About Dr. Shahzad

I am a heart doctor with experience across the UK and Ireland. Holding MBBS, MRCPI, MPH, FRSPH, and MFSEM, I specialise in cardiovascular medicine, public health, and sports cardiology. Passionate about patient care, research, and teaching, I have contributed to multiple publications and clinical trials. Beyond medicine, and actively engage in medical education, fitness, and motivational outreach, using digital platforms to promote health awareness and lifestyle interventions. For more insights, research work, and patient education resources, follow his journey!

2026 ESC Heart Failure Guidelines: Practical Changes for Clinicians

Posted on September 19, 2026 by Dr. Shahzad

The 2026 European Society of Cardiology (ESC) guideline is a substantial update to heart-failure practice. It replaces the 2021 guideline and its 2023 focused update as the current ESC reference. Its main clinical message is to treat heart failure across a continuum: reduce risk early, recognise structural disease before symptoms where possible, and apply evidence-based treatment promptly once heart failure is established.1 2

The most visible changes are a simplified ejection-fraction classification, a stage-based framework, revised terminology for therapy, and new recommendations on mineralocorticoid-receptor antagonists (MRAs) and obesity treatment. These changes should improve clarity, but they do not replace careful phenotyping, aetiological investigation, or local prescribing and device pathways.

What has changed?

1. The LVEF classification has been simplified

The ESC now uses two heart-failure phenotypes based on left-ventricular ejection fraction (LVEF): heart failure with reduced ejection fraction (HFrEF) for LVEF <50%, and heart failure with preserved ejection fraction (HFpEF) for LVEF ≥50%. The previous separate category of heart failure with mildly reduced ejection fraction (HFmrEF; LVEF 41–49%) has been removed.1 3

This reflects the view that patients with LVEF in the 41–49% range often have a similar biology and treatment response to those with lower LVEF. It should not lead to treatment decisions being made from a single LVEF value. Image quality, loading conditions, rhythm, method of measurement and biological variation all matter. A patient with an LVEF close to 50% still needs an integrated assessment of symptoms, congestion, natriuretic peptides, structural heart disease, co-morbidity and cause.

The guideline also replaces the broad label acute heart failure with decompensated heart failure. This better captures patients whose deterioration is progressive rather than abrupt.3

2. Heart failure is framed as a staged condition

The new framework places greater emphasis on prevention and earlier intervention. It follows the progression from people at risk of heart failure (stage A), through pre-heart failure with structural or functional abnormalities but no symptoms (stage B), to symptomatic heart failure (stage C) and advanced heart failure (stage D).1 3

For day-to-day practice, this reinforces three points. First, hypertension, diabetes, obesity, chronic kidney disease, coronary disease and cardiotoxic exposure should be addressed before symptomatic heart failure develops. Second, asymptomatic left-ventricular dysfunction or structural heart disease warrants active follow-up rather than passive labelling. Third, advanced-heart-failure referral should not be delayed until every conventional option has been exhausted.

3. The guideline uses clearer treatment language

The ESC separates therapy into three groups.1 2

Term	Meaning in the guideline	Practical implication
Foundational medical therapy (FMT)	Medical therapies with the strongest evidence for an unselected heart-failure population.	Establish and optimise these first, unless contraindicated or not tolerated.
Additional medical therapy (AMT)	Therapies with benefit in defined clinical settings or for selected outcomes.	Add according to phenotype, rhythm, symptoms, co-morbidity and residual risk.
Guideline-directed interventional therapy (GDIT)	Recommended device or structural interventions.	Consider after appropriate medical optimisation and multidisciplinary assessment.

For symptomatic HFrEF, the familiar disease-modifying foundation remains a beta-blocker, renin–angiotensin system inhibition with an angiotensin-converting-enzyme inhibitor or an angiotensin-receptor neprilysin inhibitor, an MRA, and an SGLT2 inhibitor, tailored to clinical status and tolerance. The guideline recommends reviewing and uptitrating foundational treatment at least every one to two weeks, guided by symptoms, observations and laboratory results.1

Treatment updates most likely to affect practice

MRA treatment now spans the LVEF spectrum

A major change is the Class I recommendation for an MRA in chronic heart failure irrespective of LVEF.3 This is an important move beyond the previous evidence boundary between reduced and preserved ejection fraction.

The recommendation is supported by the established mortality and hospitalisation benefit of steroidal MRAs in HFrEF, together with newer evidence in patients with LVEF ≥40%. In FINEARTS-HF, finerenone reduced the rate of the composite of total worsening heart-failure events and cardiovascular death. The observed benefit was driven mainly by fewer worsening heart-failure events; cardiovascular death alone was not clearly reduced. Hyperkalaemia was more frequent.4

This does not mean that MRAs are interchangeable or suitable for every patient. Choice of agent, renal function and potassium thresholds, monitoring, interaction checks, local formulary rules and the product licence remain essential. In particular, this recommendation should not be used to bypass the need for repeat renal-function and potassium testing after initiation or dose change.

Obesity is treated as a therapeutic target in selected HFpEF-spectrum patients

The guideline gives a Class IIa, Level B recommendation that semaglutide or tirzepatide should be considered for patients with symptomatic heart failure, LVEF ≥45% and body-mass index ≥30 kg/m², regardless of diabetes status, to reduce weight and improve exercise capacity and quality of life.1

This recommendation is deliberately selective. In STEP-HFpEF, semaglutide improved symptoms, physical limitations, 6-minute walk distance and weight loss over 52 weeks in patients with HFpEF and obesity.5 In SUMMIT, tirzepatide reduced the composite of cardiovascular death or worsening heart failure and improved health status in patients with HFpEF and obesity; the trial was not powered to establish a reduction in cardiovascular death alone.6

For practice, these agents should be considered in addition to, not instead of, foundational heart-failure care, congestion management, rehabilitation and structured lifestyle support. Patient selection still requires attention to frailty, nutritional risk, gastrointestinal adverse effects, renal function, diabetes treatment and local eligibility or commissioning arrangements.

Selected therapies have a clearer place after foundational treatment

The guideline retains a selective role for cardiac glycosides. Digoxin or digitoxin should be considered in patients with symptomatic HFrEF, LVEF ≤40%, despite optimal foundational treatment, to reduce heart-failure hospitalisation.1 This is not a return to routine digoxin prescribing: there remains no established mortality benefit, and renal function, potassium, dose, interactions and toxicity risk must guide use. See our related review: Digoxin in Contemporary Heart-Failure Practice.

For selected patients with stable symptomatic HFrEF and severe secondary mitral regurgitation despite optimised foundational therapy and cardiac resynchronisation therapy where indicated, mitral transcatheter edge-to-edge repair is recommended when defined clinical and echocardiographic criteria are met.1 This remains a Heart Team decision, not an alternative to medical optimisation.

What should change in a practical heart-failure review?

A useful review now starts by recording the current phenotype as HFrEF (<50%) or HFpEF (≥50%), while documenting the actual LVEF and its context. Avoid carrying the historical HFmrEF label forward as if it were a current ESC category.

For a patient with symptomatic chronic heart failure, establish whether foundational treatment is complete and tolerated before moving to additional therapies. In HFrEF, this includes early sequencing and regular review rather than prolonged, single-drug titration. For all phenotypes, assess congestion, blood pressure, renal function, potassium, rhythm, iron status, diabetes, kidney disease, obesity, frailty and adherence.

For a patient with LVEF ≥45% and obesity, assess whether semaglutide or tirzepatide fits the individual’s phenotype and goals. The strongest guideline-supported outcomes are weight loss, exercise capacity and quality of life; treatment should not be presented as a universal heart-failure mortality therapy.

For every patient, reinforce self-management, medication review, exercise-based cardiac rehabilitation where appropriate, multidisciplinary follow-up and an early plan for deterioration. The guideline gives these elements a central—not optional—place in care.1

Pitfalls and limitations

The new LVEF threshold does not eliminate measurement uncertainty. A value near 50% should prompt clinical interpretation, not automatic reclassification without context.

An ESC Class I recommendation for MRAs does not remove safety constraints. Hyperkalaemia, worsening renal function, hypotension and interacting medication remain common barriers and require proactive monitoring.

The obesity recommendation applies to a defined symptomatic population with LVEF ≥45% and BMI ≥30 kg/m². It should not be extrapolated automatically to HFrEF below this range, to patients without obesity, or to those who cannot safely tolerate weight-reducing treatment.

ESC guidance informs practice in the UK, but it is not a substitute for NICE guidance, a medicine’s UK licence, local formulary approval or a specialist heart-failure pathway. Where these differ, clinicians should follow local governance while considering the evidence and the patient’s circumstances.

Key learning points

The 2026 ESC guideline replaces the separate HFmrEF category with HFrEF <50% and HFpEF ≥50%.
Heart failure is now framed as a staged condition, strengthening prevention, earlier recognition and timely referral.
The guideline uses the terms foundational medical therapy, additional medical therapy and guideline-directed interventional therapy to clarify treatment priorities.
MRAs now have a Class I recommendation in chronic heart failure across the LVEF spectrum, but agent choice and renal/potassium surveillance remain individualised.
Semaglutide or tirzepatide should be considered only for selected patients with symptomatic HF, LVEF ≥45% and BMI ≥30 kg/m²; the recommended aims are weight loss, exercise capacity and quality of life.
Digoxin remains a selected, safety-sensitive additional therapy rather than foundational treatment.

Educational note: This article summarises guideline changes for clinicians. It is not a prescribing protocol. Treatment decisions should incorporate the current medicine licence, local pathway, renal function, potassium, haemodynamics, co-morbidity and patient preference.

Publication date: 19 September 2026
Last reviewed: 19 September 2026

References

Left Atrial Myxoma: Diagnosis, Differential Diagnosis and Management

Posted on September 19, 2026 by Dr. Shahzad

Audience: echocardiographers, cardiologists and acute physicians. Evidence reviewed: September 2026.

Key message

A left-atrial mass attached near the fossa ovalis is suggestive of myxoma, but attachment, mobility, vascularity and clinical context must be defined before diagnosis. Important mimics include thrombus, other tumours, vegetation and extracardiac compression. Once a probable myxoma is identified, prompt specialist surgical assessment is usual because embolic and obstructive complications can be sudden.

Clinical presentation

Obstruction: exertional dyspnoea, orthopnoea, syncope or positional symptoms from intermittent mitral inflow obstruction.
Embolism: cerebral, coronary, retinal or systemic arterial events.
Constitutional features: fever, weight loss, raised inflammatory markers and anaemia.
Incidental discovery: an asymptomatic mass found during unrelated imaging.

Echocardiographic assessment

Transthoracic echocardiography is the usual first test. Record the mass in multiple planes and describe size, shape, surface, mobility, stalk, precise attachment and relationship to the mitral valve and pulmonary veins. Assess functional mitral obstruction with Doppler at a stated heart rate, associated regurgitation, chamber size, pulmonary-pressure probability and pericardial effusion.

Transoesophageal echocardiography improves definition of attachment, small lesions and surgical anatomy. Three-dimensional echo may clarify the stalk and spatial relationship. Avoid declaring histology from echogenicity alone.

Possibility	Features that may support it	Important caution
Myxoma	Mobile pedunculated mass, often arising from interatrial septum near fossa ovalis	Atypical attachment occurs.
Thrombus	Atrial fibrillation, mitral stenosis, low-flow state, left-atrial appendage location	Organised thrombus can mimic tumour.
Vegetation	Valve-related oscillating mass with infection or valve destruction	Blood cultures and clinical criteria are essential.
Other tumour/metastasis	Broad attachment, infiltration, multiple lesions or known malignancy	Requires tissue and multimodality context.

When CT or CMR helps

CMR can assess tissue signal, perfusion and enhancement; CT defines calcification, coronary anatomy and extracardiac disease. Neither modality removes the need for pathology. If malignancy or thrombus remains plausible, imaging and treatment decisions should be coordinated across cardiology, radiology, oncology/infectious diseases and surgery as relevant.

Management

Probable cardiac myxoma is generally referred promptly for surgical excision, including the attachment site where feasible. Urgency reflects mobility, prior embolism, obstruction, tumour size and clinical stability. Coronary assessment follows age, symptoms and surgical protocol; tumour neovascularisation may occasionally be demonstrated.

Histopathology confirms the diagnosis. Follow-up echocardiography checks for recurrence, which is uncommon after complete excision but more likely in familial syndromes, multiple tumours or incomplete resection. Younger patients, multiple or recurrent myxomas, or suggestive endocrine/skin features should prompt consideration of Carney complex and genetic assessment.

Selected references

Educational material only. A suspected intracardiac tumour or thrombus requires timely specialist assessment; acute obstruction or embolism is an emergency.

Acute Coronary Syndrome with Complex Coronary Disease: When CABG Belongs in the Inpatient Pathway

Posted on September 19, 2026 by Dr. Shahzad

Audience: acute-cardiology, interventional-cardiology and cardiothoracic teams. Evidence reviewed: September 2026.

Key message

In acute coronary syndrome (ACS), culprit treatment and complete revascularisation are related but distinct decisions. CABG should remain in the index-admission pathway when anatomy, diabetes, ventricular dysfunction, mechanical complications or PCI feasibility suggests a prognostic or technical advantage—provided timing balances recurrent-ischaemia and bleeding risks.

Stabilise first, then define the problem

Immediate management follows ACS severity: resuscitation, antithrombotic therapy, urgent angiography and culprit reperfusion when indicated. Cardiogenic shock, ongoing ischaemia, failed PCI or a mechanical complication demands rapid multidisciplinary escalation; the ideal revascularisation mode may differ from that in a stable NSTEMI patient.

Anatomy that should trigger surgical discussion

Significant left-main disease, especially complex distal bifurcation disease.
Complex three-vessel disease not amenable to durable complete PCI.
Diabetes with multivessel coronary disease where long-term evidence favours surgery in suitable patients.
Need for concomitant valve, aortic or mechanical-complication surgery.
Failed or complicated PCI with ongoing jeopardised myocardium.

The index-admission Heart Team

Domain	Questions
Clinical stability	Ongoing pain, shock, arrhythmia, heart failure or mechanical complication?
Coronary anatomy	Left main, complexity, targets, chronic occlusions, likelihood of complete revascularisation?
Myocardium	LV function, infarct territory, viability where genuinely uncertain?
Patient factors	Frailty, cognition, renal/pulmonary disease, prior surgery, preferences and rehabilitation potential?
Treatment constraints	Recent P2Y12 inhibitor, bleeding, anticoagulation, infection and theatre availability?

Timing is an individual risk balance

Emergency CABG may be necessary for failed reperfusion, anatomy unsuitable for PCI with ongoing ischaemia, or mechanical complications. In stable patients, surgery is often delayed sufficiently to reduce perioperative bleeding and allow antiplatelet washout, but unnecessary discharge can expose patients to recurrent ischaemia and fragmented decision-making. The plan should state the reason for timing, antithrombotic strategy and triggers for acceleration.

Routine platelet-transfusion or bridging strategies should not be improvised. Follow the current guideline, local surgical protocol and patient-specific thrombotic and bleeding risks. Aspirin is commonly continued, while interruption intervals for P2Y12 inhibitors depend on the agent and urgency.

Communication standard

Document: culprit and residual anatomy; whether PCI achieved stable reperfusion; why CABG, PCI or medical therapy is preferred; estimated surgical and bleeding risk; antiplatelet stop dates; intended timing; contingency plan; and the patient’s informed preference. “For outpatient discussion” is not an adequate plan when prognostically important disease remains untreated.

Selected references

Educational material only. Revascularisation strategy and timing require case-specific Heart Team decisions and current local antithrombotic/surgical protocols.

Digoxin in Contemporary Heart-Failure Practice: A Selective, Safety-First Approach

Posted on September 19, 2026 by Dr. Shahzad

Audience: heart-failure clinicians, general physicians and trainees. Evidence reviewed: September 2026.

Key message

Digoxin remains useful for selected patients, but it is not a foundational mortality-reducing therapy for heart failure. Its narrow therapeutic index makes indication, renal function, dose, drug interactions and clinical monitoring inseparable from prescribing.

Two distinct indications

Setting	Potential role	What it does not establish
HFrEF in sinus rhythm	May reduce heart-failure hospitalisation in persistently symptomatic patients despite guideline-directed therapy	No proven survival benefit in the pivotal DIG trial
HFrEF with atrial fibrillation	May support resting rate control, often with another agent	Less reliable rate control during exertion

Evidence in HFrEF

In the Digitalis Investigation Group trial, digoxin did not reduce all-cause mortality but reduced hospital admission for worsening heart failure. The trial pre-dated angiotensin-receptor neprilysin inhibitors, SGLT2 inhibitors and widespread modern device therapy, so absolute benefits in present practice are uncertain. Contemporary guidelines therefore position digoxin as an option for selected symptomatic HFrEF rather than routine foundational treatment.

Choosing and monitoring treatment

Confirm the goal: symptom/hospitalisation reduction or ventricular-rate control.
Use a low maintenance dose tailored to age, lean body mass and renal function; loading is rarely needed in stable chronic care.
Check renal function and potassium before treatment and after clinically important changes.
Review interacting medicines, including amiodarone, verapamil, macrolides and other P-glycoprotein inhibitors.
If a serum concentration is required, sample at steady state and at least 6–8 hours after the last dose; interpret the result with symptoms, ECG and renal function.

For heart failure, many experts aim for a low serum concentration, commonly 0.5–0.9 ng/mL, when measurement is clinically indicated. A number within a laboratory “therapeutic range” does not exclude toxicity, particularly in older adults, renal impairment, hypokalaemia, hypomagnesaemia or hypothyroidism.

Recognising toxicity

Toxicity may cause anorexia, nausea, confusion, visual disturbance, bradyarrhythmia, atrioventricular block or almost any tachyarrhythmia. Stop digoxin, obtain an ECG, electrolytes, renal function and an appropriately timed level, and assess severity urgently. Life-threatening arrhythmia or significant hyperkalaemia may require digoxin-specific antibody fragments under emergency/toxicology guidance.

When to reconsider

Reassess digoxin when renal function changes, interacting therapy is added, bradycardia develops, the original indication disappears or adherence/monitoring is unreliable. Withdrawal may worsen symptoms or rate control in some patients, so deprescribing should be planned rather than automatic.

Selected references

Educational material only. Dose and monitoring must follow the current product information, renal function, local formulary and individual clinical context.

Symptomatic Obstructive Hypertrophic Cardiomyopathy: A Practical Management Pathway

Posted on September 19, 2026 by Dr. Shahzad

Audience: cardiology clinicians and trainees. Evidence reviewed: September 2026.

Key message

In symptomatic obstructive hypertrophic cardiomyopathy (HCM), first confirm that dynamic left-ventricular outflow-tract (LVOT) obstruction explains the symptoms. Treatment then proceeds from physiology-aware medical therapy to specialist myosin-inhibitor or septal-reduction strategies, while sudden-death risk is assessed on a separate track.

1. Confirm the phenotype and mechanism

Document maximal wall thickness, distribution of hypertrophy and LV systolic/diastolic function.
Identify systolic anterior motion, mitral–septal contact and the mechanism/severity of mitral regurgitation.
Measure resting and provoked LVOT gradients with correctly aligned CW Doppler. Exercise stress echocardiography is valuable when symptoms and resting/Valsalva gradients disagree.
Use CMR for anatomy, apical disease, scar burden and alternative diagnoses.
Exclude important mimics and contributors such as hypertension, valve disease, coronary disease, anaemia and arrhythmia.

2. Define what limits the patient

Record NYHA class, exertional chest pain, presyncope/syncope, palpitations and exercise capacity. Review volume status, blood pressure and drugs that reduce preload or afterload. New atrial fibrillation can sharply worsen filling and symptoms and requires prompt rhythm/rate and anticoagulation assessment.

3. Start physiology-directed treatment

A non-vasodilating beta-blocker is generally first-line for symptoms attributable to obstruction. Verapamil or diltiazem may be considered when beta-blockers are ineffective or not tolerated, but caution is required with hypotension, severe obstruction or advanced congestion. Disopyramide can reduce obstruction when added under expert supervision, with attention to anticholinergic effects and QT prolongation.

Step	Decision	Safety focus
Initial drug	Non-vasodilating beta-blocker	Heart rate, blood pressure, conduction disease
Alternative	Verapamil or diltiazem in selected patients	Hypotension, pulmonary congestion, drug interactions
Add-on	Disopyramide in expert care	QT interval and anticholinergic burden
Advanced option	Cardiac myosin inhibitor where licensed and appropriate	Serial LVEF, interactions and mandated monitoring

4. Escalate persistent severe symptoms

Patients with substantial symptoms despite maximally tolerated therapy should be referred to an experienced HCM centre. Options include a cardiac myosin inhibitor and septal reduction. Surgical myectomy is preferred when concomitant cardiac surgery or complex mitral/subvalvular anatomy requires correction. Alcohol septal ablation is an alternative for selected anatomy and risk profiles. Operator and centre experience materially affect outcomes.

5. Run parallel risk pathways

Sudden-cardiac-death risk assessment is not replaced by symptom control or gradient reduction. Evaluate previous cardiac arrest or sustained ventricular tachycardia, unexplained syncope, family history, maximal wall thickness, apical aneurysm, LV systolic dysfunction, non-sustained ventricular tachycardia and CMR scar within the applicable guideline framework. Also address genetics and family screening, atrial fibrillation, stroke prevention, pregnancy, exercise and endocarditis advice.

Selected references

Educational material only. Myosin-inhibitor and septal-reduction decisions require specialist HCM-centre assessment and current local prescribing guidance.

FINEARTS-HF: Trial Design, Results and Clinical Interpretation

Posted on September 19, 2026 by Dr. Shahzad

Audience: heart-failure clinicians, trainees and evidence-based-medicine readers. Evidence reviewed: September 2026.

Bottom line

FINEARTS-HF showed that finerenone reduced the rate of the composite of total worsening heart-failure events and cardiovascular death in symptomatic heart failure with left-ventricular ejection fraction (LVEF) ≥40%. The benefit was driven mainly by fewer worsening heart-failure events, with more hyperkalaemia but less hypokalaemia.

Clinical question

Does the non-steroidal mineralocorticoid-receptor antagonist finerenone improve outcomes in patients with heart failure and mildly reduced or preserved ejection fraction?

Design and population

FINEARTS-HF was an international, double-blind, randomised, placebo-controlled trial. It enrolled 6,001 patients aged 40 years or older with symptomatic heart failure, LVEF ≥40%, structural heart disease and elevated natriuretic peptides. Participants received finerenone or placebo in addition to usual therapy. The primary endpoint was a recurrent-event composite: total worsening heart-failure events plus cardiovascular death.

Feature	Why it matters
Recurrent-event analysis	Counts first and subsequent worsening-HF events rather than only time to first event.
LVEF ≥40%	Addresses HFmrEF/HFpEF, where evidence for steroidal MRAs had been uncertain.
Biomarker and structural criteria	Enriched the population for objectively supported heart failure.
Active contemporary background care	Improves relevance, although uptake of some newer therapies varied.

Results

During a median follow-up of 32 months, 1,083 primary-outcome events occurred in the finerenone group and 1,283 in the placebo group. The rate ratio was 0.84 (95% confidence interval 0.74–0.95; P=0.007). Worsening heart-failure events numbered 842 versus 1,024 (rate ratio 0.82, 95% CI 0.71–0.94). Cardiovascular death occurred in 8.1% versus 8.7% of participants; the trial did not demonstrate a clear mortality reduction.

Treatment effects were broadly consistent across prespecified subgroups, including the range of LVEF studied. Finerenone increased creatinine and hyperkalaemia risk but reduced hypokalaemia. The clinical trade-off therefore includes renal-function and potassium surveillance.

Strengths and limitations

Strengths: large randomised design, blinded outcome assessment, broad geography and clinically meaningful recurrent-event endpoint.
Endpoint interpretation: the primary benefit was morbidity rather than proven cardiovascular survival.
Generalisability: trial eligibility and monitoring may not represent frail patients, advanced kidney disease or routine-care adherence.
Background therapy: evolving SGLT2-inhibitor use complicates direct extrapolation to every present-day regimen.

Clinical application

Finerenone is a disease-modifying option for appropriately selected patients with HFmrEF/HFpEF, particularly when recurrent decompensation risk is important. Before initiation, confirm the indication, estimated glomerular filtration rate, serum potassium, interacting medicines and the ability to repeat blood tests. Do not assume interchangeability with spironolactone or eplerenone: molecular properties, evidence bases and licensed indications differ.

Selected references

Educational critical appraisal only. Prescribing must follow the current licence, formulary, renal/potassium criteria and local heart-failure pathways.

Arrhythmogenic Cardiomyopathy: An Integrated Echo and CMR Approach

Posted on September 19, 2026 by Dr. Shahzad

Audience: cardiology trainees, imagers and inherited-cardiac-condition teams. Evidence reviewed: September 2026.

Key message

Arrhythmogenic cardiomyopathy (ACM) is a spectrum that may be right-dominant, biventricular or left-dominant. Imaging supports—but does not independently establish—the diagnosis. Electrical, structural, tissue, genetic and family data must be integrated.

When to suspect ACM

Ventricular arrhythmia with morphology suggesting RV or LV origin.
Unexplained regional ventricular dysfunction or aneurysm.
Disproportionate RV dilatation or dysfunction.
Subepicardial or ring-like non-ischaemic scar on CMR.
A pathogenic variant or family history of ACM or premature sudden death.

Echocardiography

Perform a complete study with an RV-focused apical view. Assess RV dimensions, fractional area change, TAPSE, S′, free-wall strain and regional motion. Examine the RV outflow tract in parasternal long- and short-axis views. For the LV, quantify volumes and ejection fraction, examine regional deformation and look for subtle inferolateral dysfunction.

Regional akinesia, dyskinesia or aneurysm is more specific than subjective hypokinesia, but normal variants and poor windows are common. Prominent trabeculation or the moderator band is not diagnostic. Isolated mild RV enlargement in an athlete requires careful differentiation using proportional chamber remodelling, function, arrhythmia burden and tissue characterisation.

Cardiovascular magnetic resonance

CMR provides reproducible biventricular volumes and ejection fractions, regional cine assessment and myocardial tissue characterisation. Late gadolinium enhancement can identify non-ischaemic fibrosis; fat-sensitive observations alone are neither sufficiently specific nor central to modern diagnosis. Image quality, arrhythmia and partial-volume effects must be documented.

Modality	Strength	Limitation
Echo	Accessible, dynamic haemodynamics, serial follow-up	Geometry and acoustic-window dependence
CMR	Volumes, regional motion and fibrosis	Availability, artefact and device/renal considerations
ECG/Holter	Electrical phenotype and arrhythmia burden	May be intermittent or non-specific
Genetics	Aetiology and cascade testing	Variants require expert classification and counselling

Criteria and differential diagnosis

The 2020 Padua criteria broadened assessment beyond classic right-dominant disease and incorporated CMR tissue criteria. The 2024 European Task Force criteria further address clinical diagnosis and phenotype. Apply the chosen framework explicitly and avoid mixing thresholds from different systems without explanation.

Important mimics include athlete’s heart, myocarditis, cardiac sarcoidosis, dilated cardiomyopathy, congenital shunts, pulmonary hypertension and idiopathic RV outflow-tract arrhythmia. Coronary disease should be considered for LV-predominant abnormalities.

Management implications

Management belongs in an inherited-cardiac-condition and electrophysiology pathway. It includes arrhythmic risk assessment, exercise counselling, family screening, genotype interpretation and consideration of an implantable cardioverter-defibrillator. Imaging severity alone should not determine sudden-death prevention.

Selected references

Educational material only. Suspected ACM requires specialist assessment, genetic counselling where appropriate and individualised arrhythmic-risk evaluation.

Tricuspid Valve Anatomy and Stenosis: Echocardiographic Assessment and Clinical Context

Posted on September 19, 2026 by Dr. Shahzad

Audience: echocardiographers, cardiology trainees and valve teams. Evidence reviewed: September 2026.

Key message

Tricuspid stenosis is uncommon and usually coexists with regurgitation or left-sided valve disease. Diagnosis requires anatomy, haemodynamics and loading conditions to agree; a gradient alone is insufficient.

Anatomy first

The tricuspid apparatus comprises a large non-planar annulus, leaflets, chordae, papillary muscles, right ventricle and right atrium. Three-dimensional imaging often identifies anterior, posterior and septal leaflet segments more reliably than a single two-dimensional plane. Describe leaflet thickening, doming, restriction, commissural fusion, calcification, subvalvular involvement and device-lead interaction.

Causes

Rheumatic disease, often with mitral involvement.
Carcinoid heart disease.
Congenital abnormality or prior repair.
Endocarditis-related destruction or obstruction.
Device leads, intracardiac masses and rare drug-related disease.

Echocardiographic approach

Question	Method	Caution
Is the valve anatomically restricted?	Multiple 2D views; 3D en-face imaging where feasible	Do not infer stenosis from colour aliasing alone.
Is inflow obstructed?	CW Doppler aligned with tricuspid inflow; average several beats	Gradient rises with heart rate and flow.
What is the consequence?	RA size, IVC/hepatic veins, RV size/function, systemic venous congestion	Coexistent TR may dominate haemodynamics.
Is another lesion driving flow?	Full valve and shunt assessment	Pregnancy, anaemia and left-sided disease alter gradients.

Acquire CW Doppler from the window with the most parallel inflow alignment, commonly apical or parasternal RV inflow. Use a slow sweep speed and measure at end-expiration when appropriate. Average at least three beats in sinus rhythm and more in atrial fibrillation. Report heart rate with the mean gradient. Valve area by pressure half-time is less robust for the tricuspid valve and is influenced by right-sided compliance and loading.

Severity and clinical integration

Severe disease is supported by clear anatomical restriction, persistently raised mean diastolic gradient at a stated heart rate, prolonged inflow, reduced valve area where measurement is credible, right-atrial enlargement and systemic venous congestion. Discordant data should trigger image review and, when necessary, transoesophageal echo, CT, CMR or invasive haemodynamics.

The 2025 ESC/EACTS guideline recommends intervention for symptomatic severe tricuspid stenosis and supports tricuspid surgery when severe stenosis is present during left-sided valve surgery. Decisions should be made by a multidisciplinary valve team, accounting for aetiology, regurgitation, RV function, pulmonary vascular disease and operative risk.

Reporting checklist

Aetiology and leaflet/subvalvular morphology.
Mean gradient, heart rate, rhythm and number of beats averaged.
Degree and mechanism of associated TR.
RA/RV remodelling, RV systolic function and estimated right-atrial pressure.
Other valve lesions and evidence of systemic congestion.

Selected references

Educational material only. Valve-intervention decisions require specialist multidisciplinary assessment.

Right-Sided Doppler and Filling Pressures: Acquisition, Interpretation and Pitfalls

Posted on September 19, 2026 by Dr. Shahzad

Audience: echocardiographers and cardiology trainees. Evidence reviewed: September 2026.

Key message

Right-sided filling pressure cannot be read reliably from one Doppler waveform. Integrate inferior vena cava behaviour, tricuspid inflow, annular tissue Doppler, hepatic-vein flow, chamber morphology and the clinical setting.

Acquire physiology, not just traces

Record rhythm, heart rate, respiration and ventilation status. Tricuspid inflow is sampled at the leaflet tips in the apical four-chamber view. Tissue Doppler is obtained from the lateral tricuspid annulus. Hepatic-vein pulsed-wave Doppler is usually acquired from the subcostal window with a sample volume positioned within a hepatic vein, avoiding the vena caval junction.

Signal	Expected information	Major confounders
Tricuspid E and A	Early filling and atrial contribution	Age, heart rate, respiration, rhythm and significant TR
Lateral e′	Annular relaxation velocity	Regional dysfunction, tethering and translational motion
Hepatic-vein S, D and atrial reversal	Right-atrial pressure pattern and systolic forward flow	TR, AF, pacing and ventilation
IVC size and collapse	Estimate of right-atrial pressure	Mechanical ventilation, athletic physiology and abdominal pressure

How to interpret the components

Tricuspid E/A and deceleration time change with relaxation and pressure but have substantial overlap between normal and abnormal states. The E/e′ ratio on the right side has a weaker and more context-dependent relationship with right-atrial pressure than its familiar left-sided counterpart; it should not be used in isolation.

Normal hepatic-vein flow is generally systolic dominant. Reduced systolic predominance may accompany raised right-atrial pressure, but systolic flow reversal is particularly associated with severe tricuspid regurgitation. In atrial fibrillation, the atrial reversal wave disappears and beat selection becomes critical.

IVC diameter and inspiratory collapse provide a conventional estimate of right-atrial pressure in spontaneously breathing adults, but intermediate or discordant findings should prompt secondary signs rather than false precision. Mechanical ventilation invalidates simple application of spontaneous-breathing cut-offs.

Constrictive and restrictive physiology

Marked respiratory variation in atrioventricular inflow, hepatic-vein expiratory diastolic reversal, preserved or increased medial mitral e′ and septal shift can support constrictive physiology. No single sign is definitive. Technical quality, chronic obstructive pulmonary disease, volume status, rhythm and intrathoracic-pressure changes must be considered.

A practical synthesis

First decide whether the signal is technically valid.
Describe IVC findings and the assumptions used to estimate right-atrial pressure.
Assess TR severity before interpreting hepatic-vein systolic reversal.
Integrate RV size/function, septal configuration and pulmonary-pressure probability.
State uncertainty when signals conflict or ventilation/rhythm limits interpretation.

Selected references

Educational material only. Haemodynamic estimates require clinical correlation and invasive confirmation when management depends on precise pressure measurement.

Right Ventricular Size and Systolic Function: An Integrated Echocardiographic Assessment

Posted on September 19, 2026 by Dr. Shahzad

Audience: echocardiographers and cardiology clinicians. Evidence reviewed: September 2026.

Key message

The right ventricle is geometrically complex and load dependent. Its assessment should integrate size, shape, regional motion, haemodynamic context and more than one systolic-function index.

Acquisition before measurement

Use a dedicated RV-focused apical four-chamber view rather than assuming the standard apical view is adequate. Rotate and tilt until the maximal RV long axis and cavity are displayed without foreshortening. Add parasternal long- and short-axis, RV inflow, subcostal and inferior vena cava views. Record end-expiratory images when respiration materially changes dimensions.

What to report

Domain	Measures	Interpretive caution
Size	Basal, mid-cavity and longitudinal dimensions; indexed area or 3D volumes where available	Off-axis imaging can over- or underestimate size.
Longitudinal function	TAPSE and lateral tricuspid annular S′	Angle and loading dependent; may overestimate function after surgery.
Global area change	Fractional area change (FAC)	Requires accurate endocardial tracing and excludes RV outflow contribution.
Deformation	RV free-wall longitudinal strain	Vendor, tracking and loading conditions affect values.
Volumetric function	3D RV ejection fraction	Best when image quality and full-volume capture are adequate.

Core measurements

TAPSE measures longitudinal displacement of the lateral tricuspid annulus by M-mode. Tissue-Doppler S′ measures peak systolic annular velocity. FAC is calculated as (end-diastolic area − end-systolic area) / end-diastolic area × 100. Free-wall strain should exclude the septum when labelled “RV free-wall strain”; specify the convention because strain is normally reported as a negative percentage.

Thresholds are aids, not diagnoses. Current guidance should be checked for laboratory-, sex- and method-specific reference limits. Discordance is common: preserved TAPSE with reduced FAC or strain may reflect regional dysfunction, altered loading or postoperative mechanics.

Context changes interpretation

Pressure overload: look for hypertrophy, septal flattening, reduced pulmonary acceleration time and pulmonary-hypertension signs.
Volume overload: consider significant tricuspid or pulmonary regurgitation and shunts.
Acute RV pressure load: chamber size and regional patterns may be more informative than wall thickness.
Post-cardiotomy or transplant: longitudinal indices may fall despite preserved global output.
Arrhythmia: average representative beats and state the rhythm.

Common failure modes

A single normal TAPSE does not exclude RV dysfunction. A visually “normal” RV should not replace measurements when clinical decisions depend on function. Severe tricuspid regurgitation can produce apparently vigorous annular movement despite impaired effective forward performance. Poor endocardial definition should be acknowledged rather than converted into a falsely precise FAC or strain value.

Suggested report language

“The right ventricle is [normal/mildly/moderately/severely dilated]. Global systolic function is [preserved/impaired], supported by TAPSE [x] mm, lateral S′ [x] cm/s, FAC [x]% and/or free-wall strain [x]%. Interpretation is made in the context of [loading condition/rhythm/image limitation].”

Selected references

Educational material only; individual findings require clinical integration and local reference ranges.