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.

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

• Solomon SD et al. Finerenone in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2024.
• FINEARTS-HF primary publication.
• 2026 ESC guideline for acute and chronic heart failure.

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

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.

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

• International criteria for diagnosis of arrhythmogenic cardiomyopathy: the Padua criteria.
• 2024 European Task Force criteria for clinical diagnosis of arrhythmogenic cardiomyopathy.
• 2023 ESC cardiomyopathy guideline.

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

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

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

• 2025 ESC/EACTS valvular-heart-disease guideline.
• 2025 ESC/EACTS guideline—PubMed record.
• BSE guideline for tricuspid and pulmonary valve echocardiography.

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

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.

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

• ASE 2025 right-heart and pulmonary-hypertension guideline.
• BSE right-heart assessment guideline.
• 2022 ESC/ERS pulmonary-hypertension guideline.

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

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

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

• ASE 2025 right-heart and pulmonary-hypertension guideline.
• BSE practical guideline for right-heart assessment.
• ASE/EACVI chamber quantification.

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

Audience: echocardiographers, cardiology trainees and clinicians interpreting cardiac ultrasound. Evidence reviewed: September 2026.

Key message

An echocardiographic image is a physical measurement, not a photograph. Diagnostic confidence depends on understanding how pulse frequency, propagation, beam geometry, signal processing and Doppler assumptions shape what appears on screen.

Learning objectives

• Relate frequency, wavelength and propagation speed to image quality.
• Distinguish axial, lateral and elevational resolution.
• Choose pulse-repetition frequency, scale, gain and filters intelligently.
• Recognise common artefacts before they become diagnostic errors.

How the pulse becomes an image

Piezoelectric elements convert electrical energy into ultrasound and returning mechanical energy into voltage. In soft tissue, scanners assume a propagation speed of approximately 1540 m/s. Depth is estimated from round-trip travel time. Because this speed is assumed rather than measured in each tissue, speed error can misplace structures.

Wavelength equals propagation speed divided by frequency. Higher-frequency imaging shortens wavelength and generally improves resolution, but attenuation rises and penetration falls. Adult transthoracic studies therefore require a compromise: use the highest frequency that still visualises the structure of interest.

Resolution is directional

Doppler: measure the component along the beam

The Doppler shift depends on transmitted frequency, blood velocity and the cosine of the insonation angle. Alignment matters: an angle error causes velocity underestimation and the error is amplified when velocity is squared in the simplified Bernoulli equation, ΔP = 4v².

Pulsed-wave Doppler provides range specificity but aliases when the Doppler shift exceeds the Nyquist limit, equal to half the pulse-repetition frequency. Continuous-wave Doppler measures high velocities without aliasing but cannot assign them to a unique depth. Colour Doppler displays mean velocity and variance within each sample region; it is a mapping tool, not a direct measure of regurgitant severity.

Controls that change the answer

• Overall gain and time-gain compensation: optimise signal without manufacturing tissue or erasing weak boundaries.
• Depth and sector width: keep only the anatomy needed to improve frame rate.
• Focus: place at or just below the structure of interest.
• Velocity scale and baseline: adjust to the expected flow; a low colour scale increases sensitivity but also blooming.
• Wall filter: suppresses low-frequency tissue motion but can remove genuine low-velocity flow.
• Dynamic range: changes contrast; excessive compression can conceal subtle boundaries.

Artefacts worth naming

Reverberation creates repeated interfaces; acoustic shadowing follows strongly attenuating structures; mirror artefact duplicates anatomy across a strong reflector; side lobes and grating lobes place off-axis reflectors in the main beam; refraction may duplicate or laterally displace anatomy. Confirm a suspected mass, defect or dissection plane in orthogonal views and with altered transducer position and settings.

A disciplined optimisation sequence

Begin with the clinical question. Select the window and frequency, minimise depth and sector width, position the focus, then adjust gain and compression. For Doppler, align the beam, choose the correct modality, optimise scale and sweep speed, and record several representative beats—more when rhythm or respiration varies. Measurements should follow current chamber and valve standards rather than a visually attractive but non-standard view.

Selected references

• ASE: comprehensive adult transthoracic echocardiography guideline.
• British Society of Echocardiography protocols and guidelines.
• ASE/EACVI chamber-quantification recommendations.

Educational material only. Apply local protocols, equipment-specific guidance and specialist review to individual patients.

Audience: cardiology trainees, sonographers and clinicians interpreting adult echocardiography.
Evidence reviewed: 19 September 2026.

Key message: echocardiography estimates the probability and consequences of pulmonary hypertension (PH). It does not establish PH from a single pulmonary artery systolic pressure cut-off. Right-heart catheterisation (RHC) remains the reference method when haemodynamic confirmation will affect management.

Learning objectives

• Acquire and interpret peak tricuspid-regurgitation velocity correctly.
• Combine TR velocity with supporting signs from the ventricles, pulmonary artery and IVC/right atrium.
• Estimate RV systolic pressure while recognising major sources of error.
• Report RV adaptation and likely aetiology, not pressure alone.

Start with the invasive definition

The 2022 ESC/ERS definition of PH is a resting mean pulmonary artery pressure above 20 mmHg measured at RHC. Classification additionally requires pulmonary arterial wedge pressure and pulmonary vascular resistance. An echo-derived PASP cannot replace these measurements.

1. Measure peak TR velocity

Use continuous-wave Doppler from multiple windows, including the RV-focused apical four-chamber, parasternal RV inflow, parasternal short-axis and subcostal views where useful. Record the highest complete, well-aligned envelope. Do not trace artefact, excessive spectral broadening, an incomplete envelope or a post-ectopic beat.

In sinus rhythm, use representative beats. In atrial fibrillation or marked beat-to-beat variation, average five to seven suitable beats acquired under comparable loading conditions. A weak or absent TR signal does not exclude PH.

2. Determine echocardiographic probability

The BSE probability algorithm uses peak TR velocity as its first branch. A peak velocity above 3.4 m/s supports high probability. A velocity at or below 2.8 m/s supports low probability only when additional PH signs are absent. Intermediate values require supporting evidence. The 2025 ASE guideline similarly emphasises an integrated approach rather than fixed PASP severity bands.

Use findings from more than one domain. No single adjunctive sign is diagnostic in isolation.

3. Estimate RV systolic pressure carefully

When there is no RVOT or pulmonary-valve obstruction:

RVSP = 4 × (peak TR velocity)² + estimated right-atrial pressure

If peak TR velocity is 3.0 m/s and estimated RAP is 15 mmHg, RVSP is 4 × 9 + 15 = 51 mmHg. Report this as an estimate. Do not label PH mild, moderate or severe from fixed PASP bands.

RAP estimation is less reliable with positive-pressure ventilation, raised intra-abdominal pressure, pregnancy, athletic remodelling, severe TR and poor subcostal imaging.

Important pitfalls

• Underestimation: poor alignment, incomplete envelope, weak TR, advanced RV failure, severe free-flowing TR or early RV–RA pressure equalisation.
• Overestimation: tracing noise, excessive gain, spectral broadening, a post-ectopic beat or an incorrect RAP estimate.
• RVSP approximates PASP only when there is no obstruction between the RV and pulmonary artery.
• An ultrasound-enhancing agent may improve a weak envelope, but overgaining creates a falsely traceable signal.

Assess the RV and seek the cause

Report RV geometry, basal diameter, wall thickness where relevant, TAPSE, lateral S′, FAC, RV free-wall strain when available, RA size, TR mechanism/severity and pericardial effusion. Consider left-heart disease, valve disease, congenital shunt, lung disease/hypoxia, chronic thromboembolic disease, pulmonary arterial hypertension and mixed causes.

Suggested report

Peak TR velocity is 3.2 m/s. RV dilatation, systolic septal flattening and a dilated IVC with reduced inspiratory collapse indicate a high echocardiographic probability of pulmonary hypertension. RV systolic function is reduced by FAC and RV free-wall strain. Clinical correlation and specialist assessment are advised. Consider RHC if confirmation and haemodynamic classification will alter management.

References

1. Mukherjee M, et al. ASE right-heart and PH guideline. JASE. 2025;38:141–186.
2. Humbert M, et al. 2022 ESC/ERS PH guideline. Eur Heart J. 2022;43:3618–3731.
3. Augustine DX, et al. BSE PH protocol. Echo Res Pract. 2018;5:G11–G24.
4. Zaidi A, et al. BSE right-heart guideline. Echo Res Pract. 2020;7:G19–G41.

Educational content for clinicians. It does not replace patient-specific assessment, local protocols or specialist advice.