European Journal of Heart Failure最新文献

Aims: Dyspnoea accounts for nearly 5% of emergency department (ED) visits. Our aim was to describe the in-hospital and long-term outcomes of patients admitted to the ED for dyspnoea, based on their underlying aetiology, and to determine if prognosis varies according to the hospitalization setting.

Methods: We analyzed 18 903 consecutive patients (48% male, average age 73 years) hospitalized after an ED visit for dyspnoea from January 2010 to December 2019, as part of the PARADISE cohort (PAthwAy of Dyspneic patIent in Emergency-NCT02800122). Dyspnoea causes were classified as acute heart failure (AHF), respiratory infection (RI), chronic obstructive pulmonary disease (COPD), pulmonary embolism (PE), or asthma.

Results: RI (30%), AHF (28%), and COPD (13%) were the predominant discharge diagnoses. In-hospital mortality stood at 12% overall, ranging from 1.1% in asthma to 15% in AHF and RI. Five-year all-cause mortality for patients discharged alive was 75% in AHF, 66% in RI, 62% in COPD, 37% in PE, and 26% in asthma. Hospitalization in specialized wards was associated with significantly reduced in-hospital mortality across all aetiologies, and with a decreased long-term mortality for RI and AHF (adjusted-HR 0.90, 95% CI 0.82-0.99, P = 0.02 for RI and adjusted-HR 0.90, 95% CI 0.82-0.99, P = 0.03 for AHF).

Conclusion: Patients hospitalized for dyspnoea face a high-risk of mortality both in-hospital and post-discharge. In view of the strikingly high mortality in dyspneic patients and the potential benefits of specialized management, our study calls for rapidly setting up personalized in-hospital and post-discharge dyspnoea pathways.

Aims: Peripartum cardiomyopathy (PPCM) is characterized by left-ventricular systolic dysfunction. Plasminogen-activator-inhibitor 1 (PAI-1) and 16K-prolactin (PRL) are known drivers of PPCM. Treatment of cardiogenic shock (CS) complicating PPCM is challenging. The calcium sensitizer levosimendan (LS) is considered as a beneficial therapy in CS. There are only sparse data regarding the safety and efficacy of LS-treatment in PPCM. We aimed to investigate the molecular effects and safety of LS-treatment in the PPCM mouse model (cardiomyocyte-specific-knockout of signal-transducer-and-activator-of-transcription 3 (STAT3), CKO) and in patients from the German PPCM registry.

Methods and results: In the PPCM mouse model, LS-treatment aggravated postpartum heart failure associated with fibrosis, reduced capillary density, and enhanced mortality, whereas LS-treatment together with the PRL-inhibitor bromocriptine (BR) preserved cardiac function. In CKO hearts, LS induced PAI-1 expression via the upregulation of thrombospondin-1/-4, transforming-growth-factor-β, and activation of SMAD2 that could be prevented by combination with BR. In the German PPCM registry, 17 PPCM patients with CS were treated with LS and BR. Despite the severity of CS, all these patients survived the acute phase, and most patients showed cardiac recovery in the ensuing course of the disease (left ventricular ejection fraction at 3-month follow-up: 40 ± 19%).

Conclusion: Thus, the combination therapy with LS and BR seems to be a safe and potentially beneficial therapeutic concept for the treatment of PPCM patients with CS. As experimental PPCM mouse data suggest that treatment of PPCM patients in CS with LS alone may worsen cardiac function by enhancing the PRL/PAI-1-dependent pathomechanism, treatment of LS in PPCM patients should always be accompanied by BR treatment.

Aims: Reductions in NT-proBNP during hospitalization for acute heart failure (AHF) are linked with improved outcomes. Whether this association holds along the entire spectrum of left ventricular ejection fraction (LVEF), particularly in patients with supranormal LVEF (≥65%), remains unclear. We aimed to evaluate whether the prognostic significance of early NT-proBNP changes varies across LVEF categories.

Methods and results: We included 3276 consecutive patients hospitalized for AHF across three tertiary centres. NT-proBNP was measured at admission and within 48-72 hours. The relative change (ΔNT-proBNP) was calculated, and patients were stratified into four LVEF categories: ≤40%, 41-49%, 50-64%, and ≥65%. Primary outcomes were all-cause mortality, cardiovascular death, and recurrent HF hospitalizations, analyzed using multivariable Cox and negative binomial models. The proportion of patients with LVEF ≤40%, 41%-49%, 50%-64%, and ≥65% was 36.3%, 13.3%, 31.5%, and 19.9%, respectively. Median ΔNT-proBNP was 8.8% (-38.7 to 22.9), and 32.3% of patients exhibited a decline of ≥30%. Over a median follow-up of 1.65 years (0.40-2.66), 1420 deaths (43.4%) and 1979 HF-readmissions occurred in 1045 patients. After multivariate analyses, a significant interaction was found between ΔNT-proBNP and LVEF category for all outcomes (P for interaction <.05). Greater NT-proBNP reduction was independently associated with lower risk of all outcomes, but this association weakened at higher LVEF categories and was no longer evident in patients with LVEF ≥65%.

Conclusions: Early NT-proBNP reduction is a robust prognostic marker in AHF with LVEF up to 64%. Its utility is limited in patients with supranormal LVEF.

Heart failure (HF) remains a major global health challenge, characterized by high morbidity, mortality, and healthcare costs despite substantial advances in pharmacological, device-based, and structural therapies. Its increasing prevalence reflects population ageing, improved survival after myocardial infarction, and the rising burden of cardiometabolic disease, while growing clinical heterogeneity across the ejection fraction spectrum demands more precise diagnostic and therapeutic strategies. This state-of-the-art review summarizes contemporary HF evidence published in the European Journal of Heart Failure and ESC Heart Failure Journal, integrating recent advances in epidemiology, aetiology, diagnostics, and treatment. Emerging data underscore the role of multi-parametric biomarkers, advanced imaging, and artificial intelligence-based tools in enabling earlier diagnosis, refined risk stratification, and personalized management. Aetiology-specific insights-including hypertensive and ischaemic heart disease, cardiomyopathies, amyloidosis, and pregnancy-related HF-are reshaping clinical pathways and therapeutic decision-making. Major developments in guideline-directed medical therapy are reviewed, including early and intensive initiation strategies, expanding evidence for sodium-glucose cotransporter 2 inhibitors and mineralocorticoid receptor antagonists across the spectrum of ejection fraction, and persistent gaps between trial evidence and real-world implementation. Advances in decongestion, cardio-renal interactions, structural valve interventions, and device-based monitoring further illustrate the evolving complexity of HF care. Despite an expanding therapeutic armamentarium, delayed diagnosis, underuse of evidence-based therapies, and organizational barriers continue to limit clinical impact. Bridging this implementation gap through earlier prevention, precision phenotyping, and integrated multidisciplinary care is essential to improving outcomes for HF patients.