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.

BACKGROUND:Sympathetic overactivity is associated with hepatic steatosis. Renal denervation (RDN) is an approved treatment for uncontrolled hypertension through sympathetic modulation; however, its hepatic effects are unknown. This study aimed to assess the effects of RDN on noninvasive tests for hepatic steatosis. METHODS:This single-center study included patients with uncontrolled hypertension and cardiometabolic comorbidities undergoing RDN (n=32) or a sham procedure (n=10). Noninvasive tests for hepatic steatosis, including the hepatic steatosis index (HSI) and fatty liver index (FLI), were calculated at baseline and follow-up visits. An external cohort from the UK Biobank was used to validate the correlation between proton density fat fraction magnetic resonance imaging scans of the liver and these surrogates. RESULTS:Compared with the control group, RDN significantly reduced HSI at 3 months (0.4±0.5 versus -1.3±0.3; P=0.009), 6 months (0.0±0.9 versus -2.6±0.5; P=0.027), and 12 months (0.0±0.6 versus -2.1±0.5; P=0.013), as well as FLI at 3 months (2.6±2.2 versus -3.8±1.2; P=0.021), 6 months (4.1±2.4 versus -5.7±1.2; P=0.002), and 12 months (2.0±2.7 versus -6.2±1.3; P=0.018). No significant differences were found in HSI (-1.9±0.7 versus -2.2±0.7; P=0.77) and FLI (-7.1±1.8 versus -5.3±1.7; P=0.49) between subjects in the intervention group whose office blood pressure decreased above or below the median of 19.5 mm Hg after 12 months. In the UK Biobank, correlation analysis showed a significant relationship between proton density fat fraction magnetic resonance imaging and HSI (r=0.40; P<0.0001) and FLI (r=0.27; P<0.0001). CONCLUSIONS:RDN significantly reduced HSI and FLI in patients with uncontrolled hypertension and cardiometabolic comorbidities, suggesting a potential role of sympathetic modulation in metabolic disorders.

The sympathetic nervous system (SNS) plays a critical role in regulating inflammatory responses after myocardial infarction (MI). We aimed to investigate whether modulation of the SNS through renal denervation (RDN) influences myocardial remodeling following MI. MI in rats was induced 2 days after bilateral RDN or Sham surgery. Cardiac MRI showed that left ventricular ejection fraction was significantly higher in RDN-treated MI rats compared to Sham-treated MI rats. RNA sequencing of left ventricular tissue revealed that RDN suppresses fibrosis and inflammation related pathways at the whole transcriptome level, with clear separation of the experimental groups. These findings were confirmed by histochemical, gene, and protein expression analyses, which found a significantly higher extent of fibrosis and CD206 expression in the MI rats compared to RDN-treated MI rats. To simulate SNS activity, PMA-differentiated THP-1 cells were incubated with the β-adrenoceptor agonist isoprenaline. This resulted in upregulation of profibrotic macrophage gene expression, which was not the case after co-stimulation with a β1-adrenoceptor antagonist. Modulation of the SNS through RDN mitigates left ventricular remodeling post-MI by reducing myocardial fibrosis and scar size. Heightened SNS activity promotes a profibrotic macrophage phenotype. These findings support investigation into the therapeutic potential of RDN for managing MI patients.

In elite athletes, differentiation between physiological and pathological cardiac remodelling can be challenging. Left ventricular (LV) strain has become part of the standard in echocardiography. Data on right ventricular (RV), left atrial (LA) and right atrial (RA) strain are sparse in elite athletes. Transthoracic echocardiography including longitudinal strain analysis of all cardiac chambers was performed using a GE Vivid iq in 112 male elite professional cyclists aged 24–32 years. All athletes were actively participating in top level international races and included race champions and Olympic medallists. The results were compared to published reference values of healthy males of similar age. LV average global longitudinal strain (LV aGLS) was –21.7

Heart failure with reduced ejection fraction (HFrEF) imposes a significant clinical burden on patients and a major economic burden on healthcare systems. In HFrEF, mineralocorticoid receptor antagonists (MRAs) constitute a cornerstone of guideline-directed medical therapy (GDMT) reducing both mortality and hospitalisation. Their use in practice remains suboptimal, largely because of physicians' concerns about adverse events, particularly hyperkalaemia, which may deprive eligible patients of benefit. Only the steroidal MRAs spironolactone and eplerenone are approved for HFrEF, and this consensus document is restricted to these agents. We summarise contemporary evidence across multiple domains related to MRA therapy in HFrEF, including pharmacoepidemiology, the role of biomarkers in predicting outcomes and response to MRA, the pathological role of aldosterone and the pharmacology and clinical efficacy of steroidal MRAs. Practical, evidence-based guidance is provided on the prevention and management of hyperkalaemia, the timing of MRA initiation, and strategies to overcome barriers to MRA use. The positioning of MRAs in current guidelines is outlined to reinforce their central role in HFrEF. The process of consensus finding was started in April 2025 with a core group by online conference. We searched PubMed with the terms "MRA, eplerenone and heart failure with reduced ejection fraction". Articles published in English with no date restriction were considered. The final manuscript passed two rounds of final approval by all authors. As a result, this consensus statement advocates proactive, evidence-based approaches to optimise MRA use to improve outcomes. These recommendations aim to mitigate the persistent underuse of MRAs in clinical practice.

Background Chronic kidney disease (CKD) is an independent cardiovascular risk factor. Patients with CKD develop uremic cardiomyopathy characterized by activation of the sympathetic nervous system, left ventricular hypertrophy, and accumulation of uremic toxins such as indoxyl sulfate (IS). The aim of this study was to assess the effects of renal denervation (RDN) on uremic cardiomyopathy in a rat model of CKD. Methods Sprague–Dawley rats were fed a standard chow (control group, n=6) or a 0.25% adenine‐enriched chow (n=16) for 16 weeks to induce CKD. After 4 weeks, CKD rats with CKD were subjected to bilateral RDN (AD‐RDN, n=8) or to sham operation (AD, n=8). Blood pressure measurements, echocardiography, and cardiac magnetic resonance imaging were deployed during the experiment. Left ventricular hypertrophy was evaluated histologically. IS was measured using ELISA. In H9C2 cardiomyoblasts, the hypertrophic effects of IS were characterized in vitro. Results In AD rats, left ventricular septal wall thickness (2.37±0.036 versus 1.91±0.014 mm in CTRL, P <0.0001), E/A ratio, and cardiomyocyte size were significantly increased. Following RDN, left ventricular wall thickness (P <0.0001 versus AD), E/A ratio (P <0.0001 versus AD), and myocyte hypertrophy were significantly reduced. Plasma IS was increased in AD (0.79±0.07 versus 0.2±0.12 μg/mg in the control group, P=0.0044) and reduced in AD‐RDN (P=0.0073 versus AD). Urinary IS remained unchanged after RDN, whereas hepatic concentration of IS decreased after RDN (P=0.023). Plasma IS correlated with left ventricular hypertrophy (r=0.779, P <0.0001). Stimulation of H9C2 cardiomyoblasts with IS or serum from AD rats showed an increase in cell size (P=0.0015), whereas AD‐RDN serum showed no effect. Conclusions In a rat model of CKD, improved cardiac function following RDN was associated with reduced plasma concentrations of IS. To the present, IS remains a persistent clinical concern in patients with CKD due to its inefficient removal by conventional hemodialysis and its significant role in promoting both kidney and myocardial disease. Thus, RDN may ameliorate uremic cardiomyopathy by reducing IS and potentially represents a treatment option for patients with CKD and cardiovascular disease. Clinical trials are warranted to investigate the effects of RDN on cardiovascular outcomes in patients with CKD.

Microsampling enables decentralized adherence monitoring by capturing defined volumes of capillary blood. We developed, validated, and cross-evaluated a volumetric absorptive microsampling (VAMS) and Capitainer-B workflow for 15 cardiovascular drugs using high-resolution liquid chromatography Orbitrap analysis. Amlodipine, atenolol, atorvastatin, bisoprolol, carvedilol, clopidogrel, diltiazem, lercanidipine, metoprolol, nebivolol, prasugrel, rosuvastatin, salicylic acid, simvastatin hydroxy acid, and verapamil were included. Sampling by VAMS and Capitainer-B should be evaluated and compared. VAMS tips and Capitainer-B disks loaded with 10 μL whole blood were extracted with 200 μL methanol, shaken and centrifuged, evaporated to dryness, reconstituted, and injected for analysis. The method met international validation criteria for most analytes, with quantification and selectivity achieved for all except prasugrel. Capitainer-B generally exhibited higher matrix effects than VAMS, while accuracy and precision were within acceptance limits except for lercanidipine across both devices and for atorvastatin on Capitainer-B. Under long-term storage, VAMS showed >15 % loss for carvedilol, lercanidipine, and simvastatin hydroxy acid after two weeks, whereas Capitainer-B showed no degradation. In a proof-of-concept involving 30 patients, finger-prick concentrations from VAMS and Capitainer-B were interchangeable, supporting the suitability of these adherence workflows but reference ranges for capillary blood remain necessary to enable routine clinical interpretation. In summary, this work established a reliable, LC-Orbitrap-based microsampling platform for monitoring adherence and identified stability issued amongst others that guide future method selection and development.

Atemwegsinfektionen mit Influenza‑, SARS-CoV-2(„severe acute respiratory syndrome coronavirus 2“)- und respiratorischen Synzytialviren (RSV) sowie Pneumokokken, aber auch eine endogene Reaktivierung des Varizella-Zoster-Virus in Form eines Herpes Zoster sind mit unerwünschten kardiovaskulären Ereignissen wie Myokardinfarkt oder Hospitalisierung für Herzinsuffizienz assoziiert. Eine wirksame Prävention dieser Ereignisse ist v. a. für die Influenza- und die Pneumokokkenimpfung gut belegt und kostengünstig. Trotz vorhandener Leitlinienempfehlungen, ältere Patienten und Menschen mit Risikofaktoren zu impfen, sind die Impfraten in diesen Bevölkerungsgruppen nach wie vor niedrig und im internationalen Vergleich unterdurchschnittlich. Dieser Beitrag beschäftigt sich mit der Assoziation von durch Impfungen vermeidbaren Erkrankungen mit kardiovaskulären Komplikationen und den protektiven Wirkungen der entsprechenden Impfungen. Außerdem werden Empfehlungen zur praktischen Vorgehensweise bei der Impfung von Risikopatienten abgegeben.

Respiratory tract infections with influenza, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and respiratory syncytial (RS) viruses and pneumococci as well as endogenous reactivation of varicella zoster viruses presenting as herpes zoster, are associated with adverse cardiovascular outcomes, such as myocardial infarction or hospitalization for heart failure. Effective prevention of these events, particularly through influenza and pneumococcal vaccination, is well established and cost-effective. Despite guideline recommendations to vaccinate older patients and people at risk, vaccination rates in these population groups remain suboptimal and below average in international comparison. This article sheds light on the association of vaccine preventable diseases with cardiovascular complications and demonstrates the protective effect of the respective vaccinations. Additionally, recommendations on the practical approach to vaccinating high-risk patients are given.

Graphical Abstract Figure: Concepts of cardiac aging. Abbreviations: E/e’, transmitral early velocity to early diastolic mitral annular velocity; EF, ejection fraction; LV, left ventricular; LVEDD, left ventricular end-diastolic diameter; M/V left, ventricular mass to volume ratio.

Introduction: N-terminal B-type natriuretic peptide (NT-proBNP) is an established biomarker in pulmonary hypertension (PH). Data are limited for other biomarkers. We assessed several biomarkers for their diagnostic value in the diagnosis of precapillary PH (pPH). Methods: Blood samples were collected from 58 patients with pPH (PAH N=38, Lung Disease N=14, CTEPH N=6) and from 21 healthy individuals. MR-proANP analysis was performed with the automated Kryptor platform, NT-proCNP, DNP, sST2 and sVEGFR-1 via ELISA. The diagnostic value of the individual biomarkers for the diagnosis of PH was investigated using group comparisons and ROC analyses. In addition, the serum levels of the biomarkers were correlated with various haemodynamic parameters. Results: MR-proANP level differed significantly between the group of PH patients and controls (118,9 [55,5-222,4] vs 26,1 [17,5-54,2] p<0,001). sST2 level differed between the PH and controls (510,3 [327,9-845,3] vs 173,1 [92,3-388,7] p<0,001) too. None of the other biomarkers showed relevant differences between the groups. MR-proANP and sST2 also correlated with haemodynamic parameters such as RAP, PAPm, TPG and SvO2. ROC analyses showed that both MR-proANP and sST2 were indicative of the presence of PH AUC 0,885 and 0,778, respectively, p<0,001 each. Conclusions: Of the biomarkers studied, MR-proANP and sST2 in particular were indicators of the presence of PH and disease severity and could therefore be useful for screening and monitoring patients with pPH