Camilla Hage

Background: Effective decongestion is a key therapeutic goal during hospitalisation for acute heart failure (HF), but the clinical significance of intravenous loop diuretic-induced weight loss and its relationship with biomarker changes remain uncertain. Methods: We included patients hospitalised for HF in the nationwide Swedish Heart Failure Registry (2017–2021) who received intravenous loop diuretics, survived to discharge and had body weight recorded at admission and discharge. Weight loss was defined as ≥2 kg between admission and discharge. Associations between weight loss, changes in biomarkers (estimated glomerular filtration rate (eGFR), N-terminal pro-B-type natriuretic peptides (NT-proBNP), haemoglobin, sodium and potassium) and outcomes were evaluated. The primary outcome was rehospitalisation for HF (re-HHF); the secondary outcome was the composite of cardiovascular death or re-HHF at 30 days and 1 year. Results: Among 4979 patients (median age 80 years; 57% male), median weight change during hospitalisation was −2.5 kg and 2949 (59%) achieved weight loss ≥2 kg. Male sex, atrial fibrillation, obesity, higher admission NT-proBNP and mineralocorticoid receptor antagonist use were independently associated with weight loss. Weight change showed no meaningful association with change in eGFR. Weight loss was independently associated with a lower risk of re-HHF (HR 0.59, 95% CI 0.53 to 0.67) and the composite of cardiovascular death or re-HHF (HR 0.76, 95% CI 0.69 to 0.84) within 30 days but not thereafter. These associations were consistent irrespective of biomarker changes, including worsening renal function. Conclusions: In this nationwide cohort of patients hospitalised for HF and treated with intravenous loop diuretics, diuretic-induced weight loss, a pragmatic marker of decongestion, was associated with improved short-term clinical outcomes without an accompanying decline in renal function and irrespective of biomarker changes, including worsening renal function.

This paper discusses the considerations for multidimensional and multidisciplinary management of heart failure (HF) patients with frailty. Frailty is a multidimensional, dynamic and potentially reversible state, defined by clinical, functional, psycho-cognitive and social domains. Frailty is seldom systematically assessed in clinical practice in HF patients. Paradoxically, although the absolute benefit of HF guideline-directed medical treatment in frail HF patients seems greater, it is under-prescribed. This therapeutic gap could be related to different reasons, such as concerns about safety, polypharmacy and the lack of specific evidence-based data. Frail HF patients require a comprehensive, multidimensional therapeutic strategy that integrates available evidence-based pharmacological interventions with targeted non-pharmacological modalities across multiple clinical disciplines to optimise patient outcomes. The four domains of frailty should be objectively and routinely assessed with a multidimensional approach to facilitate a more individualised and comprehensive care plan delivered by a multidisciplinary team. In the future, we need more dedicated studies and randomised clinical trials that include frail HF patients.

Background Constrictive pericarditis (CP) and heart failure with preserved ejection fraction (HFpEF) exhibit overlapping clinical and echocardiographic characteristics, making differentiation challenging. We therefore examined whether serial echocardiographic measurements could aid in distinguishing these conditions. Methods In a single-centre retrospective study, patients with CP were matched 1:2 with patients with HFpEF based on age and sex. Echocardiographic assessments at baseline and at follow-up were analysed for each patient. Differences in longitudinal changes in ventricular and atrial sizes, stroke volume and ejection fraction were compared between study groups using linear mixed-effects model. Results In total, seven CP and 14 HFpEF patients were included. Median time between examinations was 18 months (IQR 3-39) in the CP group and 29 months (IQR 15-44) in the HFpEF group. Compared with HFpEF, CP showed greater reductions in left ventricular end-diastolic diameter (−13.9 mm, 95% CI −22.4 to −5.47), left ventricular end-systolic diameter (−9.7 mm, 95% CI −18.2 to −1.26), right atrial volume index (−10.9 mL/m2, 95% CI −20.4 to −1.36), stroke volume (-18.7 95% CI −27.6 to −9.7), indexed stroke volume (−9.8 mL/m2, 95% CI −18.7 to −0.926) and in ejection fraction (−8.9%, 95% CI −17.3 to −0.40). Conclusion CP was associated with greater longitudinal reductions in left ventricular dimensions and stroke volume compared with HFpEF. These findings suggest that comparing ventricular dimensions and stroke volume with prior echocardiographic assessments, may provide complementary diagnostic information to facilitate earlier differentiation of CP from HFpEF.

Aims: To build a comprehensive biobank integrated in the Swedish Heart Failure Registry (SwedeHF) comprising comprehensive clinomic data, proteomic, transcriptomic and genomic information in combination with clinical and diagnostic characteristics and additional ICD-code registry data. Methods: Blood and urine samples will be biobanked at SwedeHF registration with an optional second sampling after six months in patients with HF attending routine clinical visits at nine hospitals with access to healthcare integrated biobanking. Circulating and urine biomarkers will be investigated by proteomic, metabolomic, transcriptomic profiling, explored with genetic data. Sample size assessments were based on the BIOSTAT-CHF cohort and doubled to fulfil all aims targeting 5000 patients. Results: The first 1348 enrolled patients were median 72 years, 30% females, 65% HFrEF and 11% HFpEF. Median NT-proBNP was 1240 (interquartile range 470 - 2830) pg/ml. This was comparable to the 8506 patients with an index registration in SwedeHF during 2023 with 52% HFrEF and 20% HFpEF, age 75 years, 36% females and NT-proBNP 1560 [629 - 3617] pg/ml. Conclusions: We are building a high-quality detailed biobank linked to SwedeHF, the world’s largest continuous HF registry, consisting of plasma, serum, whole blood and urine samples. The Biobank will enable studies exploring underlying disease mechanisms in HF and response to HF treatment, paving the way for precision medicine and novel drug targets. It will also generate a structure for biobanking in Registry-based Randomized Controlled Trials within the national SwedeHF registry.

The role of the nurse in the heart failure (HF) multi-disciplinary team (MDT) has become well-established, with clear evidence of improved patient outcomes and recommended by professional guidelines. Recognizing the change in the HF landscape since the publication of the first Heart Failure Association (HFA) of the European Society of Cardiology (ESC) HF nurse curriculum in 2016, and the expanding role of HF nurses of in the HF MDT, the HFA in collaboration with the Association of Cardiovascular Nursing and Allied Professions (ACNAP) of the ESC prioritized this update to the curriculum. Standardized training programmes for HF nurses improve the quality of care provided to patients with HF and their caregivers. Recognizing the variability of education background and clinical autonomy across Europe and beyond, this curriculum is designed in a flexible way to be able to be adapted and adjusted based on individual country regulations and forms. Endorsement of this curriculum from national professional bodies or Nursing Councils would ensure uniformity and enhance the profession's contribution to HF care. The updated specialist HF nurse curriculum provides the basis for the advanced level of knowledge, skills and attitudes required for the appropriate expansion of the role of the HF nurse that can be adapted across Europe and beyond, while complying with professional legislation of different healthcare systems and supporting nurses who move between countries.

Acyl ghrelin increases cardiac output (CO) and contractility in patients with heart failure with reduced ejection fraction (HFrEF). In healthy humans, acyl ghrelin increases gastric emptying rate (GER) and hunger, a potential add-on benefit for HFrEF patients suffering from cachexia with symptoms of delayed gastric emptying and loss of appetite. The aim of this study was to determine if post-prandial acyl ghrelin infusion increases GER and hunger in HFrEF patients compared to CO. HFrEF patients ( n = 29) arrived fasted and received a 500-kcal breakfast followed by 1.5 g paracetamol. They next received placebo (vehicle, n = 15) or acyl ghrelin infusion (0.1 µg/kg/min, n = 14) for 120 min. Blood was tapped for plasma at 0, 30, 60, 120, and 150 min into the meal. Hunger scores and CO were recorded. Plasma paracetamol was measured to assess GER. Paracetamol concentration peaked at 30 min in 8 of 14 (57%) in the treatment group versus 1 of 15 (7%) in the placebo group (Mann–Whitney test, P = 0.004). Remaining patients peaked at later time points. The acyl ghrelin treatment group data was segregated into rapid (peak at 30 min, n = 8) and slow (peak > 30 min, n = 6) GER sub-groups. The rapid sub-group had an acyl ghrelin treatment effect on CO (one-way repeat measures, P < 0.001) and the highest median increase in hunger across all time points. Acyl ghrelin increases GER and in tandem with increasing CO. Effects on hunger are more difficult to resolve due to variability in subjective scores. Some HFrEF patients may benefit from this add-on effect.

Introduction: Heart failure (HF) with preserved (HFpEF) and reduced (HFrEF) ejection fraction may be driven by different pathophysiologies. We explored novel biomarkers, associations with clinical characteristics, discrimination between LVEF categories and associations with outcomes. Methods and results: In HFpEF(n = 76) and HFrEF(n = 36), 19 plasma biomarkers were measured including seven novel research assays for ANGPT2, BMP10, DKK3, FABP3, FGF23, IGFBP7, and MYBPC3. Heart failure with preserved ejection fraction patients were older (73 vs 63 years), more often female (50% vs 14%). All seven novel biomarkers except FABP3 tended to be higher in HFrEF vs HFpEF and associated with worse NYHA class and lower eGFR in both LVEF categories. MYBPC3 and FGF23 (higher in HFrEF) discriminated best between LVEF categories (AUC 85.8 and 80.0 respectively). In HFpEF, higher ANGPT2 was associated with worse right (TAPSE: β = −1.03;P = .04) and left ventricular function (LV-GLS; β = 1.29;P = .03) and left atrial strain (LA-GLS: β = 5.03;P < .001) whereas higher IGFBP7 and MYBPC3 with diastolic dysfunction (E/eʹ: β = 4.09;P = .02 and β = 1.36;P = .01 respectively). All biomarkers except DKK3 were positively associated with the outcome (HFpEF:all-cause death, HF hospitalization;HFrEF: all-cause death, LVAD or heart transplantation). Specifically ANGPT2 [HR 1.45(95% CI 1.00–2.13)] more strongly in HFpEF and IGFBP7 [2.51(0.95–6.64)] more strongly in HFrEFand MYBPC3 [1.62(0.99–2.64)]. Conclusion: Among seven novel biomarker assays, higher MYBPC3 (reflecting muscle injury and myopathy) and FGF23 (endothelial dysfunction, oxidative stress) distinguished HFrEF from HFpEF. Higher MYBPC3 was most prognostic in HFrEF while higher ANGPT2 and IGFBP7 (endothelial dysfunction and oxidative stress) in HFpEF. These hypothesis-generating findings support primary cardiomyocyte injury as a driver of HFrEF and systemic inflammation and oxidative stress as a driver of HFpEF. Clinical Trial Registration: ClinicalTrials.gov NCT00774709