 0.001] and neutrophil gelatinase associated lipocalin (NGAL) [from 127 (95–260) ng/mL to 167 (104–263) ng/mL, P = 0.004] increased during hospitalization in AHF. Conclusions: Echocardiographic parameters and plasma biomarkers of cardiac and venous pressures improved during AHF hospitalization in both acute HFPEF and HFREF patients, while cardiac chamber dimensions, cardiac output, and estimated plasma volume showed minimal changes., This study was supported by a grant from the European Union funded by the Seventh Framework Programme for Health in 2010 (FP7-HEALTH-2010-MEDIA; Luxembourg) (F.Z., P.R., A. M) and research fellowship from Japan Heart Foundation (E. A.). P.R., N.G., T.C., and F.Z. are supported by a public grant overseen by the French National Research Agency (ANR) as part of the second “Investissements d’Avenir” programmes Fighting Heart Failure (reference: ANR-15-RHU-0004), GEENAGE Impact Lorraine Université d’Excellence and by the Contrat de Plan Etat Lorraine IT2MP and FEDER Lorraine. LNLVA is supported by a training grant from the European Society of Cardiology (2015) and a travelling award from the International Society for Heart and Lung Transplantation (August 2015 and 2016). LNLVA gratefully acknowledges the financial support from the Fund for Cardiac Surgery through the Jacqueline Bernheim prize 2015.

Background We studied the course of plasma concentrations of 4 cardiovascular biomarkers: natriuretic peptides (BNP, NT-proBNP; mid-regional (MR) pro-atrial NP); and soluble endothelial CD146 (sCD146), in patients with severe mitral valve stenosis undergoing percutaneous mitral commissurotomy (PMC) to identify potential markers of procedural success. Methods Biomarkers were tested in 40 patients the day before and the day after PMC. Success was defined as mitral valve area ≥ 1.5 cm2; or an increase of ≥0.5 cm2 in mitral valve area associated with echocardiographic mitral regurgitation Results Average age was 63.5 ± 12.7 years; 32(80%) were female. Before PMC, mean valve area was 1.1 ± 0.2 cm2, mean gradient 9.1 ± 3.5 mmHg. PMC was successful in 30 (75%) and unsuccessful in 10 (25%). PMC yielded a significant reduction in MR-proANP and sCD146, driven by a significant reduction in these biomarkers in patients with successful procedure, whereas no reduction was observed in patients with unsuccessful procedure. A significant correlation was found between changes in plasma sCD146 and the relative change in mitral valve area. Elevated pre-procedural sPAP correlated with high sCD146, and accordingly, a significant correlation between the decrease in sPAP and sCD146 after PMC was shown. Conclusions MR-proANP and plasma sCD146 decreased significantly immediately after successful PMC. They appear to be markers of immediate success of PMC and of the hemodynamic improvement achieved by this procedure in patients with MS. Trial registration This study is part of the cohorts registered with ClinicalTrials.gov on June 16, 2011 under the number NCT01374880.

Acute heart failure (AHF) is a syndrome defined as the new onset (de novo heart failure (HF)) or worsening (acutely decompensated heart failure (ADHF)) of symptoms and signs of HF, mostly related to systemic congestion. In the presence of an underlying structural or functional cardiac dysfunction (whether chronic in ADHF or undiagnosed in de novo HF), one or more precipitating factors can induce AHF, although sometimes de novo HF can result directly from the onset of a new cardiac dysfunction, most frequently an acute coronary syndrome. Despite leading to similar clinical presentations, the underlying cardiac disease and precipitating factors may vary greatly and, therefore, the pathophysiology of AHF is highly heterogeneous. Left ventricular diastolic or systolic dysfunction results in increased preload and afterload, which in turn lead to pulmonary congestion. Fluid retention and redistribution result in systemic congestion, eventually causing organ dysfunction due to hypoperfusion. Current treatment of AHF is mostly symptomatic, centred on decongestive drugs, at best tailored according to the initial haemodynamic status with little regard to the underlying pathophysiological particularities. As a consequence, AHF is still associated with high mortality and hospital readmission rates. There is an unmet need for increased individualization of in-hospital management, including treatments targeting the causative factors, and continuation of treatment after hospital discharge to improve long-term outcomes. Acute heart failure (AHF) is a syndrome characterized by signs and symptoms of heart failure (typically systemic congestion) that occurs in the presence of an underlying cardiac dysfunction (previously diagnosed, undiagnosed or new-onset) and precipitating factors. AHF is associated with high mortality and hospital readmission rates.

Cardiogenic shock (CS) is a complex multifactorial clinical syndrome with extremely high mortality, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large spectrum of CS presentations resulting from the interaction between an acute cardiac insult and a patient's underlying cardiac and overall medical condition. Phenotyping patients with CS may have clinical impact on management because classification would support initiation of appropriate therapies. CS management should consider appropriate organization of the health care services, and therapies must be given to the appropriately selected patients, in a timely manner, whilst avoiding iatrogenic harm. Although several consensus-driven algorithms have been proposed, CS management remains challenging and substantial investments in research and development have not yielded proof of efficacy and safety for most of the therapies tested, and outcome in this condition remains poor. Future studies should consider the identification of the new pathophysiological targets, and high-quality translational research should facilitate incorporation of more targeted interventions in clinical research protocols, aimed to improve individual patient outcomes. Designing outcome clinical trials in CS remains particularly challenging in this critical and very costly scenario in cardiology, but information from these trials is imperiously needed to better inform the guidelines and clinical practice. The goal of this review is to summarize the current knowledge concerning the definition, epidemiology, underlying causes, pathophysiology and management of CS based on important lessons from clinical trials and registries, with a focus on improving in-hospital management. Chioncel, O (corresponding author), Univ Med & Pharm Carol Davila, Inst Emergency Cardiovasc Dis Prof CC Iliescu, Bucharest 950474, Romania. ochioncel@yahoo.co.uk

Objective: To investigate whether patients with an acute heart failure (AHF) episode triggered by infection present different outcomes compared to patients with no trigger and the effects of early antibiotic administration (EAA) and hospitalisation. Methods: Two groups were made according to the AHF trigger: infection (G1) or none identified (G2). The primary outcome was 13-week (91-days) all-cause mortality, and secondary outcomes were 13-week post-discharge mortality, readmission or combined endpoint. Comparisons are presented as unadjusted and adjusted (MEESSI risk score) hazard ratios (uHR/aHR) for G1 compared to G2 patients, also estimated by weeks. Stratified analysis by EAA (provided/not provided) and patient disposition (discharged/hospitalised) was performed. Results: We included 6727 patients (G1 = 3973; G2 = 2754). The 13-week mortality uHR was 1.11 (0.99-1.25; p = 0.06; with significant increases in the first 3 weeks), and the aHR was 0.91 (0.81-1.02; p = 0.11). There were no differences in unadjusted secondary post-discharge outcomes; however, G1 outcomes significantly improved after adjustment: aHR 0.83 (0.71-0.96; p = 0.01) for mortality, 0.92 (0.84-0.99; p = 0.04) for readmission, and 0.92 (0.85-0.99; p = 0.04) for the combined endpoint. We found a differentiated effect of hospitalisation (p < 0.05 for interaction; better post-discharge readmission and combined outcomes in G1), and a trend (p = 0.06) to lower mortality in G1 patients with EAA. Additionally, there were some differences between groups in baseline and acute episode characteristics. Conclusion: AHF triggered by infection is not associated with a higher mid-term mortality and has better post-discharge outcomes; however, the first 3 weeks are an extremely vulnerable period. Since hospitalisation could have a role in limiting adverse post-discharge events, and EAA in reducing mortality, these relationships should be prospectively explored in further studies.

Une femme de 64 ans nous a ete adressee pour des investigations diagnostiques approfondies en raison de syncopes repetees. La patiente souffrait depuis deux semaines de quintes de toux d’intensite croissante.

Eine 64-jahrige Frau wurde zur weiteren Diagnostik und Behandlung zugewiesen aufgrund wiederholter Synkopen. Die Patientin berichtete von seit zwei Wochen bestehenden Hustenattacken mit zunehmendem Schweregrad.

Background Accurate volume status evaluation and differentiation of cardiac and non-cardiac components of overhydration (OH) are fundaments of optimal haemodialysis (HD) management. Methods This study, by combining bioimpedance measurements, cardiovascular biomarkers and echocardiography, aimed at dissecting OH into its major functional components, and prospectively tested the association between cardiac and non-cardiac components of OH with mortality. In the first part, we validated soluble CD146 (sCD146) as a non-cardiac biomarker of systemic congestion in a cohort of 30 HD patients. In the second part, we performed a prospective 1-year follow-up study in an independent cohort of 144 HD patients. Results sCD146 incrementally increased after the short and long intervals after HD (+53 ng/mL, P = 0.006 and +91 ng/mL, P

Aims Congestion is a central feature of acute heart failure (HF) and its assessment is important for clinical decisions (e.g. tailoring decongestive treatments). It remains uncertain whether patients with acute HF with preserved ejection fraction (HFpEF) are comparably congested as in acute HF with reduced EF (HFrEF). This study assessed congestion, right ventricular (RV) and renal dysfunction in acute HFpEF, HFrEF and non-cardiac dyspnoea. Methods and results We compared echocardiographic and circulating biomarkers of congestion in 146 patients from the MEDIA-DHF study: 101 with acute HF (38 HFpEF, 41 HFrEF, 22 HF with mid-range ejection fraction) and 45 with non-cardiac dyspnoea. Compared with non-cardiac dyspnoea, patients with acute HF had larger left and right atria, higher E/e', pulmonary artery systolic pressure and inferior vena cava (IVC) diameter at rest, and lower IVC variability (all P 0.05) compared with HFrEF. Conclusion In acute conditions, HFpEF and HFrEF presented in a comparable state of venous congestion, with similarly altered RV and kidney function, despite higher BNP in HFrEF.

Aims Heart failure oral therapies (HFOTs), including beta-blockers (BB), renin–angiotensin system inhibitors (RASi) and mineralocorticoid receptor antagonists, administered before hospital discharge after acute heart failure (AHF) might improve outcome. However, concerns have been raised because early administration of HFOTs may worsen patient's condition. We hypothesized that HFOTs at hospital discharge might be associated with better post-discharge survival. Methods and results The study population was composed of 19 980 AHF patients from the GREAT registry. The primary and secondary outcomes were 90-day and 1-year all-cause mortality, respectively. Survival was estimated with univariate and covariate-adjusted Cox proportional hazards regression models for the whole population and after propensity-score matching. HFOTs at discharge were consistently associated with no excess mortality in the unadjusted and adjusted analyses of the whole and matched cohorts. In the matched cohort, BB and RASi at discharge were associated with lower 90-day mortality risks compared to the respective untreated groups [hazard ratio (HR) 0.56, 95% confidence interval (CI) 0.46–0.69; and HR 0.53, 95% CI 0.42–0.66, respectively]. The favourable associations of BB and RASi at discharge with 90-day mortality were present in many subgroups including patients with reduced or preserved left ventricular ejection fraction and persisted up to 1 year after discharge. The combination of RASi and BB was associated with an even lower risk of death than RASi or BB alone. Conclusions Administration of HFOTs at hospital discharge is associated with better survival of AHF patients.