Heart Failure: Contemporary Assessment and Management

Illustrative overview using the ESC 2026 classification; treatment eligibility is individualized.

Heart failure is a complex clinical syndrome caused by structural and/or functional cardiac abnormalities that impair the heart’s ability to meet the circulatory needs of the body or do so only at the expense of elevated filling pressures.

Its clinical importance extends well beyond reduced ejection fraction. Heart failure encompasses a broad spectrum of phenotypes, etiologies and disease trajectories and remains associated with recurrent hospitalization, impaired quality of life, progressive functional limitation and substantial cardiovascular mortality.

Contemporary management has therefore shifted toward earlier identification, prevention, accurate phenotyping, rapid implementation of disease-modifying therapy, management of congestion and comorbidities, multidisciplinary care and repeated reassessment.

The 2026 ESC guideline places particular emphasis on prevention and early intervention, while the Second Universal Definition of Heart Failure recognizes HF as a dynamic condition that may progress, stabilize, improve or enter remission.

When to Seek Urgent Help

Severe breathlessness at rest, chest pain, collapse or fainting require emergency assessment. In Qatar, call 999 for a medical emergency. [10]

Increasing breathlessness, swelling or rapid unexpected weight gain should prompt contact with your treating team according to your personal care plan. Do not wait for a routine website enquiry to be answered.

A New 2026 Classification

The 2026 ESC guideline simplifies the traditional ejection-fraction classification.

Heart Failure with Reduced Ejection Fraction — HFrEF

HFrEF is now defined in the ESC framework as:

LVEF <50% together with symptoms and/or signs of heart failure.

This is a major change. The previous category of heart failure with mildly reduced ejection fraction, traditionally covering LVEF 41–49%, has been removed because contemporary evidence suggests substantial overlap in pathophysiology and treatment response with the reduced-EF population.

Heart Failure with Preserved Ejection Fraction — HFpEF

HFpEF is defined as:

LVEF ≥50% with symptoms and/or signs of HF plus objective evidence of structural and/or functional cardiac abnormalities.

The diagnosis therefore requires more than a normal ejection fraction combined with dyspnea. Objective evidence supporting abnormal cardiac structure, filling pressure or function remains essential.

This article uses the 2026 ESC classification. Earlier guidelines and clinical trials may use different LVEF categories. A change in terminology does not make treatment evidence identical across all ejection-fraction ranges. [1]

The 2026 Second Universal Definition takes a complementary approach, emphasizing reduced, preserved and improved EF phenotypes while cautioning against excessive reliance on rigid numerical cutoffs because EF varies with age, sex, imaging methodology and disease trajectory.

Classification and terminology sources: ESC guideline [1]; Second Universal Definition expert consensus, JACC version [2].

Heart Failure Is a Continuum: Stages A to D

The ESC has now adopted the stage-based model:

Stage A — At risk for HF: risk factors are present, but there are no symptoms, signs or established cardiac abnormalities.

Stage B — Pre-HF: structural, functional or biomarker abnormalities are present without current or previous HF symptoms.

Stage C — Symptomatic HF: structural or functional cardiac abnormalities are present with current or previous symptoms and/or signs of HF.

Stage D — Advanced HF: severe disease with persistent symptoms, recurrent decompensation or progressive dysfunction despite optimized therapy.

This framework is important because heart failure prevention begins long before the first hospitalization.

Prevention: Treat the Substrate Before Heart Failure Develops

Prevention of HF begins with aggressive management of cardiovascular risk.

Key targets include:

• hypertension

• diabetes

• obesity

• coronary artery disease

• chronic kidney disease

• atrial fibrillation

• valvular disease

• cardiotoxic cancer therapies

• excessive alcohol exposure

• sleep-disordered breathing

• sedentary lifestyle

• inherited cardiomyopathies

Blood-pressure control, optimal diabetes therapy, smoking avoidance, healthy body weight, exercise, lipid management and identification of structural heart disease can substantially influence the lifetime risk of developing symptomatic HF.

Patients with Stage B or pre-HF represent a particularly important opportunity for intervention before progression to overt disease.

Diagnostic Pathway

Symptoms and signs of HF are often nonspecific.

Typical manifestations include:

• exertional dyspnea

• orthopnea

• paroxysmal nocturnal dyspnea

• fatigue

• reduced exercise tolerance

• peripheral edema

• elevated jugular venous pressure

• pulmonary congestion

• rapid weight gain from fluid retention

The diagnostic process should establish three things:

Is heart failure present?
What phenotype is present?
What caused it?

Natriuretic Peptides

BNP and NT-proBNP remain central to the evaluation of suspected HF.

Low concentrations can make significant HF less likely, whereas elevated values support further cardiac evaluation. Interpretation must remain clinical because values can be affected by age, atrial fibrillation, renal dysfunction and other conditions.

Conversely, obesity can result in lower natriuretic peptide concentrations despite clinically important HF, which is particularly relevant in HFpEF.

The 2026 ESC guideline identifies natriuretic peptides and echocardiography as key diagnostic tools.

Echocardiography

Transthoracic echocardiography is fundamental.

It provides information regarding:

• LVEF

• LV dimensions and remodeling

• diastolic function

• left atrial enlargement

• right ventricular function

• pulmonary pressures

• valvular heart disease

• pericardial disease

• regional wall-motion abnormalities

• potential infiltrative or cardiomyopathic patterns

In HFpEF, echo findings suggesting elevated filling pressure, abnormal relaxation, atrial remodeling or pulmonary hypertension can provide crucial objective evidence.

Search for the Cause

Heart failure should never be regarded as the final etiological diagnosis.

The clinician should actively investigate potentially treatable causes, including:

• ischemic heart disease

• hypertension

• valvular disease

• arrhythmia-mediated cardiomyopathy

• myocarditis

• genetic cardiomyopathy

• cardiac amyloidosis

• iron overload

• toxic cardiomyopathy

• endocrine disease

• peripartum cardiomyopathy

• congenital heart disease

Cardiac magnetic resonance, coronary imaging, genetic evaluation, laboratory testing or nuclear imaging may be required according to the suspected phenotype.

The ESC 2026 guideline specifically emphasizes multimodality assessment to identify treatable etiologies.

Contemporary Heart Failure Therapy

One of the major conceptual changes in the 2026 ESC guideline is the new treatment terminology.

Foundational Medical Therapy — FMT

Treatments with a Class I recommendation for the general HF population and convincing evidence of reducing hospitalization and/or mortality.

Additional Medical Therapy — AMT

Therapies recommended for selected populations, specific phenotypes, symptoms, quality of life or additional outcome reduction.

Guideline-Directed Interventional Therapy — GDIT

Recommended device and procedural therapies, including ICD, CRT and selected structural interventions.

HFrEF: Foundational Medical Therapy

For HFrEF, contemporary foundational therapy consists of four major therapeutic components:

1. ACE inhibitor / ARNI / ARB

ACE inhibitors, ARNI and ARBs represent alternatives within this component, not treatments to be administered simultaneously.

2. Evidence-based beta-blocker

3. Mineralocorticoid receptor antagonist

4. SGLT2 inhibitor

These treatments act through complementary mechanisms and collectively reduce hospitalization, disease progression and mortality.

The 2026 ESC guideline emphasizes that there is no evidence requiring a rigid sequencing strategy. Foundational agents can be introduced rapidly and in parallel, with individualization according to blood pressure, heart rate, renal function, potassium, congestion and tolerance.

Although ESC 2026 groups LVEF 41–49% within HFrEF, the evidence base is not equally direct for every drug across this range. Large prospective trials exclusively enrolling patients with LVEF 41–49% have not established the effects of ACE inhibitors/ARNI/ARBs or beta-blockers in isolation. [1]

RAAS and Neprilysin Inhibition

ARNI therapy, ACE inhibitors and ARBs reduce adverse neurohormonal activation and ventricular remodeling.

Sacubitril/valsartan has an established role in symptomatic HFrEF and should be considered within the contemporary foundational approach when clinically appropriate.

ACE inhibitors remain effective disease-modifying therapy when ARNI is not used, while ARBs remain appropriate when ACE inhibitors are not tolerated and ARNI is not feasible.

Treatment choice must account for blood pressure, kidney function, potassium and prior angioedema.

Beta-Blockers

Evidence-based beta-blockers reduce mortality and HF hospitalization in HFrEF.

They should generally be initiated in clinically stable patients and titrated toward guideline-supported target or maximally tolerated doses.

Dose decisions should consider:

• heart rate

• blood pressure

• congestion

• conduction disease

• atrial fibrillation

• symptoms of low output

Persistent congestion or hemodynamic instability may require stabilization before aggressive titration.

Mineralocorticoid Receptor Antagonists: A Major 2026 Change

One of the most important changes in the 2026 ESC guideline is that MRAs are now recommended as foundational treatment in symptomatic chronic HF independent of LVEF.

This means MRA therapy is no longer conceptually limited to traditional HFrEF.

Renal function and serum potassium must be monitored carefully because hyperkalemia remains a major limiting factor.

MRA selection should reflect the phenotype and the evidence for the individual drug. Spironolactone and eplerenone have established roles in reduced-EF HF, while finerenone has direct outcomes evidence in patients with LVEF ≥40%. These agents should not be presented as interchangeable or routinely combined. [3,4]

The 2026 ACC HFpEF Expert Consensus Decision Pathway favors finerenone as the MRA of choice in HFpEF, with alternatives considered according to tolerance, access and clinical circumstances. Kidney function, potassium, interactions and applicable prescribing information must guide selection and monitoring. [7]

FINEARTS-HF demonstrated a reduction in the composite of total worsening-HF events and cardiovascular death, driven predominantly by fewer worsening-HF events. This should not be described as a separately established reduction in cardiovascular mortality. [4]

SGLT2 Inhibitors Across the EF Spectrum

Dapagliflozin and empagliflozin have fundamentally changed HF treatment.

They reduce HF hospitalization and improve clinical outcomes across a broad spectrum of LVEF, whether or not diabetes is present.

The ESC 2026 guideline recommends SGLT2 inhibitors as foundational therapy in symptomatic HF regardless of LVEF.

In HFrEF, benefit includes reduction in HF hospitalization and cardiovascular mortality. In HFpEF, the principal outcome benefit is driven predominantly by fewer HF hospitalizations.

Their effects occur relatively rapidly and extend beyond glucose lowering.

Diuretics and Congestion

Loop diuretics remain central for treatment of congestion.

Their principal objective is to:

• relieve dyspnea and edema

• restore euvolemia

• reduce filling pressures

• improve functional status

Unlike major disease-modifying therapies, diuretics are primarily used for volume management rather than mortality reduction.

The dose should be individualized according to congestion, renal function, blood pressure and previous diuretic response.

Persistent congestion despite escalating therapy requires reassessment of adherence, renal function, sodium intake, perfusion status and potential diuretic resistance.

Additional Therapy in HFrEF

Despite optimal FMT, some patients remain symptomatic or at high risk.

Additional therapies may include, in appropriately selected patients:

• ivabradine

• vericiguat

• hydralazine plus isosorbide dinitrate

• digoxin or digitoxin

• other phenotype-specific therapies

Selection depends on rhythm, heart rate, blood pressure, renal function, recent worsening HF, tolerability and comorbidity profile.

Digitalis: Evidence and Important Distinctions

DIGIT-HF evaluated digitoxin, not digoxin, as an addition to contemporary therapy. It reduced the combined outcome of all-cause death or first hospitalization for worsening HF. The individual mortality component was not statistically significant. [8]

The 2026 ESC guideline states that a cardiac glycoside may have an additional role in selected patients with symptomatic HFrEF and LVEF ≤40% despite optimal foundational treatment, aiming to reduce HF hospitalization. It is not a routine substitute for foundational therapy. [1]

Digitoxin and digoxin differ in pharmacology and supporting evidence. Findings from one agent should not automatically be transferred to the other. Serum concentrations, interactions, organ function and toxicity risk require careful monitoring.

A prespecified DECISION analysis found clinical deterioration after withdrawal of long-term digoxin. This withdrawal finding should not be interpreted as proof that initiating digoxin benefits every patient. Treatment changes require individual clinical review. [9]

HFpEF: No Longer a Therapeutic Void

HFpEF treatment has changed substantially.

The 2026 ESC guideline identifies two foundational medical therapies for symptomatic HFpEF:

SGLT2 inhibitor

Mineralocorticoid receptor antagonist

Diuretics remain necessary when congestion is present.

At the same time, HFpEF must be treated as a heterogeneous syndrome rather than a single disease.

Management should aggressively address:

• hypertension

• obesity

• atrial fibrillation

• diabetes

• CKD

• ischemia

• sleep apnea

• valvular disease

• pulmonary disease

• anemia and iron deficiency

• cardiac amyloidosis

ACE inhibitors, ARBs, beta-blockers and other therapies may still be used for specific comorbidities, but they are not universally disease-modifying in HFpEF.

Obesity-Related HFpEF

Obesity is increasingly recognized as an important HFpEF phenotype.

The STEP-HFpEF program demonstrated that semaglutide produced substantial improvements in symptoms, physical limitation, exercise capacity and body weight in patients with obesity-related HFpEF.

Clinical trial: STEP-HFpEF [5].

The SUMMIT trial subsequently showed that tirzepatide reduced the composite of cardiovascular death or worsening HF and improved health status in patients with HFpEF and obesity.

Clinical trial: SUMMIT [6].

Reflecting this evidence, the 2026 ESC guideline gives Class IIa recommendations for semaglutide or tirzepatide in appropriate patients with HFpEF and obesity.

Heart Failure with Improved EF

Improvement in LVEF does not necessarily mean the disease has disappeared.

The Second Universal Definition recognizes HF with improved EF as a clinically meaningful phenotype and emphasizes that HF is dynamic, with potential for improvement, remission and recurrence.

In general, patients who improve on disease-modifying treatment should not have effective therapy withdrawn simply because EF has normalized unless there is a compelling clinical reason.

Ongoing surveillance remains important.

Iron Deficiency: Updated 2026 Approach

Iron deficiency is common in HF and contributes to impaired exercise capacity and quality of life.

A notable 2026 ESC update is greater emphasis on transferrin saturation <20% as a practical marker of iron deficiency, because ferritin can be strongly influenced by inflammation and may not accurately identify patients most likely to benefit.

In symptomatic HFrEF with iron deficiency, intravenous iron is recommended to improve symptoms and quality of life and should be considered to reduce HF hospitalization.

Evidence in HFpEF remains substantially more limited.

Iron deficiency should also prompt evaluation for its underlying cause rather than treatment of the laboratory abnormality alone.

Atrial Fibrillation and Heart Failure

AF and HF frequently coexist and can worsen one another.

Management should address:

• thromboembolic prevention

• ventricular rate

• rhythm control where appropriate

• congestion

• precipitating factors

• underlying structural disease

AF may also be the primary driver of myocardial dysfunction in tachycardia- or arrhythmia-induced cardiomyopathy.

In appropriately selected patients, rhythm-control strategies—including catheter ablation—may improve symptoms and ventricular function.

The clinical question should not simply be whether AF is present, but whether the arrhythmia is contributing materially to HF progression.

Chronic Kidney Disease and Heart Failure

CKD is both a risk factor and consequence of HF.

Small changes in creatinine during successful decongestion do not automatically represent harmful renal injury and should be interpreted in clinical context.

Contemporary HF management increasingly seeks to preserve disease-modifying therapy rather than discontinuing it reflexively because of modest changes in renal function.

SGLT2 inhibitors and MRAs require appropriate renal and electrolyte surveillance.

Hyperkalemia, worsening kidney function and hypotension should trigger thoughtful adjustment—not automatic abandonment—of beneficial therapy.

Device and Interventional Therapy

Implantable Cardioverter-Defibrillators

ICDs remain an important strategy for prevention of sudden cardiac death in appropriately selected patients.

The 2026 ESC guideline recommends ICD therapy in selected patients with HFrEF, LVEF ≤35% and ischemic etiology, and states that it should be considered in selected patients with non-ischemic disease.

Device eligibility is individualized and is not extended to every patient with LVEF <50% by the change in terminology. [1]

The decision should incorporate:

• life expectancy

• competing non-arrhythmic mortality

• HF severity

• comorbidities

• age

• arrhythmic substrate

• patient preferences

Cardiac Resynchronization Therapy

CRT can improve ventricular synchrony, cardiac function, symptoms and outcomes in selected HFrEF patients with electrical dyssynchrony.

Benefit is greatest in carefully selected patients, particularly those with:

• persistent reduced EF despite optimized FMT

• broad QRS

• typical left bundle branch block morphology

• significant symptoms

Device decisions should follow optimized pharmacological therapy whenever clinically feasible.

Structural Intervention

Heart failure may be aggravated by severe valvular disease.

The 2026 ESC guideline strengthens the role of transcatheter structural intervention in selected patients.

For example, mitral transcatheter edge-to-edge repair is recommended in selected symptomatic HFrEF patients with persistent severe secondary mitral regurgitation despite optimized FMT and CRT where indicated and when appropriate clinical and echocardiographic criteria are fulfilled.

Decompensated Heart Failure

The 2026 ESC guideline replaces the term acute heart failure with decompensated heart failure.

This reflects the fact that deterioration may occur abruptly or gradually and does not always represent a truly acute disease process.

Management begins with assessment of:

• congestion

• perfusion

• blood pressure

• oxygenation

• renal function

• precipitating factors

Common triggers include:

• infection

• ischemia

• atrial fibrillation

• uncontrolled hypertension

• medication nonadherence

• renal deterioration

• excessive sodium or fluid intake

• valvular disease

Loop diuretics are central when congestion is present.

Patients with hypoperfusion, shock or severe end-organ dysfunction require urgent escalation and may need inotropes or temporary mechanical circulatory support.

Less severe decompensation can sometimes be managed in structured ambulatory HF programs when appropriate.

Advanced Heart Failure

Stage D HF requires timely recognition.

Warning features include:

• recurrent HF hospitalization

• persistent severe symptoms

• progressive renal or hepatic dysfunction

• refractory congestion

• intolerance of foundational therapy

• recurrent ventricular arrhythmia

• worsening functional capacity

• dependence on intravenous therapies

Referral should occur before irreversible end-organ dysfunction develops.

Advanced therapies may include:

• durable mechanical circulatory support

• heart transplantation

• selected continuous inotropic strategies

• specialized multidisciplinary care

The ESC 2026 guideline upgraded aspects of durable mechanical circulatory support based on contemporary evidence.

Palliative and supportive care should also be integrated according to symptoms, prognosis and patient goals rather than viewed solely as an end-of-life intervention.

Cardiac Rehabilitation and Multidisciplinary Care

Heart failure treatment does not end with medication.

The ESC recommends multidisciplinary HF management programs and cardiac rehabilitation.

Exercise-based cardiac rehabilitation improves:

• exercise capacity

• functional status

• quality of life

• short-term hospitalization risk

Exercise should be individualized according to clinical stability, functional capacity and cardiovascular risk.

The 2026 ESC Cardiac Rehabilitation Guideline specifically recommends exercise training in stable chronic HF and supports early rehabilitation after decompensated HF once decongestion and hemodynamic stability have been achieved.

Patient education should include:

• daily symptom awareness

• weight monitoring when appropriate

• medication adherence

• recognition of worsening congestion

• physical activity

• nutrition

• vaccination

• blood pressure monitoring

• appropriate fluid and sodium advice

• when to seek medical assistance

Agree on a written action plan with your clinical team, including when to report worsening symptoms and whether any medication adjustments are authorized. Fluid and sodium advice should be individualized; do not apply a universal restriction or change diuretic doses without an agreed plan.

Long-Term Follow-Up

Heart failure requires repeated reassessment because the phenotype can change.

Follow-up should evaluate:

• symptoms and NYHA class

• congestion

• blood pressure

• heart rate and rhythm

• renal function

• potassium

• iron status

• medication tolerance

• adherence

• LVEF and structural evolution when clinically indicated

• comorbidities

• device function

• functional capacity

• psychosocial health

The objective is not only stabilization.

The goal is to prevent disease progression, maintain foundational therapy, reduce hospitalization and mortality, improve quality of life and identify patients who require advanced intervention before deterioration becomes irreversible.

A Contemporary Perspective

Modern heart failure management has moved well beyond the traditional concept of treating congestion after symptoms appear.

The 2026 framework begins with prevention, recognizes pre-HF, simplifies phenotypes, expands disease-modifying therapy across the EF spectrum and emphasizes rapid initiation of foundational treatment.

For HFrEF, ACE-I/ARNI/ARB, beta-blocker, MRA and SGLT2 inhibition form the therapeutic foundation.

For HFpEF, SGLT2 inhibition and MRA therapy are now foundational, while obesity-related HFpEF can additionally benefit from targeted weight-loss therapies in appropriate patients.

The modern objective is therefore broader than improving ejection fraction.

It is to prevent HF where possible, identify disease earlier, reduce congestion and hospitalization, prevent sudden death, treat the underlying cause, preserve organ function, improve functional capacity and extend meaningful survival.