Heart failure (HF) is a significant clinical burden contributing to many deaths and hospitalisations worldwide, and congestion lies at its core, both as the chief culprit of acute decompensation events and a key therapeutic target.1,2 In this Cardiac Failure Review special collection, four complementary, state-of-the-art papers explore congestion from unique perspectives: pathophysiology, biomarkers, device-based strategies and the challenge of residual congestion.
This editorial synthesises insights gained from these papers and places them in the context of contemporary clinical practice, including the latest European Society of Cardiology (ESC) guidelines on HF and the ESC’s 2023 focused update, as well as recent trial findings.3,4 The central message we hope to convey is that congestion is not merely a phenomenon of excess water in a patient with HF, but instead is a complex, multifaceted process that requires nuanced assessment and a multimodal diagnostic and therapeutic approach.5
Pathophysiology and Phenotypes of Congestion in HF
Traditionally, clinicians have perceived congestion in HF as simple fluid overload. In their review, Kumric et al. challenge this oversimplification, providing mechanistic insights into how acute HF decompensation can arise from internal volume redistribution without a net gain in total body water.6 They differentiate two overlapping congestion phenotypes: intravascular congestion (elevated cardiac filling pressures due to central shifting of venous blood) versus extravascular congestion (excess fluid sequestered in interstitial tissues). In clinical practice, these phenotypes often coexist, and patients may transition between them during the clinical course.
Distinguishing between these two types of congestion is important because each may require different therapeutic strategies. For example, sympathetic activation and venous constriction can acutely redistribute venous blood and raise filling pressures (intravascular congestion) even if weight gain is minimal. Conversely, sodium retention by the kidneys and fluid accumulation over weeks lead to expanded interstitial volume (extravascular congestion) with clinical manifestations of oedema. Kumric and colleagues emphasise that the severity of congestion is not linearly related to left ventricular systolic function. Notably, some patients with only mild cardiac dysfunction are profoundly congested, while others with significantly reduced left ventricular ejection fraction (LVEF) and frank HF, such as those with heart failure with reduced ejection fraction (HFrEF), may remain euvolaemic. This discordance between the degree of congestion and left ventricular function teaches us to assess congestion directly rather than infer it from LVEF or the degree of structural disease on echocardiography.
Another key insight is the inherent limitation of established signs and symptoms in quantifying the degree of congestion. Physical findings (such as pitting oedema or pulmonary crackles) and patient-reported symptoms of dyspnoea have limited sensitivity and specificity for haemodynamically significant congestion. Orthopnoea and elevated jugular venous pressure primarily reflect high intracardiac pressures, whereas peripheral oedema and pleural effusions reflect interstitial volume. However, patients may have one without the other. For these reasons, additional tools are needed to characterise congestion phenotypes, including laboratory biomarkers and cardiac imaging. Natriuretic peptides (brain natriuretic peptide [BNP] and/or NT-proBNP) increase with rising intravascular volume and pressure load and remain the cornerstone biochemical markers of congestion. In contrast, biomarkers such as carbohydrate antigen 125 (CA125) correlate with serosal fluid accumulation and thus mirror extravascular tissue congestion. A tailored, holistic approach to congestion that integrates clinical examination findings with laboratory biomarkers and cardiac imaging provides a window of opportunity to capture both fluid redistribution and fluid retention dynamics among patients presenting with HF-related congestion.
Biomarkers for Congestion: Not All Congestion is Created Equal
Building on the proposition that congestion is a heterogeneous entity, Parlati et al. provide an in-depth review of biomarkers as pragmatic, everyday tools to detect and manage congestion in HF.7 They reinforce that natriuretic peptides remain the most widely used and validated markers in both acute and chronic HF, aiding in diagnosis, risk stratification and treatment guidance. Biological increases in BNP/NT-proBNP concentrations reflect high intracardiac pressures and intravascular volume, while decreasing levels of these peptides due to HF-directed treatment are associated with clinical improvement. However, the authors cautiously state that no single biomarker can capture all layers of congestion. Emerging experimental biomarkers may track different ‘compartments’ of fluid overload. For example, adrenomedullin (ADM), particularly its stable plasma fragment bio-ADM, increases in concentration in response to endothelial stretch and vascular leakage, indicating systemic and tissue congestion and portending a worse prognosis. This has potential therapeutic implications: the monoclonal antibody adrecizumab is being tested to bind ADM and shift fluid from tissues back into the vascular compartment, potentially improving vascular integrity and alleviating oedema. Another emerging biomarker, soluble CD146, is shed by endothelial cells during venous engorgement, and preliminary studies suggest that it correlates strongly with congestion burden.
The take-home messages from the biomarker review are optimistic, but cautious. The authors convey that many of these biomarkers (ADM, CA125, CD146 and others such as soluble ST2, galectin-3, FGF-23, endothelin-1) expand our toolkit to pinpoint and profile congestion more precisely than symptoms alone. When combined with robustly established markers such as natriuretic peptides, a proposed ‘multi-marker’ strategy may provide a more comprehensive assessment of congestion, helping to distinguish, for example, acute haemodynamic stress from chronic peripheral fluid accumulation.
It needs to be emphasised that many novel biomarkers remain experimental and are currently of limited value in contemporary clinical practice. We need further validation of the independent prognostic value of these biomarkers and must determine whether they offer any meaningful incremental value beyond the gold standard – natriuretic peptides. Equally, we need evidence that acting on their levels improves patient outcomes. At present, natriuretic peptides remain the workhorse indicators of congestion (and the 2023 ESC guidelines recommend measuring BNP/NT-proBNP at admission and again at discharge as a surrogate of congestion status).4 Other measures, such as haemoconcentration, increased CA125 or ADM levels, or persistently low serum sodium, may identify high-risk patients with residual congestion at discharge, but their routine use is not yet endorsed by practice guidelines. As research efforts intensify, a composite congestion score integrating biomarkers with clinical and cardiac imaging data could enable timely, targeted intervention before overt fluid overload develops.
Device-based Monitoring and Guideline-Directed Medical Therapy
Pharmacological advances in HF have transformed outcomes over the past few decades, however, their uptake in practice remains suboptimal. Laborante et al. examine congestion through the lens of therapeutic inertia and technology, arguing for a paradigm shift in how we prevent and manage fluid accumulation.8
A central theme is that guideline-directed medical therapy (GDMT) modifies the course of HF. The combination of β-blockers, renin–angiotensin system inhibitors, angiotensin receptor-neprilysin inhibitors (ARNI), mineralocorticoid receptor antagonists (MRAs) and SGLT2 inhibitors not only improves survival, but also has intrinsic decongestant effects. Traditionally, diuretics have been the cornerstone drugs for congestion relief and symptom improvement in HF. However, emerging evidence summarised by Laborante et al. offers a provocative premise: early and aggressive implementation of GDMT can mitigate congestion by modulating the neurohormonal drivers of sodium and water retention. For instance, SGLT2 inhibitors promote osmotic diuresis and natriuresis, and studies using implantable monitors have demonstrated a rapid decrease in pulmonary artery pressures (PAP) soon after treatment initiation, reflecting relief of intravascular congestion. ARNI therapy has likewise been associated with reduced left ventricular filling pressures, offering the possibility of down-titrating loop diuretics over time.
These observations fit well within a contemporary HF treatment framework: rather than reflexively escalating diuretics for weight gain or oedema accumulation, clinicians should prioritise up-titrating the ‘fantastic four’ of HF pharmacological armamentarium (as tolerated), which address the root causes of fluid retention and maladaptive volume distribution. The STRONG-HF trial recently showed that an early post-discharge protocol of rapid GDMT up-titration resulted in faster resolution of clinical congestion and fewer HF rehospitalisations, and that this was achieved with lower total diuretic doses than standard care.9
Of note, diuretics remain indispensable for acute decompensation events. On the other hand, simply piling on more diuretics yields diminishing returns. Two recent randomised trials, ADVOR (acetazolamide added to loop diuretics) and CLOROTIC (high-dose thiazide added), produced only modest additional symptom relief and/or higher diuresis but no improvement in clinical outcomes among patients with acute HF.10,11 These findings generally tone down the enthusiasm for escalating diuretic combinations and have influenced guidelines to avoid routine add-on diuretics for all-comer patients with acute HF.4
Instead, the focus is shifting towards smarter congestion management: remote monitoring and early intervention based on haemodynamic trends and measurements. Implantable devices, such as the CardioMEMS PAP sensor, have shown that increases in filling pressures occur in an occult mode of action and precede overt clinical decompensation by days to even weeks. This knowledge can help clinicians to adjust and escalate decongestive therapies in a timely fashion before symptoms become clinically apparent. Earlier trials demonstrated reduced HF hospitalisations with PAP-guided therapy, leading the ESC guidelines to cautiously endorse implantable pressure monitoring in advanced HF (class IIb).3,4 However, some trials, such as GUIDE-HF, did not clearly improve outcomes across a broad spectrum of HF populations, suggesting that technology is only as good as the clinical strategy around it – patient selection and timely therapeutic responses remain critical.12 Finally, the authors propose that non-invasive options such as wearable thoracic impedance devices, lung ultrasound (LUS) to detect B-lines and connected weight/BP solutions are promising, but larger trials are required to demonstrate their clinical usefulness and impact on patient outcomes. Laborante et al. envision an integrated future in which digital health solutions support clinical decision-making, enabling rapid up-titration of GDMT and patient self-management to keep congestion under control. Embracing such a paradigm could mitigate therapeutic inertia and reduce preventable decompensation events in this vulnerable patient population.
Tackling Residual Congestion and Improving Outcomes in Acute HF
Despite IV diuretic use and apparent haemodynamic stabilisation, a substantial proportion of patients leave hospital with residual congestion – a condition characterised by persistent elevated filling pressures and tissue fluid retention despite the impression that patients are clinically ‘dry’. Siniarski and Gąsecka spotlight this phenomenon, noting that a vast majority of acute HF admissions are precipitated by congestion and that a staggering proportion – up to 40% of patients who seem euvolaemic on clinical examination – still have occult pulmonary congestion detectable by ultrasound at discharge.¹³ These patients experience a poorer prognosis in the weeks following discharge.
Consequently, early post-discharge HF readmissions remain common (with a steady rate of around 30% at 3 months), and residual congestion is the dominant driver of these events. Every unplanned HF readmission carries a steep prognostic price by significantly increasing the risk of short-term mortality. The authors underscore an important message: achieving complete decongestion before hospital discharge and maintaining it thereafter is critical to breaking this vicious cycle.
What practical steps can we undertake in everyday HF practice? First, we should systematically assess for residual congestion prior to discharge. This can be achieved using a checklist encompassing clinical signs, orthopnoea, jugular venous distension, daily weight measurements and, where available, point-of-care tools such as lung ultrasound or circulating natriuretic peptide testing. The latest 2023 update of the ESC HF guidelines explicitly states that patients should be congestion-free prior to discharge, and pre-discharge measurement of NT-proBNP is recommended as an objective marker reflecting haemodynamic stabilisation.4
Secondly, early post-discharge follow-up is essential. As laid out in the STRONG-HF paradigm, we should see patients within 6 weeks of discharge at the latest, monitor their symptoms, renal function and weight, adjust diuretics and rapidly titrate GDMT, aiming to initiate all four pillars of therapy prior to discharge whenever possible.9
Furthermore, device-based therapies and advanced interventions should be considered in patients with persistent congestion despite optimal medical therapy in guideline-recommended doses. The overarching principle should be clear: do not let the patient leave hospital ‘wet’, and if they do, ensure there is a clear plan to achieve euvolaemia promptly.
Conclusion
Congestion in HF is an age-old clinical problem, but it also represents the frontier of modern HF care. Collectively, these papers illustrate how our understanding and management of HF congestion are evolving. We should recognise congestion as a dynamic continuum with a direct impact on outcomes at every stage of HF. For practitioners, adopting this comprehensive approach – from meticulous volume assessment and biomarker use to early guideline-directed therapy, monitoring and follow-up – will help translate the latest evidence into better patient outcomes.