Patients' quality of life is a key consideration of chronic kidney disease care. Nonetheless, qualitative research on patients' experience, quality of life, and frequent associated comorbidities remains limited. This study identifies aspects of the disease experience, healthcare journey, and caregiver experience contributing to quality of life for early-stage (stage 3 CKD) and advanced chronic kidney disease (stages 4-5) patients and their caregivers. In this cross-sectional, observational, multicenter study based on qualitative methodology, participants completed a general (Short Form-36) and disease-specific (Kidney Disease Quality of Life Short Form-36) quality of life assessment and semi-structured interviews. Quota and convenience sampling were used to enroll 36 patients selected by clinicians based on chronic kidney disease stage and the presence of key comorbidities (heart failure, hyperkalemia). Twelve caregivers were also invited to participate in patient interviews. All data were examined thematically. Three themes emerged: (1) Impact of chronic kidney disease on quality of life throughout the patient journey (physical, social, and emotional); (2) attitudes toward the disease (characterized by 'acceptance' or 'powerlessness'); and (3) caregivers' role and burden. Patients' characteristics and caregiver support must be considered for designing medical interventions and improvement of patient-doctor communication. Family caregivers are pillars clinicians should rely on to raise awareness about chronic kidney disease's relevance among patients and families.

Introduction and objectives: Dapagliflozin improves clinical outcomes in patients with chronic heart failure (HF), irrespective of left ventricular ejection fraction. However, its effects on circulating biomarkers that reflect distinct pathophysiological pathways remain incompletely understood.Methods: DAPA-MODA is a prospective, multicenter, single-arm study that enrolled patients with stable chronic HF receiving optimized guideline-directed medical therapy, excluding sodium-glucose cotransporter-2 inhibitors. In a predefined biomarker substudy (n = 156; 63.5% men; age 70.5 ± 10.6 years; 67.9% with left ventricular ejection fraction > 40%), 11 biomarkers representing 5 key biological pathways (cardiac stress, inflammation, neurohormonal activation, congestion, and fibrosis) were measured at baseline, 1 month, and 6 months.Results: At baseline, markers of myocardial stress were frequently elevated (NT-proBNP [95.5%] and MR-proANP [34.8%]), as was troponin for myocardial injury (73.5%). Inflammatory (IL-6 [40%], CRP [35%], GDF-15 [56%]) and neuro-endocrine stress (copeptin [43%]) markers were also commonly raised. In contrast, elevations in congestion (MR-proADM, CA-125) and fibrosis markers (ST2, PINP) were less frequent, reflecting diverse pathophysiological involvement. Dapagliflozin led to significant reductions in NT-proBNP and MR-proADM levels by 6 months. Reductions in MR-proANP, CRP, IL-6, copeptin, and PINP were confined to patients with elevated baseline levels. ST2 and CA-125 remained unchanged, while GDF-15 levels increased modestly.Conclusions: Dapagliflozin favorably modulates several key pathophysiological pathways involved in chronic HF progression, with differential effects among biomarkers by acting particularly on those that are elevated at baseline.

BACKGROUND AND AIMS:Urinary sodium (uNa+) is a promising tool to guide diuretic therapy in acute heart failure (AHF), yet its real-world adoption is uncertain. We aimed to evaluate current practices, perceived utility, and barriers to uNa⁺-guided management among physicians managing AHF in Spain. METHODS:We conducted a nationwide cross-sectional electronic survey in June 2025 of clinicians from cardiology, internal medicine, emergency medicine, and nephrology. The questionnaire assessed the frequency and timing of uNa+ monitoring in inpatient and outpatient settings, thresholds for poor response, therapeutic adjustments, and perceived benefits and barriers. RESULTS:A total of 413 physicians responded: 138 (33%) from cardiology, 159 (39%) from internal medicine, 78 (19%) from emergency medicine, and 38 (9%) from nephrology. Overall, 70% reported measuring uNa+ during AHF hospitalization, but only 18% did so routinely. Outpatient application remained infrequent (32%). Nephrologists showed the highest usage in both inpatient (90%) and outpatient (61%) settings. The most frequent cut-off to define diuretic resistance was <50 mmol/l. Therapeutic strategies differed by specialty: loop diuretic escalation was more frequent in cardiology and emergency medicine, while thiazides were preferred in internal medicine and nephrology. Most participants (78%) considered uNa⁺ monitoring clinically useful. Major barriers included lack of standardized protocols, limited training, therapeutic inertia, and logistical constraints. CONCLUSIONS:While uNa⁺ monitoring is valued by clinicians, its use in AHF in Spain remains inconsistent across specialties. Addressing implementation barriers through education, protocols, and decision-support tools is critical to a broader adoption of uNa⁺ guided therapy in routine care.

AIMS:Congestion is a major cause of hospitalisation in patients with heart failure (HF), and the persistence of congestive signs at discharge is a robust predictor of early readmission. Currently, there is increasing interest in the comprehensive assessment of subclinical congestion, as it can increase residual risk in individuals who appear to be euvolemic. Our aim was to investigate the prevalence and prognostic impact of subclinical venous congestion assessed by ultrasound. METHODS AND RESULTS:This is a two-centre, prospective observational study. Patients admitted for HF between June 2021 and March 2023 were selected. Clinical [physical examination (PE)] and subclinical venous congestion [Venous Excess Ultrasound score (VExUS)] were assessed. The prognostic impact was assessed through a composite endpoint of death from any cause, HF readmissions, or unscheduled visits requiring intravenous diuretic administration at 6-month follow-up. 120 patients were included (62% male, mean age 75 ± 15 years). Congestion parameters decreased during hospitalisation but tended to worsen at the first outpatient visit. At discharge, 24% showed subclinical venous congestion. This group had a significantly higher incidence of adverse outcomes, comparable to those with overt clinical congestion. Subclinical congestion was an independent predictor of the composite endpoint (HR 2.84; 95% CI: 1.01-8.01, P value = 0.048) after adjustment for age, chronic kidney disease, NYHA class at admission, and NT-proBNP level at discharge. CONCLUSION:Clinical and subclinical congestion decreased during hospitalisation but worsened shortly after discharge. A quarter of patients had residual venous congestion, which was associated with a worse prognosis at 6 months.

Heart failure with ejection fraction ≥40% is associated with high mortality and risk of decompensation, as well as poorer quality of life. SGLT2 inhibitors are currently considered the standard therapy for these patients. However, despite treatment with these drugs, patients continue to have a high risk of adverse events. Overactivation of the mineralocorticoid receptor promotes the release of inflammatory and profibrotic factors, which contribute to the development and progression of this entity. However, not all mineralocorticoid receptor antagonists have demonstrated clinical benefit in these patients. The FINEARTS-HF study demonstrated that finerenone, a nonsteroidal mineralocorticoid receptor antagonist, significantly reduces the risk of cardiovascular death or heart failure decompensation, with consistent results across all patient subgroups analyzed. Consequently, in the treatment of these patients the combination of SGLT2 inhibitors and finerenone should be considered.

Background/Objectives: Congestion is a hallmark of heart failure (HF) and a major determinant of outcomes. Non-invasive tools enable detection of subclinical congestion, but their correlation and prognostic relevance remain incompletely defined. The present study aimed to assess the prevalence, evolution, interrelationships, and prognostic impact of clinical and subclinical congestion markers in patients hospitalized for HF. Methods: This single-centre, prospective cohort study included adults admitted with HF who underwent serial evaluations at admission, 72 h, pre-discharge, early outpatient follow-up and at 6 months. Clinical congestion was assessed using a standardized physical examination score. Subclinical congestion was evaluated using lung ultrasound (LUS), Venous Excess Ultrasound Score (VExUS), and Remote Dielectric Sensing (ReDS). Patients were classified according to the presence of clinical and/or subclinical congestion at discharge. The primary endpoint was a composite of all-cause mortality, HF readmission, or unscheduled visits requiring intravenous diuretics within six months. Results: Ninety-four patients (mean age 74 ± 11 years, 68% male) were included. While clinical congestion improved significantly during hospitalization, approximately 30% of patients remained clinically congested at discharge. Among clinically euvolemic patients, only 47% showed no evidence of subclinical congestion. Correlations between congestion markers were weak to moderate, suggesting complementary pathophysiological information. At discharge, pulmonary B-lines were the strongest predictor of the composite endpoint (hazard ratio [HR] 3.50, 95% CI 1.41-8.72), followed by clinical congestion (HR 2.67, 95% CI 1.13-6.30). Patients with clinical and subclinical congestion exhibited lower event-free survival. Conclusions: Subclinical congestion is common despite apparent clinical euvolemia and is associated with worse outcomes. Integrating clinical assessment with non-invasive congestion markers may improve post-discharge risk stratification in HF.

Managing cardiorenal syndrome in acute decompensated heart failure remains a major challenge in contemporary cardiology. While pharmacological decongestion with diuretics is the cornerstone of therapy and is effective in most patients, worsening renal function and diuretic resistance continue to pose challenges in selected cases. Device-based therapies are increasingly explored to target key pathophysiological mechanisms underlying cardiorenal dysfunction. This expert review builds on a conceptual framework for device-based therapies. Rather than cataloguing individual technologies, we apply a functional framework that classifies devices according to their primary mode of action: reduction of venous or lymphatic congestion ('pullers'), augmentation of arterial perfusion ('pushers'), and direct removal of sodium and/or fluid ('removers'). For each category, we integrate pathophysiological rationale with available clinical evidence, highlighting the predominance of early-phase physiological evidence and the need for randomized studies demonstrating benefit beyond optimized contemporary medical care.

Introducción y objetivos Los incrementos de creatinina durante el tratamiento de la insuficiencia cardiaca aguda pueden aparecer junto con hemoconcentración y descongestión, pero los rangos de creatinina asociados con menor riesgo, seguridad o daño no están bien definidos.Métodos Se estudiaron 2.043 ingresos consecutivos por insuficiencia cardiaca aguda entre 2014 y 2021. Las exposiciones principales fueron el incremento máximo intrahospitalario de creatinina (ΔCr) y el cambio de hemoglobina (ΔHb). Los modelos incluyeron splines cúbicos restringidos para ΔCr, ΔHb continua y su interacción. La mortalidad y los episodios compuestos se analizaron con modelos de Cox; la primera rehospitalización por cualquier causa y por insuficiencia cardiaca, con modelos de Fine-Gray. El contraste principal de ΔHb fue el contraste basado en el rango intercuartílico observado (+1,3 g/dl), no un punto de corte de subgrupo.Resultados La mediana de edad fue de 77 años [69-83] y el 57,6% de los ingresos correspondieron a varones. En contexto de hemoconcentración, se identificaron rangos de ΔCr asociados con menor riesgo para mortalidad (0,10-0,18 mg/dl), primera rehospitalización por cualquier causa (0,06-0,25 mg/dl), primera rehospitalización por insuficiencia cardiaca (0,00-0,32 mg/dl) y muerte o primera rehospitalización por cualquier causa (0,10-0,23 mg/dl). Los umbrales de daño aparecieron por encima de 0,61, 0,98 y 0,91 mg/dl respectivamente; no se identificó umbral de daño para rehospitalización por insuficiencia cardiaca.Conclusiones Entre los ingresos por insuficiencia cardiaca aguda con hemoconcentración, pequeños incrementos de creatinina se asociaron con menor riesgo, mientras que incrementos mayores se relacionaron con pérdida de beneficio y, para algunos episodios, daño. Estos hallazgos apoyan una interpretación continua y dependiente del contexto del empeoramiento de la función renal durante la descongestión.

Background:Infective endocarditis (IE) carries a significant risk of recurrence. European clinical guidelines recommend performing follow-up blood cultures (BCs), although evidence regarding their utility is limited. We aimed to assess the yield of follow-up BCs in these patients. Methods:Single-center post hoc analysis of a prospective cohort including IE survivors diagnosed between 2012 and 2023 with at least 12 months of follow-up. Results:Among 225 patients included, follow-up BCs were performed in 153 (68.0%). Recurrence was diagnosed in 19 patients (8.4%). Patients with recurrence had higher mortality during follow-up (15.8% vs 4.4%, P = .025).Among patients with follow-up BCs, there was 1 contaminant (0.7%) and 2 true-positive results (1.3%), both of them representing IE reinfections due to different microorganisms. One of them had fever at BC extraction. The 1-year recurrence rate and IE-associated mortality (including complications or recurrences) were similar in patients with and without BCs (7.8% vs 9.7%, P = .789 and 1.4% vs 0.7%, P = .538, respectively).In the index IE episode, patients with recurrence more frequently presented with previous IE (21.1% vs 5.3%, P = .035), fungal etiology (10.5% vs 1.5%, P = .010), and mycotic aneurysms (15.8% vs 1.0%, P = .004), while they had a lower frequency of native-valve (31.6% vs 54.6%, P = .049) and Staphylococcus aureus (5.3% vs 23.2%, P = .012) endocarditis. Conclusions:Follow-up BC after an IE episode appears to have low utility, with similar rates of true positives and contaminants. Patients with follow-up BCs did not have more recurrences diagnosed or lower mortality during follow-up.

BACKGROUND:Chronic obstructive pulmonary disease (COPD) is a frequent comorbidity in chronic heart failure (CHF) and is associated with greater symptom burden and worse prognosis. Carbohydrate antigen 125 (CA125) has emerged as a biomarker of congestion and mesothelial/inflammatory activation in heart failure; however, its relationship with COPD in ambulatory CHF populations has not been systematically evaluated. We aimed to (1) determine the prevalence of COPD in a CHF outpatient cohort, (2) compare CA125 levels according to COPD status, and (3) evaluate whether COPD independently predicts CA125 levels. METHODS:COPA-HF was a multicenter prospective observational study conducted in five outpatient HF units in Madrid, Spain (May-June 2025). Consecutive adults with HF were enrolled during routine follow-up visits after providing written informed consent. COPD was defined by spirometry according to GOLD criteria in patients with tobacco exposure or respiratory symptoms, using a post-bronchodilator. CA125 and NT-proBNP were measured at inclusion. Multivariable linear regression was used to identify variables independently associated with CA125. RESULTS:A total of 171 patients were included. Median age was 87.4 years (IQR 82.9-90.9), 55.6% were women, and HFpEF predominated (83%). COPD was present in 61 patients (35.7%). Compared to non-COPD patients, those with COPD were younger, predominantly male, more symptomatic (NYHA class III: 32.8% vs 13.6%; p = 0.011), and showed higher pulmonary artery systolic pressure (40 vs 30 mmHg; p = 0.010) and more frequent B-lines on lung ultrasound. CA125 levels were higher in patients with COPD (23.0 vs 18.0 U/mL; p = 0.034), whereas NT-proBNP did not differ between groups. On multivariable analysis, COPD (β = 16.38; 95% CI 3.59-29.17; p = 0.013) and pleural effusion (β = 20.42; 95% CI 0.58-40.26; p = 0.044) were independently associated with higher CA125. CONCLUSIONS:COPD was highly prevalent in this cohort of ambulatory HF patients and was independently associated with elevated CA125 levels, together with pleural effusion. COPD should therefore be considered when interpreting CA125 during outpatient heart failure follow-up.

Introduction and objectives: Creatinine increases during acute heart failure treatment may occur in the setting of hemoconcentration and decongestion, but the ranges of creatinine increase associated with lower risk, safety, or harm remain poorly defined.Methods: We studied 2043 consecutive hospitalizations for acute heart failure between 2014 and 2021. The main exposures were the maximum in-hospital increase in creatinine (ΔCr) and hemoglobin change (ΔHb). Models used restricted cubic splines for ΔCr, continuous ΔHb, and their interaction. Mortality and composite endpoints were analyzed with Cox models; first all-cause and heart failure rehospitalization were analyzed using Fine-Gray models. The primary ΔHb contrast was the observed interquartile range reporting contrast (+1.3 g/dL), rather than a subgroup cutoff.Results: The median age was 77 [69-83] years and 57.6% of hospitalizations involved male patients. In the context of hemoconcentration, ΔCr ranges associated with lower risk were identified for mortality (0.10-0.18 mg/dL), first all-cause rehospitalization (0.06-0.25 mg/dL), first heart failure rehospitalization (0.00-0.32 mg/dL), and the composite of death or first all-cause rehospitalization (0.10-0.23 mg/dL). Harm thresholds were observed above 0.61, 0.98, and 0.91 mg/dL, respectively; no harm threshold was identified for heart failure rehospitalization.Conclusions: Among patients hospitalized with acute heart failure who achieved hemoconcentration, small creatinine increases were associated with lower risk, whereas larger increases were associated with a loss of benefit and, for some endpoints, harm. These findings support a continuous, context-dependent interpretation of worsening renal function during decongestive therapy.

Introduction and objectives: Kidney dysfunction is common in chronic heart failure (CHF), but its prognostic significance in contemporary populations remains uncertain. We evaluated 1-year outcomes according to kidney function stage and the prognostic role of the estimated glomerular filtration rate (eGFR).Methods: We analyzed 1105 patients with CHF enrolled in the CARDIOREN Registry (13 centers, 2021-2022). Kidney function was categorized according to CKD-EPI eGFR (≥ 60, 30-59, < 30 mL/min/1.73 m²). The primary endpoint was the composite of all-cause death or worsening heart failure at 1 year; all-cause mortality was analyzed separately. Associations were assessed using multivariable Cox regression models with fractional polynomial modeling.Results: Median age was 75 years, 63% of patients were men, and 38% had heart failure with preserved ejection fraction. Overall, 59% had eGFR < 60 mL/min/1.73 m². At 1 year, the composite endpoint occurred in 24% of patients, and all-cause mortality occurred in 13%. Event rates increased progressively with worsening kidney function categories for the primary endpoint (11%, 31%, and 38%; P < .001) and for all-cause mortality (4%, 16%, and 26%; P < .001). In multivariable analysis, N-terminal pro-B-type natriuretic peptide, hemoglobin, and furosemide-equivalent dose were independently associated with both outcomes. Hemoglobin showed a U-shaped association, with higher risk at both low and high concentrations. CA125 was independently associated with all-cause mortality. eGFR was not independently associated with the composite endpoint but remained independently associated with all-cause mortality, showing a nonlinear inverse relationship.Conclusions: In this contemporary CHF population, worse kidney function identified patients with a more adverse clinical profile and poorer outcomes, although these associations were attenuated after adjustment for congestion markers and disease severity.

Heart failure (HF) is a major cause of hospitalization and mortality. Early initiation of guideline-directed medical therapy (GDMT) improves outcomes in heart failure with reduced ejection fraction (HFrEF). This study assesses the impact of starting GDMT with an SGLT2i in newly diagnosed HFrEF patients. The XXXX1 multicenter prospective registry enrolled consecutive newly diagnosed HFrEF patients between October 2021 and March 2022 to evaluate the influence of medical treatment schedules in newly diagnosed HFrEF. In this substudy, patients were grouped by initial GDMT with or without an SGLT2i. Over six months, clinical variables, echocardiographic and laboratory parameters, and clinical events (hospitalizations, emergency visits) were collected. The primary aim was to compare GDMT implementation (quadruple therapy rates), with secondary aims assessing efficacy (target doses) and safety (adverse events). Of 518 patients, 400 initiated treatment with an SGLT2i, while 118 did not, with no differences in the baseline characteristics. At six months, 81.5

AIMS:Acute decompensated heart failure (ADHF) is often treated with diuretic agents in both the inpatient and ambulatory settings, yet fluid overload frequently persists and is associated with rehospitalization and death. In patients with predominant interstitial fluid expansion but without intravascular overload, increasing the loop diuretic dose or adding a second diuretic may cause intravascular volume depletion, electrolyte disturbance, and worsening renal function without clearing the excess tissue fluid. COMPRESSION-HF tests whether adding lower limb compression to standard diuretic treatment improves early decongestion in patients with ADHF, predominant peripheral oedema, and inferior vena cava (IVC) diameter ≤21 mm. METHODS:COMPRESSION-HF (NCT06418932) is an investigator-initiated, multicentre, randomized, double-blind, sham-controlled trial in which adults with ADHF, bilateral leg oedema (grade II or higher of IV), N-terminal pro-B-type natriuretic peptide (NT-proBNP >1000 pg/ml), and IVC diameter ≤21 mm were assigned 1:1 to active bilateral lower limb compression (two-layer inelastic-elastic bandaging; manufacturer-specified nominal ankle pressure, approximately 20 mm Hg) plus parenteral furosemide or to sham bandaging plus parenteral furosemide, for up to 72 h. The two co-primary endpoints are 24-h urinary sodium excretion and change in body weight from baseline. Secondary endpoints include changes in lower limb circumference, clinical congestion score, and IVC diameter, together with NT-proBNP at 72 h, cumulative 72-h furosemide-equivalent dose, carbohydrate antigen 125 (CA-125) at day 15 ± 3, and 30-day safety. Continuous endpoints will be analysed with mixed-effects analysis of covariance or repeated-measures models including centre as a random intercept. Recruitment is complete (106 patients randomized); the trial was powered to detect a 20 mmol between-group difference in 24-h urinary sodium excretion. CONCLUSIONS:COMPRESSION-HF will show whether adding lower limb compression to standard loop diuretic treatment increases natriuresis and weight loss in patients with ADHF and predominant peripheral oedema, and will describe the relationship between tissue congestion, intravascular refilling, and the diuretic response.

Heart failure (HF) management has evolved substantially over recent decades, transitioning from predominantly symptomatic treatment to a strategy grounded in disease-modifying therapies that improve survival and reduce hospitalizations. This review provides a structured and clinically oriented synthesis of landmark randomized controlled trials (RCTs) that have shaped contemporary guideline-directed medical therapy across the spectrum of left ventricular ejection fraction (LVEF). Evidence from pivotal large-scale RCTs is presented according to pharmacological classes, encompassing both foundational and selected adjunctive therapies. In HF with reduced LVEF, multiple drug classes consistently reduce mortality and HF hospitalizations, forming the basis of contemporary quadruple therapy. In contrast, evidence in HF with mildly reduced or preserved LVEF remains more heterogeneous, with sodium-glucose co-transporter-2 inhibitors emerging as the only class with consistent benefit across the full LVEF spectrum. Additional therapies, including digoxin, vericiguat, intravenous iron, and emerging incretin-based agents, provide incremental benefits in selected clinical contexts. Differences in trial populations, design, and background therapy limit direct comparisons but highlight the progressive refinement of HF treatment strategies. Despite the strength of the evidence base, a persistent gap remains between guideline recommendations and real-world implementation. Bridging this gap, improving representation of under-represented populations in clinical trials, and advancing precision medicine approaches remain key priorities for future research.

The cardiovascular-kidney-metabolic framework recognizes the interconnected biological, clinical, and societal drivers of cardiovascular disease, chronic kidney disease, diabetes, and obesity. To advance an integrated perspective, aligned with the kidney community focus, the International Society of Nephrology convened an International Expert Forum, bringing together a global and multidisciplinary team of leaders in this field. This meeting report synthesizes key discussions spanning cardiovascular-kidney-metabolic risk stratification, lifestyle interventions, guideline-directed medical therapies, emerging late-stage therapeutics, and models of care delivery. Participants emphasized the importance of early, integrated case finding; long-term, joint kidney-cardiovascular risk assessment; and timely use of evidence-informed therapies to reduce kidney disease progression, kidney failure, and cardiovascular events. Persistent gaps, including therapeutic inertia, fragmented care, and global inequities in access to care, were highlighted, alongside promising multidisciplinary and system-level care models. Emerging therapies targeting residual risk further underscore the need for adaptive implementation strategies. Aligned with the International Society of Nephrology's mission, this forum represents a foundational step toward connecting disciplines, bridging evidence-to-practice gaps, and building global capacity to improve equitable cardiovascular-kidney-metabolic outcomes.

Background/Objectives: Congestion is a hallmark of heart failure (HF) and a major determinant of outcomes. Non-invasive tools enable detection of subclinical congestion, but their correlation and prognostic relevance remain incompletely defined. We aimed to assess the prevalence, evolution, interrelationship, and prognostic impact of clinical and subclinical congestion markers in patients hospitalized for HF. Methods: This single-centre, prospective cohort study included adults admitted with HF who underwent serial evaluations at admission, 72 hours, pre-discharge, early outpatient follow-up and at 6-month. Clinical congestion was assessed using a standardized physical examination score. Subclinical congestion was evaluated using lung ultrasound (LUS), Venous Excess Ultrasound Score (VExUS), and Remote Dielectric Sensing (ReDS). Patients were classified according to the presence of clinical and/or subclinical congestion at discharge. The primary endpoint was a composite of all-cause mortality, HF readmission, or unscheduled visits requiring intravenous diuretics within six months of follow-up. Results: Ninety-four patients (mean age 74±11 years, 68% male) were included. While clinical congestion improved significantly during hospitalization, approximately 30% of patients remained clinically congested at discharge. Among clinically euvolemic patients, only 47% showed no evidence of subclinical congestion. Correlations between congestion markers were weak to moderate, suggesting complementary pathophysiological information. At discharge, pulmonary B-lines were the strongest predictor of the composite endpoint (hazard ratio [HR] 3.50, 95% CI 1.41–8.72), followed by clinical congestion (HR 2.67, 95% CI 1.13–6.30). Patients with both clinical and subclinical congestion had the lowest event-free survival, approximately 50% at six months of follow-up (log-rank p = 0.03). Conclusions: Subclinical congestion is common despite apparent clinical euvolemia and is associated with worse outcomes. Integrating clinical assessment with non-invasive congestion markers may improve post-discharge risk stratification and patient management in HF.