What's New in Heart Failure? October 2025

The October 2025 issue of the European Journal of Heart Failure (EJHF) is rich and diverse (Figure 1). It points to progress on three fronts: (i) definitions and risk, (ii) monitoring and devices, and (iii) cellular mechanisms. First, the field continues to redefine conceptual frameworks and risk factors for heart failure (HF). A landmark EJHF expert consensus document introduces structured definitions for HF improvement, remission, and recovery, emphasizing their prognostic and therapeutic implications.1 Additionally, a large UK Biobank analysis shows a J-shaped relationship between alcohol consumption and incident HF, with beer intake in women emerging as a novel risk signal2; an accompanying editorial underscores the absence of a universally ‘safe’ threshold of alcohol consumption and the importance of clinical context.3 Second, innovation in devices and monitoring continues to reshape HF practice. A nationwide French telemonitoring programme showed that remote monitoring of HF symptoms and body weight was associated with reduced mortality and healthcare utilization.4 Furthermore, a Swedish HF registry-based analysis suggests that cardiac resynchronization therapy (CRT) may facilitate initiation and up-titration of HF guideline-directed medical therapy (GDMT).5 Early-phase device studies, such as the cardio-microcurrent therapy trial, suggest that non-traditional bioelectrical interventions may improve function and quality of life in non-ischaemic chronic HF with reduced ejection fraction (HFrEF).6 Finally, the translational frontier is represented by scientific statements on immunometabolic crosstalk7 and mitochondrial targets,8 underlining the importance of systemic and cellular pathways in driving HF progression or recovery. A central element of this issue is the EJHF expert consensus document on HF improvement, remission, and recovery.1 It emphasizes that HF is a dynamic syndrome rather than a static condition, with trajectories that can diverge despite similar baseline characteristics. The emergence of HF with improved ejection fraction (HFimpEF) as a diagnostic entity has underscored this complexity, yet definitions remain inconsistent and largely based on left ventricular ejection fraction (LVEF) values. The consensus panel therefore proposes a taxonomy that distinguishes between improvement, remission, and recovery. Improvement denotes partial amelioration of cardiac structure or function, which may be transient. Remission indicates sustained clinical stability, supported by biomarkers and imaging, but with persistent vulnerability to relapse. Recovery, by contrast, is a rare state of durable normalization of structure and function, sometimes indistinguishable from healthy myocardium. The authors emphasize that remission is far more common than true recovery. Registry and trial data indicate that many patients who achieve an LVEF >50% on GDMT or CRT eventually relapse, with recurrent dysfunction documented in ~44% at 6 months in TRED-HF,9 and with adverse remodelling observed in ~7.5% over 24 months and therapy re-initiation required in ~21% in STOP-CRT.10 Additionally, more than one third of patients with HFimpEF experience LVEF decline during follow-up.11-14 Accordingly, the consensus document strongly discourages down-titration or withdrawal of GDMT, a message consistent with large registry analyses reporting that treatment withdrawal was independently associated with a higher risk of cardiovascular mortality and hospitalization.15 The paper also highlights critical knowledge gaps: the safety of treatment de-escalation, the contribution of genetic predisposition to relapse,16-18 and the need for integrated monitoring that goes beyond LVEF. The authors propose combining natriuretic peptides, imaging of ventricular remodelling and functional testing as a more robust approach to risk stratification, echoing the prognostic value of strain and atrial reverse remodelling.19-21 Finally, the authors call for prospective trials that stratify patients by trajectory to tailor follow-up timing and the therapeutic intensity to disease course. Taken together, this framework clarifies why patients labeled as ‘recovered’ should, in most cases, remain on lifelong GDMT, and why nuanced phenotyping is needed if the goal is to move from remission toward true recovery. Another major highlight is the large UK Biobank analysis of alcohol consumption and incident HF.2 Among >400 000 participants without baseline HF, a clear J-shaped relationship was observed after a median follow-up of 12 years. Low-to-moderate intake was associated with a lower risk of new-onset HF, with the nadir at approximately 14 units/week in men and 7 units/week in women, translating into an estimated 20% relative risk reduction versus non-drinkers. In contrast, heavy drinking conferred no protection, and beer consumption was associated with higher HF risk in women, with up to a 29% increase at intermediate doses. These findings reinforce that alcohol is not a neutral exposure in HF prevention. While modest wine intake aligned with lower risk, spirits showed neutral or adverse profiles, and beer clearly emerged as harmful for women. Sex-specific biological differences in alcohol metabolism may partly amplify these effects. Despite robust statistical adjustment, residual confounding remains possible, and the absence of a randomized trial design limits causal inference. Still, this study, together with prior cohorts and meta-analyses,22-24 provides the most comprehensive evidence to date that the alcohol–HF relationship is dose- and sex-specific. The accompanying editorial further situates these findings within the broader literature and stresses the complexity of the alcohol–HF relationship.3 Although the J-shaped curve observed in the UK Biobank is consistent with earlier cohorts,22, 24 the authors caution against overinterpreting apparent benefits of moderate drinking. Bias from misclassification of former drinkers as abstainers and residual confounding may partly account for apparently protective associations.25 Moreover, evidence on alcoholic cardiomyopathy underscores that even moderate but sustained consumption can induce myocardial dysfunction in susceptible individuals.26 The editorial argues for prudence: while low levels of alcohol may not carry major harm, the safest preventive message in HF remains to limit intake, particularly beer in women, and to recognize that any potential protective effects may be outweighed by risks for atrial fibrillation, hypertension, and liver disease. Taken together, the original report and the editorial underscore alcohol as a modifiable but double-edged risk factor in HF, warranting cautious counselling rather than permissive thresholds. This issue underscores three key studies which illustrate how innovation in monitoring and devices is reshaping HF management. The nationwide French TELESAT-HF programme evaluated over 18 000 patients using the French National Healthcare Data System database, comparing a remote monitoring programme (RMP; Satelia® Cardio) with standard of care over a median follow-up of 912 days.4 The algorithm adjusted monitoring frequency according to changes in weight and symptoms and incorporated both digital and nurse-assisted interfaces. After weighting, 5357 RMP patients were compared with 13 525 controls. RMP was associated with a 36% lower risk of all-cause mortality (hazard ratio [HR] 0.64, 95% confidence interval [CI] 0.59–0.70; p < 0.001), with consistent benefit across comorbidity and hospitalization subgroups. HF hospitalization rates were neutral (rate ratio [RR] 0.95, 95% CI 0.89–1.02), but time in hospital decreased by 2.1% (p < 0.001) and emergency visits fell by 17% (RR 0.83, 95% CI 0.75–0.92; p = 0.001). These findings suggest that structured telemonitoring can be implemented at scale, lowering mortality and acute-care utilization without increasing admissions.4, 27 Registry-based analyses explored whether CRT could facilitate optimization of GDMT.5 In the Swedish HF Registry, 1543 patients with HFrEF who received CRT were compared with 4537 matched controls. Baseline use of beta-blockers and renin–angiotensin system inhibitors was similar, but over 1.5 years CRT recipients were more likely to achieve improved use or dose of beta-blockers (46% vs. 35%; odds ratio [OR] 1.83, 95% CI 1.58–2.13) and to reduce loop diuretic requirements (30% vs. 24%; OR 1.26, 95% CI 1.07–1.48). In per-protocol analyses, CRT was also associated with greater likelihood of angiotensin receptor–neprilysin inhibitor/angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (OR 1.22, 95% CI 1.04–1.44) and mineralocorticoid receptor antagonist optimization (OR 1.25, 95% CI 1.05–1.50). These results position CRT not only as a haemodynamic intervention but also as a facilitator of full-dose HF GDMT.28 Finally, the cardio-microcurrent open-label randomized trial (C-MIC II) tested bioelectrical modulation through direct myocardial microcurrent delivery.6 The device comprises a subcutaneous generator connected to epicardial leads that continuously emit low-intensity currents to counteract pathological electrical fields linked to myocardial oedema and contractile dysfunction. In 65 ambulatory patients with non-ischaemic dilated cardiomyopathy, LVEF 25–35%, and New York Heart Association (NYHA) class III–IV, randomized to C-MIC (device group) or not (control group) on top of GDMT, 6-month outcomes favoured the device: LVEF improved versus control (mean difference +5.1%, 95% CI 3.1–7.1; p < 0.001). Clinical endpoints also favoured the device: 68.9% of patients improved by at least one NYHA class (p < 0.001), 60.0% achieved ≥5-point gains in Kansas City Cardiomyopathy Questionnaire overall summary score (p < 0.001), and 38.3% had a ≥30% increase in 6-min walk distance (p = 0.002). These findings provide proof-of-concept that targeted microcurrent therapy can favourably modulate ventricular function, symptoms, and quality of life in advanced HFrEF. This issue also advances our mechanistic understanding of HF progression through two complementary scientific statements. The first, from the Heart Failure Association of the European Society of Cardiology (ESC), reviews the bidirectional crosstalk between immune activation and myocardial metabolism.7 Chronic low-grade inflammation alters substrate utilization, impairs mitochondrial function, and promotes adverse remodelling,29 while metabolic inflexibility, in turn, amplifies immune responses, a theme grounded in contemporary immunometabolism and cardiac energetics literature.30, 31 These interactions are particularly relevant in HF with preserved ejection fraction, where comorbidity-driven systemic inflammation may drive both microvascular dysfunction and energetic failure. The statement highlights key biomarkers and emerging therapeutic targets, ranging from anti-inflammatory strategies to modulators of fatty acid and glucose oxidation. The second statement, from the ESC Working Group on Cellular Biology of the Heart and the ESC Working Group on Myocardial Function, focuses on mitochondrial biology as a therapeutic frontier in ischaemic heart disease and HF.8 Beyond their role as cellular powerhouses, mitochondria regulate cell death, redox balance, and innate immunity. The document reviews translational hurdles that have so far limited the clinical development of mitochondrial therapies, including drug delivery, off-target toxicity, and absence of standardized biomarkers. Nevertheless, advances in mitochondrial modulators, cardiolipin stabilizers, and targeted antioxidants suggest that clinical translation is feasible when paired with precise phenotyping. Taken together, these scientific statements emphasize that HF is not only a disorder of pump mechanics but also one of systemic and cellular homeostasis. By linking immune activation, metabolism, and mitochondrial biology, they outline a roadmap for next-generation therapies aimed at modifying disease at its roots. Conflict of interest: none declared.