When the Goal of Heart Failure Care Shifts

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2026 ESC Guidelines — From Advanced Heart Failure to End-of-Life Care

In Munich, at the 2026 Congress of the European Society of Cardiology, the session dedicated to the new heart failure guidelines took place in one of the venue’s largest lecture halls.

I arrived nearly half an hour before the session was scheduled to begin, yet there was hardly a single vacant seat left in a hall built for roughly a thousand attendees. People lined the walls, and some sat directly on the floor. It is rare to witness such attendance at a cardiology congress. I positioned myself along the wall as well, mindful not to get in anyone’s way.

The presentation commenced with the revised heart failure classification, modern guideline-directed medical therapy, decompensation, implantable cardiac devices, and heart transplantation. The speaker then transitioned to the central topic: advanced heart failure.

At that moment, my focus sharpened considerably. A close relative of mine experienced this very reality: severe heart failure, recurrent clinical deteriorations, and the progressively agonizing choice between the anticipated benefits of therapy and the mounting burden of its intolerance.

Right around then, an excerpt from the Patriarch’s Dormition sermon appeared on my phone screen. Reflecting on death and the final chapter of life, he remarked: “Often, someone who is already departing this world is unnecessarily burdened with various medical interventions; sometimes this happens… Passing away is merely a transition to a better realm, into eternity.”

Just moments earlier, the slides on screen had illustrated the capabilities of modern medicine: which drug to add next, when to initiate inotropes, when to deploy mechanical circulatory support, or when to proceed with heart transplantation. Yet now, an entirely different question emerged: Can a moment come when one additional intervention no longer yields genuine benefit for the patient?

In the hall, the presentation continued to examine advanced heart failure, mechanical circulatory support, and transplantation. Naturally, an existential question surfaced—one that clinicians in everyday practice do not always formulate so directly: When do we maintain life-prolonging treatment at full intensity, and when does the moment arrive when the primary goal of care must change?

The New Framework for Heart Failure

The 2026 ESC Guidelines introduce fundamental revisions to the classification of heart failure. Previously, patients were stratified into three principal categories based on ejection fraction. The updated guideline no longer maintains the intermediate category—heart failure with mildly reduced ejection fraction (HFmrEF)—as an independent grouping.

Two primary phenotypes are now defined:

  • Heart Failure with Reduced Ejection Fraction (HFrEF) — Left ventricular ejection fraction (LVEF) below 50%;

  • Heart Failure with Preserved Ejection Fraction (HFpEF) — LVEF 50% or greater.

In addition, a staged classification framework was introduced, ranging from Stage A (patients solely at risk of developing heart failure) to Stage D (corresponding to advanced heart failure).

This structural shift is consequential because it departs from viewing heart failure merely through the lens of a single cross-sectional ejection fraction measurement. Heart failure is an evolving clinical continuum spanning from early prevention to a stage demanding consideration of cardiac transplantation, mechanical circulatory support, or palliative care.

What Defines Advanced Heart Failure?

Advanced heart failure is not simply synonymous with a severely depressed ejection fraction. It describes a clinical syndrome in which, despite optimal guideline-directed medical, device, and surgical therapy, severe persistent symptoms, pronounced functional limitations, and marked cardiac dysfunction persist.

Clinically, the coexistence of several hallmark features warrants rigorous attention:

  • Severe and persistent symptoms of heart failure (typically NYHA Functional Class III–IV);

  • Severe cardiac dysfunction (advanced left- or right-sided ventricular failure, severe diastolic dysfunction, inoperable severe valvular disease, or congenital abnormalities);

  • Recurrent hospitalizations or unscheduled emergency presentations over the preceding 12 months triggered by congestion, low cardiac output, or malignant arrhythmias;

  • Pronounced functional impairment, demonstrated by very short distances on the 6-minute walk test or markedly depressed peak oxygen consumption (

    $$\text{VO}_2$$

    ).

A severely depressed ejection fraction is not an absolute prerequisite. Advanced heart failure can develop in the context of preserved ejection fraction, isolated right ventricular failure, or uncorrectable structural and congenital lesions.

The prognosis remains grave. In the HELP-HF registry, patients meeting the full diagnostic criteria for advanced heart failure demonstrated a 1-year mortality of 46.5%. Recognizing such individuals promptly is therefore not an academic exercise—it serves as a definitive clinical trigger to evaluate eligibility for heart transplantation, mechanical circulatory support, and specialized therapies without delay.

Crucially: an LVEF of 15% or 20% does not inherently indicate that therapeutic options have been exhausted.

Foundational Therapy — What Should Be Maintained?

The 2026 ESC Guidelines formalize a refined therapeutic nomenclature:

  • Foundational medical therapy comprises pharmacological classes with robust, unequivocal clinical trial evidence reducing mortality and hospital admissions across broad patient cohorts.

  • Phenotype-specific / supplementary therapies are selected based on precise clinical presentations, specific symptoms, or comorbidities.

  • Guideline-directed interventional and device therapies constitute a dedicated category encompassing implantable hardware and procedural solutions.

In heart failure with reduced ejection fraction, foundational therapy centers on four core pillars:

  1. Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors (e.g., dapagliflozin, empagliflozin);

  2. Mineralocorticoid Receptor Antagonists (MRAs) (e.g., spironolactone, eplerenone);

  3. Beta-blockers;

  4. Renin-Angiotensin System Inhibitors — ACE inhibitors, ARBs, or angiotensin receptor-neprilysin inhibitors (ARNI, such as sacubitril/valsartan).

When systemic congestion, pulmonary edema, or peripheral swelling occurs, loop diuretics serve as essential symptomatic therapy. In selected patient phenotypes, additional agents—such as ivabradine, vericiguat, or cardiac glycosides (digoxin, digitoxin)—may be indicated (the clinical value of digoxin and digitoxin has been reinforced in the 2026 guidelines based on contemporary evidence).

However, in advanced heart failure, a pivotal paradigm shift occurs compared with stable ambulatory care: reaching target guideline doses is no longer an end in itself. The clinical objective shifts toward maximizing therapeutic benefit using the exact dosages the patient can realistically tolerate.

When Should Heart Failure Medications Be Deprescribed or Down-Titrated?

As the underlying pathology advances, patients frequently experience systemic hypotension, low cardiac output, renal and hepatic hypoperfusion, electrolyte disturbances, and medication intolerance.

At this crossroad, medications should never be discontinued simply in response to an isolated numeric vital sign. Systemic hypotension does not automatically mandate the immediate withdrawal of life-prolonging pharmacotherapy. The guiding diagnostic question must always be: Does the patient exhibit true clinical hypoperfusion?

If blood pressure reads low yet extremities remain warm, urine output is preserved, mentation is clear, and renal panels remain stable, numeric hypotension alone does not warrant terminating prognostic medical regimens.

The scenario changes drastically when systemic hypoperfusion manifests:

  • Depressed cardiac output;

  • Cool, clammy extremities;

  • Oliguria;

  • Rapid deterioration of renal indices driven by poor organ perfusion;

  • Altered cognitive status / confusion;

  • Severe symptomatic hypotension;

  • Laboratory or clinical markers of hepatic and end-organ malperfusion.

Under these hemodynamically compromised conditions, medications that otherwise extend survival in compensated states can exacerbate circulatory collapse.

Beta-blockers require particular nuance. An LVEF of 15% in isolation is never a reason to halt beta-blocker therapy. However, LVEF 15% + low cardiac output + manifest end-organ hypoperfusion represents a clear rationale for deliberate dose reduction or temporary suspension. The 2026 ESC discussions highlight precisely these compromised phenotypes as candidates for tapering or withholding beta-blockers or ivabradine to preserve essential heart rate and cardiac output.

Equally important, mild fluctuations in renal parameters should not trigger premature abandonment of disease-modifying agents. In a heavily congested patient receiving intensive diuresis, a modest rise in serum creatinine is often acceptable as long as effective clinical decongestion is being achieved.

Low Cardiac Output — When Are Inotropes Indicated?

When advanced heart failure is complicated by persistent low output states, refractory hypoperfusion, or progressive organ dysfunction, continuous intravenous inotropic therapy may become necessary.

Agents such as dobutamine or milrinone are commonly employed; the specific agent is chosen based on systemic vascular resistance, arrhythmias, renal clearance, and comprehensive hemodynamic profiling.

Continuous or intermittent inotropic infusions can serve distinct clinical functions:

  • Bridge to decision;

  • Bridge to cardiac transplantation;

  • Bridge to long-term durable mechanical circulatory support;

  • Temporary stabilization to restore end-organ perfusion and determine whether candidate-qualifying therapies remain feasible.

The 2026 ESC recommendations integrate inotropes into the active pathway for managing refractory hypoperfusion and low cardiac output in advanced disease.

Nevertheless, inotropes carry substantial arrhythmogenic potential and increase myocardial oxygen demand. Their clinical intent, target dosage, and temporal duration must be pre-specified.

When durable mechanical circulatory support or cardiac transplantation is contraindicated or impossible, inotropes may occasionally find utility in a palliative setting—not to alter the underlying trajectory of disease, but to alleviate debilitating dyspnea, nausea, and cognitive fatigue caused by severe low-output states. Thus, the exact same infusion can represent a high-tech bridge to life-saving intervention in one patient, and comfort-focused symptom relief in another.

Congestion and Diuretic Resistance

One of the most vexing challenges in advanced heart failure is refractory volume overload: severe dyspnea, orthopnea, pulmonary vascular congestion, ascites, worsening cardio-renal syndrome, and diuretic resistance.

In these circumstances, the therapeutic target of loop diuretics extends far beyond simply reducing scale weight. The target is true, meaningful decongestion—lowering elevated pulmonary capillary wedge and central venous filling pressures.

Loop diuretic dosing must be dynamically titrated to volume status, renal filtration capacity, and natriuretic response. If responsiveness wanes, sequential nephron blockade using combinations of diuretic classes should be deployed to circumvent compensatory sodium reabsorption. When medical decongestion fails, ultrafiltration or renal replacement therapy may be evaluated in selected cases.

Even as end-of-life approaches, diuretics rarely lose their relevance; their importance frequently magnifies, providing direct, non-invasive relief from suffocating dyspnea and severe peripheral edema.

Advanced Heart Failure Does Not Mean the End of Life

Once Stage D heart failure is recognized, the clinician’s immediate priority must be: Is this patient a candidate for heart transplantation or durable mechanical circulatory support (MCS)? This evaluation must occur proactively, before irreversible, multi-organ failure supervenes.

In appropriately selected candidates, a left ventricular assist device (LVAD) can be utilized as:

  • Bridge to transplantation;

  • Bridge to candidacy (allowing secondary organ dysfunction or pulmonary hypertension to reverse);

  • Bridge to recovery (in rare myocardial insults);

  • Destination therapy (durable, permanent long-term circulatory support).

The 2026 ESC Guidelines consolidate and reinforce the indications for long-term durable mechanical support. In patients experiencing refractory deterioration despite optimal medical and device therapy, cardiac transplantation remains the definitive life-prolonging standard where no major contraindications exist.

Therefore, confronting a severely ill patient should never prompt an automatic assumption that they have reached the terminal end of life. An inotrope-dependent patient with an ejection fraction of 15% to 20% may be standing precisely at the therapeutic juncture where surgical advanced heart failure therapies can radically restore longevity and functional capacity.

When Does Palliative Care Begin?

Palliative care must not be conflated with comfort care delivered only during the final terminal hours. Its core components should be integrated upstream, running in parallel with aggressive, life-prolonging disease management.

Palliative interventions focus on:

  • Rigorous relief of intractable dyspnea and pain;

  • Proactive management of psychological distress, anxiety, and depression;

  • Comprehensive psychosocial support for patients and their caregivers;

  • Structured Advance Care Planning (ACP);

  • Establishing clear agreements on resuscitation parameters (DNR/DNAR orders);

  • Eliciting patient preferences regarding care settings and end-of-life location;

  • Deprescribing therapies and avoiding invasive procedures that have ceased to offer clinical utility and solely impart physical or emotional burden.

Central to the 2026 ESC palliative guidance are symptom control, health-related quality of life, patient autonomy, and proactive care planning.

When advanced surgical therapies (transplantation or LVAD) are unfeasible, clinically contraindicated, or declined by an informed patient, the primary focus of care pivots from life prolongation at all costs toward the preservation of comfort, dignity, and quality of life. This transition becomes paramount when clinical prognosis is governed not solely by cardiac reserve, but by catastrophic comorbidities—such as advanced malignancy, irreversible multi-organ failure, or end-stage neurodegenerative disease.

When Should Treatment Be Discontinued?

This represents arguably the most demanding question in clinical practice, requiring the highest degree of clinical judgment.

The ESC does not define an arbitrary threshold value at which clinicians are told to “stop treating heart failure.” There is no cut-off value based solely on:

  • LVEF 15%;

  • LVEF 10%;

  • Astronomical natriuretic peptide levels;

  • NYHA Class III–IV status;

  • Progressive azotemia;

  • Advanced chronological age.

The appropriate clinical question is entirely different: Which therapies continue to offer this specific human being tangible benefit, and which interventions now impose greater harm, suffering, or burden than value?

Here, clinical medicine must clearly delineate between two goals of care:

  1. Prognostic / Disease-Modifying Therapy:

    Its primary objective is the mitigation of future hospitalizations and premature mortality. These therapies should be sustained as long as the patient tolerates them and a realistic potential for therapeutic return persists. However, when profound hypotension, end-organ ischemia, hyperkalemia, or overt physiological intolerance arise, downward titration or outright discontinuation becomes a clinical necessity rather than a failure of care.

  2. Symptom-Targeted Palliative Therapy:

    These interventions frequently remain vital until the final moments of life. Diuretics are continued specifically to alleviate respiratory distress and peripheral swelling. Supplemental oxygen is administered when true hypoxemia causes suffering. Low-dose inotropes are occasionally continued to combat severe organ hypoperfusion and nausea. The systematic management of dyspnea, pain, terminal agitation, insomnia, and existential distress becomes the central therapeutic mandate.

Thus, at the end of life, treatment is never abandoned—the goal of treatment changes.

What Happens to Implantable Defibrillators at the End of Life?

This issue demands explicit, early clinical anticipation. A patient may be actively dying from end-stage pump failure, yet an active implantable cardioverter-defibrillator (ICD) can continue to interpret agonal ventricular arrhythmias and deliver repeated, excruciating high-energy shocks.

Comprehensive Advance Care Planning must directly address the management of cardiac implantable electronic devices alongside resuscitation status.

Deactivating the anti-tachycardia shock therapies of an ICD during terminal care does not induce cardiac arrest and does not cause death. Its sole objective is to protect the patient from painful, traumatic electric discharges when those shocks can no longer alter prognosis and run counter to established comfort-focused goals.

This discussion must be conducted proactively—in a calm, deliberate manner with the patient and family—long before acute peri-arrest decompensation occurs.

Can a Left Ventricular Assist Device (LVAD) Be Withdrawn?

An even more complex ethical and clinical landscape surrounds the elective deactivation of durable mechanical circulatory support.

Circumstances may arise where a device-dependent patient develops devastating secondary complications (such as catastrophic stroke or metastatic malignancy), experiences intolerable quality of life, or explicitly communicates a desire to withdraw life-sustaining technological support.

Such a determination transcends mere technical mechanics. It mandates an exhaustive assessment of decision-making capacity, multidisciplinary ethics consultation, palliative medicine integration, transparent family involvement, and rigorous adherence to local legal and professional frameworks. The presence of an active mechanical pump does not extinguish a patient’s ethical and legal right to participate in defining the boundaries of their medical care.

Where Is the Line Drawn?

In that Munich lecture hall, this question stood out above all others.

Contemporary medicine possesses remarkable tools: quadruple medical therapy, cardiac resynchronization, defibrillators, inotropic infusions, temporary and durable mechanical circulatory support, left ventricular assist devices, and orthotopic heart transplantation. Medicine’s technical capacity is expanding relentlessly—to introduce another drug, to attempt another intervention, to pursue another increment of survival. Yet prior to every intervention, the clinician must answer: What does this truly offer this individual patient?

In advanced heart failure, the initial priority remains the exhaustive utilization of all viable life-prolonging options. Patients warrant early referral to dedicated advanced heart failure centers to evaluate their candidacy for transplantation, mechanical support, or advanced interventions.

Yet when those possibilities have been exhausted, are contraindicated, or are declined by an informed patient, the clinical mission evolves. The clinician is confronted with the question: How long can we prolong life? To which an equally profound question must be paired: How will the patient live the time that remains?

Ultimately, managing advanced heart failure requires knowing when to deprescribe interventions that no longer serve the patient, while preserving and reinforcing everything that provides meaningful longevity, symptomatic relief, and dignified comfort.

This is not giving up on care.

This is aligning care with what truly matters.

Written by Dr. David Malidze, Cardiologist, on social media.

Primary Sources:

  • Køber L, Adamo M, et al. 2026 ESC Guidelines for the management of heart failure. European Heart Journal. 2026. doi:10.1093/eurheartj/ehag100.

  • Pagnesi M, et al. Prognostic impact of the updated HFA-ESC definition of advanced heart failure: results from the HELP-HF registry. European Journal of Heart Failure. 2022;24:1493-1503.

  • Heart Failure Association of the European Society of Cardiology. Identifying and overcoming barriers to referral in advanced heart failure. Clinical consensus statement.

  • European Society of Cardiology. 2026 ESC Guidelines for the management of heart failure — official guideline resources and congress presentation.

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