Skip to main content
MedVellum
QuestionsVideosPricing

MedVellum

Fellowship exam preparation across every specialty: source-verified topics, questions in every format, and videos.

Product

  • Specialties
  • Questions
  • Videos
  • Exam tools
  • Pricing

Verification & policy

  • Verified register
  • Editorial policy
  • Privacy
  • Terms

Account

  • Sign in
  • Create account
  • Dashboard
  • Account & billing

© 2026 MedVellum. For education only — not a substitute for clinical judgement.

llms.txtPsychiatry LLM catalogSitemap

Cardio Topicsimaging-noninvasive

Cardio · imaging-noninvasive

Echo valve quantitation: areas, gradients, regurgitation grades

Fellowship-level guide to grading valve disease on echocardiography under the 2025 ESC/EACTS and 2020 ACC/AHA valvular heart disease guidelines: the ACC/AHA 2020 stage tables for aortic stenosis, aortic regurgitation, mitral stenosis, primary and secondary mitral regurgitation and tricuspid regurgitation; the ESC/EACTS 2025 concordant and discordant aortic stenosis categories, dobutamine stress echocardiography and CT calcium scoring; mixed valve disease; prosthetic valve deterioration criteria; and the measurement pitfalls both guidelines name.

high6 referencesUpdated 9 Oct 202653 min readVerification in progress

Practise this topic

  • SAQ
  • Case

Your progress

Saved on this device.

Practise this topic

  • Short-answer question1
  • Clinical case1

Target exams

  • EECC
  • ABIM Cardiovascular Disease Certification

Red flags

  • In symptomatic severe AS (Stage D1, aortic velocity ≥4.0 m/s or mean pressure gradient ≥40 mm Hg), exercise testing should not be performed because of the risk of severe haemodynamic compromise (ACC/AHA 2020, COR 3: Harm, LOE B-NR)
  • Small-AVA, low-gradient AS with preserved LVEF: measurement errors, uncontrolled blood pressure and conditions lowering stroke volume are frequent explanations other than severe AS and must be carefully excluded (ESC/EACTS 2025 Recommendation Table 4, footnote c)
  • Chronic severe AR requires evidence of LV dilation as well as the severe haemodynamic criteria (ACC/AHA 2020 Table 15, Stages of Chronic AR, Stages C and D)
  • In secondary MR, PISA measured by 2D TTE underestimates the true ERO because of the crescentic shape of the proximal convergence (ACC/AHA 2020 Table 18 footnote)
On this page
Study tools

Your progress

Saved on this device.

Practise this topic

  • Short-answer question1
  • Clinical case1

Target exams

  • EECC
  • ABIM Cardiovascular Disease Certification

Red flags

  • In symptomatic severe AS (Stage D1, aortic velocity ≥4.0 m/s or mean pressure gradient ≥40 mm Hg), exercise testing should not be performed because of the risk of severe haemodynamic compromise (ACC/AHA 2020, COR 3: Harm, LOE B-NR)
  • Small-AVA, low-gradient AS with preserved LVEF: measurement errors, uncontrolled blood pressure and conditions lowering stroke volume are frequent explanations other than severe AS and must be carefully excluded (ESC/EACTS 2025 Recommendation Table 4, footnote c)
  • Chronic severe AR requires evidence of LV dilation as well as the severe haemodynamic criteria (ACC/AHA 2020 Table 15, Stages of Chronic AR, Stages C and D)
  • In secondary MR, PISA measured by 2D TTE underestimates the true ERO because of the crescentic shape of the proximal convergence (ACC/AHA 2020 Table 18 footnote)
Key answer
  • ESC/EACTS 2025: comprehensive TTE is the first-line examination to confirm valve dysfunction and determine its aetiology, mechanism and severity; quantitative analysis (as opposed to visual) should be the goal, and severity should be assessed with an integrative approach of all criteria checked for consistency.[1]
  • Aortic stenosis (ACC/AHA 2020 Table 13): in Stages C1, C2 and D1, severe AS is an aortic Vmax ≥4 m/s or mean ΔP ≥40 mm Hg, and in C1 and C2 AVA is typically ≤1.0 cm² but not required to define severe AS; the low-gradient Stages D2 and D3 have their own criteria. ESC/EACTS 2025 calls the mean pressure gradient the most robust parameter.[2][1]
  • Discordant AS (ESC/EACTS 2025): AS may be further categorised by flow state based on SVi, with 35 mL/m² conventionally accepted to discern low from normal flow; in low-flow, low-gradient AS with reduced LVEF, DSE can help to discriminate pseudo-severe from true severe AS in the presence of flow reserve (increase in stroke volume of ≥20%).[1]
  • CT calcium score for severe AS: ESC/EACTS 2025 says >2000 AU in men and >1200 AU in women indicate severe AS with high sensitivity and specificity (∼85%); ACC/AHA 2020 gives sex-specific thresholds of 1300 in women and 2000 in men.[1][3]
  • Severe regurgitation (ACC/AHA 2020): the severe AR criteria in Table 15 include vena contracta >0.6 cm, regurgitant volume ≥60 mL/beat, regurgitant fraction ≥50% and ERO ≥0.3 cm², and diagnosis of chronic severe AR requires evidence of LV dilation; severe primary MR in Table 17 includes vena contracta ≥0.7 cm, ERO ≥0.40 cm² and regurgitant volume ≥60 mL, with a footnote that not all criteria for each category will be present in each patient; severe TR in Table 20 includes vena contracta width ≥0.7 cm, ERO ≥0.40 cm² and regurgitant volume ≥45 mL.[2]
  • Secondary MR: ESC/EACTS 2025 says an EROA of ≥30 mm² and/or an RVol of ≥45 mL has been identified as having a significant impact on outcomes; the ACC/AHA 2020 text defines severe secondary MR as an ERO ≥40 mm², adding that outcome studies have shown poor prognosis with moderate MR (ERO ≥20 mm²).[1][3]
  • Mitral stenosis: for rheumatic MS, ESC/EACTS 2025 says an MVA of ≤1.5 cm² in conjunction with clinical factors (symptoms, high risk of thromboembolism, or haemodynamic decompensation) is indicative of clinically severe MS; ACC/AHA 2020 Table 16 uses mitral valve area ≤1.5 cm² for Stages C and D.[1][2]
  • Prosthetic valves: ESC/EACTS 2025 Table 12 gives criteria for the diagnosis of moderate or severe haemodynamic deterioration of aortic and mitral biological valves with SVD or non-structural valve dysfunction (except PVL or PPM)ᵃ/ᵇ, thrombosis, or endocarditis, where footnote ᵃ (aortic row) is obstruction by pannus; dilatation of the aortic root after stentless BHV; or AV-sparing operations, and footnote ᵇ (mitral row) is leaflet entrapment by pannus, chordae, or suture; its aortic EOA and DVI criteria are measured against the echo performed 1–3 months after the procedure.[1]

This page is about the numbers: how each valve lesion is graded on echocardiography under ESC/EACTS 2025 and ACC/AHA 2020, where the measurements mislead, and what to do when they disagree.[1][3] Treatment decisions live in Severe aortic stenosis: TAVI versus surgical valve replacement, Asymptomatic severe aortic stenosis: exercise testing and surgery triggers, Aortic regurgitation: quantitation and surgery timing, Mitral regurgitation: primary and secondary and Prosthetic heart valves: choice, anticoagulation and thrombosis.

How severity is graded

Start with the machine and the person holding the probe. ESC/EACTS 2025 says comprehensive TTE is the first-line examination to confirm valve dysfunction, and determine the aetiology, mechanism and severity of VHD, as well as cardiac chamber anatomy and damage.[1] ACC/AHA 2020 says TTE is the standard diagnostic test in the initial evaluation of patients with known or suspected VHD.[3]

  • Quantify (ESC/EACTS 2025): quantitative imaging analysis (as opposed to visual) should be the goal in all patients with relevant VHD, complemented by qualitative and semi-quantitative evaluation.[1]
  • Integrate (ESC/EACTS 2025): the severity of VHD should be assessed using an integrative approach of all criteria checked for consistency.[1]
  • Stenotic lesions (ACC/AHA 2020): key measurements are maximum velocity, mean gradient and valve area.[3]
  • Regurgitant lesions (ACC/AHA 2020): regurgitant orifice area, volume and fraction are calculated, when possible in the context of a multiparameter severity grade based on colour Doppler imaging, continuous- and pulsed-wave Doppler recordings, and the presence or absence of distal flow reversals.[3]
  • LV measures (ACC/AHA 2020): decisions are most robust when based on sequential studies, given the inherent measurement variability of LV dimensions, volumes and LVEF.[3]
  • Expertise (ACC/AHA 2020): both the performance and interpretation of these tests require meticulous attention to detail, as well as expertise in cardiac imaging and evaluation of haemodynamics.[3]

When TTE is not enough, ESC/EACTS 2025 says TOE and/or additional imaging should be applied when TTE is of poor quality or inconclusive (e.g. calcium scoring and anatomy of the valve using CCT).[1] ESC/EACTS 2025 gives TOE a central diagnostic role in specific clinical scenarios, e.g. thrombosis, prosthetic valve dysfunction, endocarditis, mitral stenosis, and assessment of MV or TV anatomy.[1] In regurgitant lesions, particularly AR, ESC/EACTS 2025 says CMR has gained key value in clinical practice.[1]

The ACC/AHA 2020 stages

ACC/AHA 2020 bases severity on multiple criteria, including symptoms, valve anatomy, valve haemodynamics, and the effects of valve dysfunction on ventricular and vascular function (e.g. end-organ damage).[3] ACC/AHA 2020 provides a classification of the progression of VHD with 4 stages (A to D), set out in its Table 4.[2]

ACC/AHA 2020 Table 4. Stages of VHD

StageDefinitionDescription
AAt riskPatients with risk factors for development of VHD
BProgressivePatients with progressive VHD (mild to moderate severity and asymptomatic)
CAsymptomatic severeAsymptomatic patients who have the criteria for severe VHD: C1: asymptomatic patients with severe VHD in whom the LV or RV remains compensated; C2: asymptomatic patients with severe VHD with decompensation of the LV or RV
DSymptomatic severePatients who have developed symptoms as a result of VHD
[2]

ACC/AHA 2020 adds a caveat worth quoting at the viva: severity is a continuous variable, and the stages simply provide a framework, or starting point.[3] Some patients will have symptoms or end-organ damage with haemodynamics that do not quite meet the severity criteria, and numerical measures may not match exactly across all categories.[3] Conversely, other patients may remain asymptomatic without obvious end-organ damage despite apparently severe VHD.[3]

Aortic stenosis: velocity, gradient and valve area

ACC/AHA 2020 names the three key measurements for decisions in AS: the maximum aortic velocity, the mean pressure gradient (calculated with the Bernoulli equation) and the valve area (calculated with the continuity equation).[3] ESC/EACTS 2025 grades on the same three, and calls the mean pressure gradient the most robust parameter.[1] Although AVA is theoretically the ideal parameter, ESC/EACTS 2025 says there are numerous technical limitations associated with its calculation.[1]

ACC/AHA 2020 Table 13. Stages of AS

StageDefinitionValve anatomyValve haemodynamicsHaemodynamic consequencesSymptoms
AAt risk of ASBAV (or other congenital valve anomaly); aortic valve sclerosisAortic Vmax <2 m/s with normal leaflet motionNoneNone
BProgressive ASMild to moderate leaflet calcification/fibrosis of a bicuspid or trileaflet valve with some reduction in systolic motion; or rheumatic valve changes with commissural fusionMild AS: aortic Vmax 2.0–2.9 m/s or mean ΔP <20 mm Hg; moderate AS: aortic Vmax 3.0–3.9 m/s or mean ΔP 20–39 mm HgEarly LV diastolic dysfunction may be present; normal LVEFNone
C: Asymptomatic severe AS
C1Asymptomatic severe ASSevere leaflet calcification/fibrosis or congenital stenosis with severely reduced leaflet openingAortic Vmax ≥4 m/s or mean ΔP ≥40 mm Hg; AVA typically is ≤1.0 cm² (or AVAi 0.6 cm²/m²) but not required to define severe AS; very severe AS is an aortic Vmax ≥5 m/s or mean P ≥60 mm HgLV diastolic dysfunction; mild LV hypertrophy; normal LVEFNone; exercise testing is reasonable to confirm symptom status
C2Asymptomatic severe AS with LV systolic dysfunctionSevere leaflet calcification/fibrosis or congenital stenosis with severely reduced leaflet openingAortic Vmax ≥4 m/s or mean ΔP ≥40 mm Hg; AVA typically ≤1.0 cm² (or AVAi 0.6 cm²/m²) but not required to define severe ASLVEF <50%None
D: Symptomatic severe AS
D1Symptomatic severe high-gradient ASSevere leaflet calcification/fibrosis or congenital stenosis with severely reduced leaflet openingAortic Vmax ≥4 m/s or mean ΔP ≥40 mm Hg; AVA typically ≤1.0 cm² (or AVAi ≤0.6 cm²/m²) but may be larger with mixed AS/ARLV diastolic dysfunction; LV hypertrophy; pulmonary hypertension may be presentExertional dyspnoea, decreased exercise tolerance, or HF; exertional angina; exertional syncope or presyncope
D2Symptomatic severe low-flow, low-gradient AS with reduced LVEFSevere leaflet calcification/fibrosis with severely reduced leaflet motionAVA ≤1.0 cm² with resting aortic Vmax <4 m/s or mean ΔP <40 mm Hg; dobutamine stress echocardiography shows AVA <1.0 cm² with Vmax ≥4 m/s at any flow rateLV diastolic dysfunction; LV hypertrophy; LVEF <50%HF; angina; syncope or presyncope
D3Symptomatic severe low-gradient AS with normal LVEF or paradoxical low-flow severe ASSevere leaflet calcification/fibrosis with severely reduced leaflet motionAVA ≤1.0 cm² (indexed AVA ≤0.6 cm²/m²) with an aortic Vmax <4 m/s or mean ΔP <40 mm Hg AND stroke volume index <35 mL/m²; measured when patient is normotensive (systolic blood pressure <140 mm Hg)Increased LV relative wall thickness; small LV chamber with low stroke volume; restrictive diastolic filling; LVEF ≥50%HF; angina; syncope or presyncope
[2] [3]

Read the AVA cells carefully: in Stages C1 and C2 the table says AVA is typically ≤1.0 cm² but not required to define severe AS, and in D1 it may be larger with mixed AS/AR.[2] Velocity or gradient defines the high-gradient stages; the low-gradient stages D2 and D3 need the extra criteria in their rows.[2]

[2]

The ACC/AHA 2020 diagnostic rows for AS

  • ACC/AHA 2020, COR 1, LOE A: in patients with signs or symptoms of AS or a BAV, TTE is indicated for accurate diagnosis of the cause of AS, assessment of haemodynamic severity, measurement of LV size and systolic function, and determination of prognosis and timing of valve intervention.[3]
  • ACC/AHA 2020, COR 1, LOE B-NR: in suspected low-flow, low-gradient severe AS with normal LVEF (Stage D3), optimisation of blood pressure control is recommended before measurement of AS severity by TTE, TEE, cardiac catheterisation or CMR.[3]
  • ACC/AHA 2020, COR 2a, LOE B-NR: in suspected low-flow, low-gradient severe AS with reduced LVEF (Stage D2), low-dose dobutamine stress testing with echocardiographic or invasive haemodynamic measurements is reasonable to further define severity and assess contractile reserve.[3]
  • ACC/AHA 2020, COR 2a, LOE B-NR: in suspected low-flow, low-gradient severe AS with normal or reduced LVEF (Stages D2 and D3), calculation of the ratio of the outflow tract to aortic velocity is reasonable to further define severity.[3]
  • ACC/AHA 2020, COR 2a, LOE B-NR: in suspected low-flow, low-gradient severe AS with normal or reduced LVEF (Stages D2 and D3), measurement of the aortic valve calcium score by CT imaging is reasonable to further define severity.[3]

The velocity ratio

The velocity ratio sidesteps the outflow tract diameter (area) measurement.[3] ACC/AHA 2020 says the outflow tract–to–aortic velocity ratio is independent of body size and eliminates potential errors in calculated valve area related to measurement of LV outflow tract diameter or area.[3] A normal ratio is close to 1.0; a ratio of ≤0.25 corresponds to a valve area 25% of normal for that patient, which is consistent with severe AS and is a predictor of symptom onset and adverse outcomes.[3] ESC/EACTS 2025 describes the ratio of the LVOT to the AV Doppler jet VTI as not requiring calculation of LVOT area, and says it may assist evaluation when other parameters are equivocal (<0.25 suggests that severe AS is highly likely).[1]

Where AS measurements go wrong

  • Missed alignment or poor images (ACC/AHA 2020): severity of AS may be underestimated if image quality is poor or if a parallel intercept angle is not obtained between the ultrasound beam and aortic jet.[3]
  • Hypertension at the scan (ACC/AHA 2020): measurements made when the patient is hypertensive may underestimate or, less often, overestimate stenosis severity; hypertension imposes a second pressure load that lowers forward stroke volume and transaortic gradient.[3]
  • Repeat when controlled (ACC/AHA 2020): if results indicate only moderate stenosis but were recorded when the patient was hypertensive, repeat measurements when blood pressure is better controlled ensure that a diagnosis of severe AS is not missed.[3]
  • Figure 6 legend note a (ESC/EACTS 2025 Figure 6, integrative imaging assessment of patients with aortic stenosis): in particular, verify LVOT diameter and multiwindow Doppler interrogation.[1]
  • Bedside examination (ACC/AHA 2020): in adult patients, physical examination may not be accurate for diagnosis of and assessment of severity of AS.[3]

Other AS measures

  • Progression (ACC/AHA 2020): with moderate AS (aortic velocity 3.0–3.9 m/s), the average annual rate of progression is an increase in velocity of 0.3 m/s, an increase in mean pressure gradient of 7 mm Hg and a decrease in valve area of 0.1 cm².[3]
  • Aortic sclerosis (ACC/AHA 2020): defined as focal areas of valve calcification and leaflet thickening with an aortic velocity <2.0 m/s; progression to severe AS occurs in about 10% of patients within 5 years.[3]
  • GLS (ESC/EACTS 2025): assessment of GLS can be useful for risk stratification, and a threshold of −15% may contribute to identifying patients with severe asymptomatic AS at increased risk of clinical deterioration or premature mortality.[1]
  • Valvuloarterial impedance (ESC/EACTS 2025): the estimated value has been shown to be prognostic of adverse clinical outcomes before and after valve replacement.[1]
  • TOE (ESC/EACTS 2025): allows morphological evaluation of the valve, planimetry of AVA and assessment of potential subvalvular obstruction (unless there is acoustic shadowing caused by calcification), and evaluation of concomitant valve disease.[1]
  • Exercise echocardiography (ESC/EACTS 2025): may provide additional prognostic information by assessing the increase in mean pressure gradient and change in LV function.[1]
  • Exercise haemodynamics (ACC/AHA 2020): recording aortic valve haemodynamics with exercise is of limited value and does not show additive value for predicting outcome when baseline severity and functional status are considered.[3]

Discordant aortic stenosis: the low-gradient pathway

The classic trap is a small valve area with a gradient that does not match.[1] ESC/EACTS 2025 says AS may be further categorised according to flow state based on SVi when there is discordance between echocardiographic parameters.[1] A threshold of 35 mL/m² is conventionally accepted to discern low from normal flow, although sex-specific thresholds have been proposed.[1]

ESC/EACTS 2025 concordant and discordant AS criteria (Section 8.2.1), with what Sections 8.2.1 and 8.4.1 say about each

Category (ESC/EACTS 2025)DefinitionWhat the guideline says about it
High-gradient AS (concordant)Mean gradient ≥40 mmHg, Vmax ≥4.0 m/s, AVA ≤1 cm² (or ≤0.6 cm²/m²)Section 8.2.1: considered severe irrespective of LV function and flow conditions
Low-flow, low-gradient AS with reduced LVEF (discordant)Mean gradient <40 mmHg, AVA ≤1 cm², SVi ≤35 mL/m², LVEF <50%Section 8.4.1 (symptomatic severe AS): reduced LV function usually improves after intervention if it is predominantly caused by excessive afterload; improvement is unlikely if the primary cause is fibrosis due to myocardial infarction or cardiomyopathy
Low-flow, low-gradient AS with preserved LVEF (discordant)Mean gradient <40 mmHg, AVA ≤1 cm², SVi ≤35 mL/m², LVEF ≥50%Section 8.4.1 (symptomatic severe AS): outcomes are improved with intervention (either TAVI or SAVR) compared with medical treatment alone; intervention should therefore be considered in patients with symptoms after careful confirmation that AS is severe
Normal-flow, low-gradient AS with preserved EF (discordant)Mean gradient <40 mmHg, AVA ≤1 cm², SVi >35 mL/m², LVEF ≥50%Section 8.2.1: patients usually have moderate stenosis. Section 8.4.1 (symptomatic severe AS): prognosis is similar to that of moderate AS
Discordant high-gradient ASMean gradient ≥40 mmHg, AVA >1 cm²Section 8.2.1: considered severe if not caused by a reversible high-flow status
[1] [1]

ESC/EACTS 2025 considers discordant high-gradient AS severe if it is not caused by a reversible high-flow status.[1] The legend of ESC/EACTS 2025 Figure 6 (integrative imaging assessment of patients with aortic stenosis) says high flow may be reversible (anaemia, hyperthyroidism, or arteriovenous fistulae).[1] The same legend gives the upper limit of normal flow using pulsed Doppler as cardiac index 4.3 L/min/m² and SVi 58 mL/m².[1]

Dobutamine stress echocardiography

ESC/EACTS 2025 says that in low-flow, low-gradient AS with reduced LVEF, dobutamine stress echocardiography can help to discriminate between pseudo-severe and true severe AS in the presence of flow reserve (an increase in stroke volume of ≥20%). ACC/AHA 2020 (COR 2a, LOE B-NR) calls low-dose dobutamine stress testing with echocardiographic or invasive haemodynamic measurements reasonable in suspected low-flow, low-gradient severe AS with reduced LVEF (Stage D2) to further define severity and assess contractile reserve.[1][3] ACC/AHA 2020 says patients with severe AS and LVEF <50% present with an aortic valve area <1.0 cm² but a low velocity and gradient (velocity <4 m/s or mean gradient <40 mm Hg) at rest.[3] It adds that in these patients, severe AS with LV systolic dysfunction attributable to afterload mismatch must be distinguished from primary myocardial dysfunction with only moderate AS.[3] Dobutamine stress echocardiography may be useful, measuring aortic velocity (or mean pressure gradient) and valve area at baseline and at higher flow rates.[3] The ACC/AHA 2020 text gives the maximum dose of dobutamine as 20 mcg/kg per minute, under appropriate clinical and haemodynamic monitoring.[3]

  • True severe AS (ACC/AHA 2020): a fixed valve area, with transaortic velocity rising to ≥4 m/s (mean gradient ≥40 mm Hg) at any flow rate, but with valve area remaining ≤1.0 cm².[3]
  • Moderate AS with primary LV dysfunction (ACC/AHA 2020): the valve area increases as volume flow rate increases, with only a modest increase in transaortic velocity or gradient.[3]
  • No flow reserve (ACC/AHA 2020): some patients fail to show an increase in stroke volume ≥20% with dobutamine, referred to as "lack of contractile reserve" or "lack of flow reserve".[3]
  • Flow reserve (ESC/EACTS 2025): in low-flow, low-gradient AS with reduced LVEF, DSE can help to discriminate between pseudo-severe and true severe AS in the presence of flow reserve (increase in stroke volume of ≥20%).[1]
  • Figure 6 legend note d (ESC/EACTS 2025): flow reserve is a ≥20% increase in stroke volume in response to low-dose dobutamine, or if the change in stroke volume is 10%–20%, calculate projected AVA.[1]

In its section on symptomatic severe AS, ESC/EACTS 2025 adds that in low-flow, low-gradient AS with reduced LVEF the absence of flow reserve is associated with increased surgical and long-term mortality.[1] Even so, it says both modes of intervention improved LVEF and clinical outcomes in observational studies.[1]

CT aortic valve calcium score

ESC/EACTS 2025 says CCT calcium AV scoring is readily available and provides important adjunctive information in low-flow, low-gradient AS, because it correlates with haemodynamic severity, progression and clinical outcomes.[1] ACC/AHA 2020 says quantitation of aortic valve calcium by CT is especially useful in low-flow, low-gradient AS of unclear severity with either a normal or reduced LVEF.[3]

Aortic valve calcium score thresholds, by guideline

SourceMenWomenWhat the source says
ESC/EACTS 2025: indicates severe AS>2000 AU>1200 AUHigh sensitivity and specificity (∼85%)
ESC/EACTS 2025: higher thresholds>3000 AU>1600 AUVery specific
ESC/EACTS 2025: severe AS unlikely<1600 AU<800 AUSevere AS becomes unlikely below these values
ACC/AHA 2020: thresholds for diagnosis of severe AS20001300Sex-specific Agatston unit thresholds; they reflect the contribution of leaflet fibrosis, in addition to calcification, to leaflet stiffness in women
[1] [3] [3] [1]

A low score does not settle every valve.[1] ESC/EACTS 2025 says cautious interpretation is required in patients who can develop severe AS without pronounced AV calcification, such as in BAV, concomitant amyloidosis, and predominantly fibrotic stenosis associated with post-rheumatic, radiation-induced and inflammatory disease.[1]

Putting the tests together

  • Complementary (ESC/EACTS 2025): in low-flow, low-gradient AS with reduced LVEF, CCT AV calcium scoring and DSE provide complementary information.[1]
  • If findings are equivocal (ESC/EACTS 2025): an integrated assessment considering all available clinical, morphological and haemodynamic factors is required.[1]
  • Invasive (ESC/EACTS 2025): in exceptional cases with unclear AS severity, right heart catheterisation can be combined with measurements of the transaortic gradients, allowing estimation of AVA; LV catheterisation is not recommended unless there are symptoms and signs of severe AS and non-invasive investigations are inconclusive.[1]
  • Invasive (ACC/AHA 2020): when non-invasive data are non-diagnostic or discrepant with the clinical evaluation, catheterisation can be helpful; aortic valve area is calculated with the Gorlin formula using a Fick or thermodilution cardiac output.[3]

Three further notes from the ESC/EACTS 2025 Figure 6 legend (integrative imaging assessment of patients with aortic stenosis) are quoted here as the legend gives them.[1]

  • Figure 6 legend note c (ESC/EACTS 2025): available evidence refers to patients with preserved LVEF; check for bradycardia or uncontrolled hypertension, which may lead to prolonged ejection time and reduced flow rate; depending on symptoms, integrated assessment complemented by CCT AV calcium scoring may be pursued.[1]
  • Figure 6 legend note e (ESC/EACTS 2025): if one test is not conclusive, complement diagnostics with the other test.[1]
  • Figure 6 legend note f (ESC/EACTS 2025): based on clinical judgement (typical symptoms without other explanation), morphological valve changes, LV hypertrophy (in absence of coexistent hypertension), and consistent findings using different modes of assessment [TTE and TOE, invasive assessment, AV planimetry by CT or MRI (cut-off 1.2 cm²)].[1]

What the grade triggers (ESC/EACTS 2025 Recommendation Table 4, selected group)

ESC/EACTS 2025 Recommendation Table 4 gives recommendations on indications for intervention in symptomatic and asymptomatic severe aortic stenosis, and the recommended mode of intervention.[1] These are its three rows under the group heading "Symptomatic patients with severe aortic stenosis"; the table's asymptomatic and mode-of-intervention rows are covered in the AS treatment topics.[1]

  • ESC/EACTS 2025, Class I, Level B: intervention is recommended in symptomatic patients with severe, high-gradient AS [mean gradient ≥40 mmHg, Vmax ≥4.0 m/s, AVA ≤1.0 cm² (or ≤0.6 cm²/m² BSA)].[1]
  • ESC/EACTS 2025, Class I, Level B: intervention is recommended in symptomatic patients with low-flow (SVi ≤35 mL/m²), low-gradient (<40 mmHg) AS with reduced LVEF (<50%) after careful confirmation that AS is severe.[1]
  • ESC/EACTS 2025, Class IIa, Level B: intervention should be considered in symptomatic patients with low-flow (SVi ≤35 mL/m²), low-gradient (<40 mmHg) AS with normal LVEF (≥50%) after careful confirmation that AS is severe.[1]
  • Footnote c to that row: explanations (such as measurement errors, uncontrolled blood pressure, and conditions lowering the stroke volume) other than severe AS for a small AVA but low gradient despite preserved LVEF are frequent and must be carefully excluded.[1]

For patients with heart failure, ESC 2026 HF Recommendation Table 17 recommends aortic valve intervention, SAVR or TAVI, in severe aortic stenosis and HF to improve symptoms and reduce the risk of death (Class I, Level B1).[5] The ESC 2026 HF footnote says the row refers to severe high-gradient AS regardless of LVEF and to low-flow, low-gradient AS with HFrEF.[5] For low-flow, low-gradient AS in HFpEF, ESC 2026 HF refers back to the 2025 ESC/EACTS valvular heart disease guideline.[5]

In its section on symptomatic severe AS, the ESC/EACTS 2025 text says that for low-flow, low-gradient AS with reduced LVEF, intervention is recommended when severe AS is confirmed by CCT (calcium scoring) or stress echocardiography, while patients with pseudo-severe AS should receive GDMT.[1] In the same section, for normal-flow, low-gradient AS with preserved LVEF, it recommends regular clinical and echocardiographic surveillance unless multimodality diagnostic evaluation clearly suggests severe AS.[1] Timing in the asymptomatic patient is covered in Asymptomatic severe aortic stenosis: exercise testing and surgery triggers, and the choice between TAVI and SAVR in Severe aortic stenosis: TAVI versus surgical valve replacement.

Stress testing: dobutamine is not exercise
  • ACC/AHA 2020: in symptomatic patients with severe AS (Stage D1, aortic velocity ≥4.0 m/s or mean pressure gradient ≥40 mm Hg), exercise testing should not be performed because of the risk of severe haemodynamic compromise (COR 3: Harm, LOE B-NR).[3]
  • ACC/AHA 2020: in asymptomatic patients with severe AS (Stage C1), exercise testing is reasonable to assess physiological changes with exercise and to confirm the absence of symptoms (COR 2a, LOE B-NR).[3]
  • The ACC/AHA 2020 dobutamine row is a different test in a different stage: low-dose dobutamine stress testing with echocardiographic or invasive haemodynamic measurements is reasonable in suspected low-flow, low-gradient severe AS with reduced LVEF (Stage D2) to further define severity and assess contractile reserve (COR 2a, LOE B-NR).[3]

Aortic regurgitation

ESC/EACTS 2025 lists what a stepwise AR evaluation should address: the severity of AR, its mechanism and aetiology, the haemodynamic impact on LV function and pulmonary pressure, and the ascending aorta.[1] ESC/EACTS 2025 says TTE assessment of AR severity follows an integrative approach considering qualitative, semi-quantitative and quantitative parameters, but remains challenging.[1] Echocardiography is the first-line modality, while CMR and CCT are more accurate for the measurement of specific parameters.[1]

ACC/AHA 2020 Table 15. Stages of Chronic AR

StageDefinitionValve anatomyValve haemodynamicsHaemodynamic consequencesSymptoms
AAt risk of ARBAV (or other congenital valve anomaly); aortic valve sclerosis; diseases of the aortic sinuses or ascending aorta; history of rheumatic fever or known rheumatic heart disease; IEAR severity: none or traceNoneNone
BProgressive ARMild to moderate calcification of a trileaflet valve BAV (or other congenital valve anomaly); dilated aortic sinuses; rheumatic valve changes; previous IEMild AR: jet width <25% of LVOT; vena contracta <0.3 cm; regurgitant volume <30 mL/beat; regurgitant fraction <30%; ERO <0.10 cm²; angiography grade 1. Moderate AR: jet width 25%–64% of LVOT; vena contracta 0.3–0.6 cm; regurgitant volume 30–59 mL/beat; regurgitant fraction 30% to 49%; ERO 0.10–0.29 cm²; angiography grade 2Normal LV systolic function; normal LV volume or mild LV dilationNone
CAsymptomatic severe ARCalcific aortic valve disease; bicuspid valve (or other congenital abnormality); dilated aortic sinuses or ascending aorta; rheumatic valve changes; IE with abnormal leaflet closure or perforationSevere AR: jet width ≥65% of LVOT; vena contracta >0.6 cm; holodiastolic flow reversal in the proximal abdominal aorta; regurgitant volume ≥60 mL/beat; regurgitant fraction ≥50%; ERO ≥0.3 cm²; angiography grade 3 to 4. In addition, diagnosis of chronic severe AR requires evidence of LV dilationC1: normal LVEF (>55%) and mild to moderate LV dilation (LVESD <50 mm); C2: abnormal LV systolic function with depressed LVEF (≤55%) or severe LV dilation (LVESD >50 mm or indexed LVESD >25 mm/m²)None; exercise testing is reasonable to confirm symptom status
DSymptomatic severe ARCalcific valve disease; bicuspid valve (or other congenital abnormality); dilated aortic sinuses or ascending aorta; rheumatic valve changes; previous IE with abnormal leaflet closure or perforationSevere AR: Doppler jet width ≥65% of LVOT; vena contracta >0.6 cm; holodiastolic flow reversal in the proximal abdominal aorta; regurgitant volume ≥60 mL/beat; regurgitant fraction ≥50%; ERO ≥0.3 cm²; angiography grade 3 to 4. In addition, diagnosis of chronic severe AR requires evidence of LV dilationSymptomatic severe AR may occur with normal systolic function (LVEF >55%), mild to moderate LV dysfunction (LVEF 40% to 55%), or severe LV dysfunction (LVEF <40%); moderate to severe LV dilation is presentExertional dyspnoea or angina or more severe HF symptoms
[2]

The line people forget sits in Stages C and D: diagnosis of chronic severe AR requires evidence of LV dilation.[2] ACC/AHA 2020 adds that qualitative measures of AR severity are adequate in many situations, but when AR is significant (Stages B and C), quantitative measures of regurgitant volume and ERO area are better predictors of clinical outcome.[3]

  • ACC/AHA 2020, COR 1, LOE B-NR: in patients with signs or symptoms of AR, TTE is indicated for assessment of the cause and severity of regurgitation, LV size and systolic function, prognosis, and timing of valve intervention.[3]
  • ACC/AHA 2020, COR 1, LOE B-NR: in patients with a BAV or with known dilation of the aortic sinuses or ascending aorta, TTE is indicated to evaluate the presence and severity of AR.[3]
  • ACC/AHA 2020, COR 1, LOE B-NR: in moderate or severe AR with suboptimal TTE images or a discrepancy between clinical and TTE findings, TEE, CMR or cardiac catheterisation is indicated for the assessment of LV systolic function, systolic and diastolic volumes, aortic size and AR severity.[3]

AR measurement points

  • Blood pressure (ESC/EACTS 2025): the evaluation needs to take the haemodynamic condition into consideration, particularly the BP, since high pressures can lead to overestimation of the regurgitant volume.[1]
  • 2D cut-offs (ESC/EACTS 2025): consequences of AR on LV size and function must be carefully assessed; cut-offs for intervention are mostly based on 2D echocardiographic measurements.[1]
  • 3D and CMR (ESC/EACTS 2025): they allow more accurate evaluation of LV volumes and LVEF than 2D echocardiography, and are useful in borderline cases.[1]
  • CMR (ACC/AHA 2020): provides accurate and reproducible measures of regurgitant volume and regurgitant fraction in AR, as well as assessment of aortic morphology, LV volume and LV systolic function.[3]
  • CMR volume cut-off (ESC/EACTS 2025): an LVESVi of ≥43 mL/m² using CMR was recently proposed to guide management of asymptomatic patients and appears to have better predictive value than LV diameter.[1]
  • Strain (ESC/EACTS 2025): strain imaging can be helpful in identifying subclinical LV dysfunction and can therefore influence the optimal timing of intervention.[1]
  • The aorta (ESC/EACTS 2025): accurate measurements of the aortic diameter are required at all levels: the annulus, sinuses of Valsalva, sinotubular junction and ascending aorta.[1]
  • Auscultation (ACC/AHA 2020): it has high specificity for detecting AR but low sensitivity and diagnostic accuracy.[3]

Mitral regurgitation

First decide which MR you are grading.[1] ESC/EACTS 2025 says the echo workup of MR includes multiparametric assessment of severity, evaluation of MV anatomy (often with 3D TOE), identification of the mechanism (PMR, ventricular SMR or atrial SMR), and evaluation of cardiac damage.[1] In its primary MR section, ESC/EACTS 2025 calls echocardiography the diagnostic method of choice for the quantification of MR, determination of its aetiology and identification of cardiac consequences.[1]

Primary MR

ACC/AHA 2020 Table 17. Stages of Chronic Primary MR

StageDefinitionValve anatomyValve haemodynamics*Haemodynamic consequencesSymptoms
AAt risk of MRMild mitral valve prolapse with normal coaptation; mild valve thickening and leaflet restrictionNo MR jet or small central jet area <20% LA on Doppler; small vena contracta <0.3 cmNoneNone
BProgressive MRModerate to severe mitral valve prolapse with normal coaptation; rheumatic valve changes with leaflet restriction and loss of central coaptation; prior IECentral jet MR 20%–40% LA or late systolic eccentric jet MR; vena contracta <0.7 cm; regurgitant volume <60 mL; regurgitant fraction <50%; ERO <0.40 cm²; angiographic grade 1+ to 2+Mild LA enlargement; no LV enlargement; normal pulmonary pressureNone
CAsymptomatic severe MRSevere mitral valve prolapse with loss of coaptation or flail leaflet; rheumatic valve changes with leaflet restriction and loss of central coaptation; prior IE; thickening of leaflets with radiation heart diseaseCentral jet MR >40% LA or holosystolic eccentric jet MR; vena contracta ≥0.7 cm; regurgitant volume ≥60 mL; regurgitant fraction ≥50%; ERO ≥0.40 cm²; angiographic grade 3+ to 4+Moderate or severe LA enlargement; LV enlargement; pulmonary hypertension may be present at rest or with exercise; C1: LVEF >60% and LVESD <40 mm; C2: LVEF ≤60% and/or LVESD ≥40 mmNone
DSymptomatic severe MRSevere mitral valve prolapse with loss of coaptation or flail leaflet; rheumatic valve changes with leaflet restriction and loss of central coaptation; prior IE; thickening of leaflets with radiation heart diseaseCentral jet MR >40% LA or holosystolic eccentric jet MR; vena contracta ≥0.7 cm; regurgitant volume ≥60 mL; regurgitant fraction ≥50%; ERO ≥0.40 cm²; angiographic grade 3+ to 4+Moderate or severe LA enlargement; LV enlargement; pulmonary hypertension presentDecreased exercise tolerance; exertional dyspnoea
[2]

*The table footnote: several valve haemodynamic criteria are provided for assessment of MR severity, but not all criteria for each category will be present in each patient.[2] Categorisation as mild, moderate or severe depends on data quality and integration of these parameters in conjunction with other clinical evidence.[2]

[2]
  • ACC/AHA 2020, COR 1, LOE B-NR: in known or suspected primary MR, TTE is indicated for baseline evaluation of LV size and function, RV function, LA size, pulmonary artery pressure, and the mechanism and severity of primary MR (Stages A to D).[3]
  • ACC/AHA 2020, COR 1, LOE C-EO: in primary MR, when TTE provides insufficient or discordant information, TEE is indicated for evaluation of the severity of MR, mechanism of MR and status of LV function (Stages B to D).[3]
  • ACC/AHA 2020, COR 1, LOE B-NR: in primary MR, CMR is indicated to assess LV and RV volumes and function, and may help with assessing MR severity when there is a discrepancy between the findings on clinical assessment and echocardiography.[3]
  • ACC/AHA 2020, COR 1, LOE B-NR: in severe primary MR undergoing mitral intervention, intraoperative TEE is indicated to establish the anatomic basis for primary MR (Stages C and D) and to guide repair.[3]
  • ACC/AHA 2020, COR 2a, LOE B-NR: in primary MR (Stages B and C) with symptoms that might be attributable to MR, haemodynamic exercise testing using Doppler echocardiography or cardiac catheterisation, or cardiopulmonary exercise testing, is reasonable.[3]
  • ACC/AHA 2020, COR 2b, LOE B-NR: in asymptomatic severe primary MR (Stages B and C1), serum biomarkers and novel measurements of LV function, such as global longitudinal strain, may be considered as an adjunct to guide timing of intervention.[3]

Primary MR measurement points

  • Integrate (ACC/AHA 2020): determination of MR severity is made by integrating all available data, including effective orifice area, regurgitant volume and fraction (by PISA or quantitative Doppler), colour jet area, vena contracta, CW Doppler intensity and the transmitral jet velocity curve.[3]
  • Quantify (ESC/EACTS 2025): quantitative parameters such as EROA have prognostic implications, and volumetric methods provide additional information on MR severity [RVol and regurgitant fraction (RF)].[1]
  • Colour settings (ESC/EACTS 2025): accurate colour flow settings must be used to avoid overestimation of MR severity.[1]
  • Prolapse (ACC/AHA 2020): in mitral valve prolapse, MR may be non-holosystolic (mid-late systole), so conventional colour Doppler parameters may overestimate its severity on a single image frame; volumetric measurements provide a better assessment in this situation.[3]
  • "Normal" LVEF (ACC/AHA 2020): favourable loading conditions in MR increase LVEF, so a "normal" LVEF in MR is approximately 70%; the onset of LV dysfunction is inferred when LVEF declines toward 60% or the LV cannot contract to a diameter <40 mm at end systole.[3]
  • Load dependence (ACC/AHA 2020): LVEF is load dependent and often overestimates LV function in MR.[3]
  • Repeat before acting (ACC/AHA 2020): because echocardiographic measurements are variable, management decisions that rest on them should be confirmed by repeat sequential TTE.[3]
  • TOE (ESC/EACTS 2025): the method of choice to assess valve anatomy, leaflet quality, motion and coaptation, as well as to confirm MR severity.[1]
  • CMR (ESC/EACTS 2025): an alternative to precisely quantify RVol and RF in cases of inconclusive or discordant measurements, and the gold standard to determine cardiac dimensions and chamber volumes; the combination of planimetered volumetric methods and phase-contrast measurement of the MV inflow is used for this purpose.[1]
  • CMR and outcomes (ACC/AHA 2020): outcome data on large numbers of patients come from echocardiography, and it is uncertain whether CMR data can be used interchangeably with echo data in predicting outcomes.[3]
  • Exercise echo (ESC/EACTS 2025): evaluates dynamic changes in regurgitant jet and pulmonary pressures at peak exercise, and might be helpful when symptoms and resting regurgitation severity are discordant.[1]
  • In theatre (ACC/AHA 2020): because anaesthesia lessens afterload, preload and mitral valve closing force, severity of MR should be evaluated at the same loading conditions as occurred during the awake state.[3]

Secondary MR

ESC/EACTS 2025 says secondary MR is present when the MV structure appears grossly normal but the valve is incompetent, owing to alterations in LV and LA geometry, dyssynchrony and imbalances between closing and tethering forces.[1] ESC/EACTS 2025 says SMR assessment should be performed after optimisation of medical therapy and in a euvolaemic and normotensive state.[1] ESC 2026 HF agrees that to assess the severity of MR adequately, the patient should be euvolaemic or as close to euvolaemia as possible.[5]

ACC/AHA 2020 Table 18. Stages of Secondary MR

StageDefinitionValve anatomyValve haemodynamics*Associated cardiac findingsSymptoms
AAt risk of MRNormal valve leaflets, chords, and annulus in a patient with CAD or cardiomyopathyNo MR jet or small central jet area <20% LA on Doppler; small vena contracta <0.30 cmNormal or mildly dilated LV size with fixed (infarction) or inducible (ischaemia) regional wall motion abnormalities; primary myocardial disease with LV dilation and systolic dysfunctionSymptoms attributable to coronary ischaemia or HF may be present that respond to revascularisation and appropriate medical therapy
BProgressive MRRegional wall motion abnormalities with mild tethering of mitral leaflet; annular dilation with mild loss of central coaptation of the mitral leafletsERO <0.40 cm²†; regurgitant volume <60 mL; regurgitant fraction <50%Regional wall motion abnormalities with reduced LV systolic function; LV dilation and systolic dysfunction attributable to primary myocardial diseaseSymptoms attributable to coronary ischaemia or HF may be present that respond to revascularisation and appropriate medical therapy
CAsymptomatic severe MRRegional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflet; annular dilation with severe loss of central coaptation of the mitral leafletsERO ≥0.40 cm²†; regurgitant volume ≥60 mL‡; regurgitant fraction ≥50%Regional wall motion abnormalities with reduced LV systolic function; LV dilation and systolic dysfunction attributable to primary myocardial diseaseSymptoms attributable to coronary ischaemia or HF may be present that respond to revascularisation and appropriate medical therapy
DSymptomatic severe MRRegional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflet; annular dilation with severe loss of central coaptation of the mitral leafletsERO ≥0.40 cm²†; regurgitant volume ≥60 mL‡; regurgitant fraction ≥50%Regional wall motion abnormalities with reduced LV systolic function; LV dilation and systolic dysfunction attributable to primary myocardial diseaseHF symptoms attributable to MR persist even after revascularisation and optimisation of medical therapy; decreased exercise tolerance; exertional dyspnoea
[2]
  • *Several valve haemodynamic criteria are provided for assessment of MR severity, but not all criteria for each category will be present in each patient; categorisation depends on data quality and integration of these parameters in conjunction with other clinical evidence.[2]
  • †The measurement of the proximal isovelocity surface area by 2D TTE in patients with secondary MR underestimates the true ERO because of the crescentic shape of the proximal convergence.[2]
  • ‡May be lower in low-flow states.[2]

Here the two guidelines read differently, so quote both.[1][3] The ACC/AHA 2020 text says severe secondary MR is defined as an ERO ≥40 mm², but outcome studies have shown poor prognosis in those with moderate MR (ERO ≥20 mm²).[3] ESC/EACTS 2025 says that when quantifying EROA and RVol in SMR, lower thresholds may apply to define severe regurgitation because of the potential elliptical regurgitant orifice and/or the low-flow state.[1] ESC/EACTS 2025 says an EROA of ≥30 mm² and/or an RVol of ≥45 mL has been identified as having a significant impact on outcomes, with prognosis improved after treatment.[1]

ESC/EACTS 2025

Europe

  • Lower thresholds may apply to define severe SMR (potential elliptical orifice and/or low-flow state)
  • EROA ≥30 mm² and/or RVol ≥45 mL identified as having a significant impact on outcomes
  • Assess after optimisation of medical therapy, euvolaemic and normotensive

ACC/AHA 2020

United States

  • Severe secondary MR defined as an ERO ≥40 mm² (text); Table 18 severe: ERO ≥0.40 cm²†, regurgitant volume ≥60 mL‡, regurgitant fraction ≥50%
  • Poor prognosis already with moderate secondary MR (ERO ≥20 mm²)
  • Table 18 footnotes † and ‡: † PISA by 2D TTE underestimates the true ERO in secondary MR (crescentic proximal convergence); ‡ on the severe regurgitant volume cell: may be lower in low-flow states
[1] [3] [2] [2] [3] [1]
  • ACC/AHA 2020, COR 1, LOE B-NR: in chronic secondary MR (Stages B to D), TTE is useful to establish the aetiology and to assess the extent of regional and global LV remodelling and systolic dysfunction, severity of MR and magnitude of pulmonary hypertension.[3]
  • CMR (ESC/EACTS 2025): used to confirm SMR severity and assess cardiac chamber function and dimensions.[1]
  • Exercise echo (ESC/EACTS 2025): owing to the dynamic nature of SMR, it may help to identify severe SMR when values at rest are inconclusive.[1]

Atrial secondary MR

ESC/EACTS 2025 says atrial SMR is most frequently defined by the presence of all four of the following key criteria, joined by AND.[1]

  • Preserved LVEF (≥50%) without regional wall motion abnormalities or leaflet tethering.[1]
  • No or mildly dilated LV cavity [LV end-diastolic dimension of <56 mm in women and <63 mm in men; indexed LV end-diastolic volume of <71 mL/m² (in women) or <79 mL/m² (in men)].[1]
  • Mitral annulus dilatation [anteroposterior diameter of >35 mm].[1]
  • Enlarged LA (LAVI >34 mL/m²).[1]

At advanced stages, it says atrial and ventricular SMR criteria can overlap in the case of late LV damage due to continuous volume overload.[1] Atrial SMR was occasionally misclassified as PMR due to pseudo-prolapse with leaflet tethering in advanced stages.[1]

Mitral stenosis

For rheumatic MS, ESC/EACTS 2025 says echocardiography is the preferred method for screening in endemic regions and for assessing the severity, the extent of anatomical lesions and the haemodynamic consequences of MS.[1] In rheumatic MS, it says mitral valve area by 2D planimetry is the most commonly used measurement of stenosis severity, but 3D TTE and TOE have additional diagnostic value.[1] In rheumatic MS, an MVA of ≤1.5 cm² in conjunction with clinical factors (symptoms, high risk of thromboembolism, or haemodynamic decompensation) is indicative of clinically severe MS.[1] In rheumatic MS, mean transvalvular gradient and pulmonary pressures reflect its consequences and have prognostic value.[1]

ACC/AHA 2020 Table 16. Stages of MS

StageDefinitionValve anatomyValve haemodynamicsHaemodynamic consequencesSymptoms
AAt risk of MSMild valve doming during diastoleNormal transmitral flow velocityNoneNone
BProgressive MSRheumatic valve changes with commissural fusion and diastolic doming of the mitral valve leaflets; planimetered mitral valve area >1.5 cm²Increased transmitral flow velocities; mitral valve area >1.5 cm²; diastolic pressure half-time <150 msMild to moderate LA enlargement; normal pulmonary pressure at restNone
CAsymptomatic severe MSRheumatic valve changes with commissural fusion and diastolic doming of the mitral valve leaflets; planimetered mitral valve area ≤1.5 cm²Mitral valve area ≤1.5 cm²; diastolic pressure half-time ≥150 msSevere LA enlargement; elevated PASP >50 mm HgNone
DSymptomatic severe MSRheumatic valve changes with commissural fusion and diastolic doming of the mitral valve leaflets; planimetered mitral valve area ≤1.5 cm²Mitral valve area ≤1.5 cm²; diastolic pressure half-time ≥150 msSevere LA enlargement; elevated PASP >50 mm HgDecreased exercise tolerance; exertional dyspnoea
[2]

The table note explains why the gradient is missing from the criteria.[2] ACC/AHA 2020 says the transmitral mean pressure gradient should be obtained and is usually >5 mm Hg to 10 mm Hg in severe MS.[2] However, because of its variability with heart rate and forward flow, it has not been included in the criteria for severity.[2]

  • ACC/AHA 2020, COR 1, LOE B-NR: in signs or symptoms of rheumatic MS, TTE is indicated to establish the diagnosis, quantify haemodynamic severity, assess concomitant valvular lesions and demonstrate valve morphology (to determine suitability for mitral commissurotomy).[3]
  • ACC/AHA 2020, COR 1, LOE C-LD (initial diagnosis of rheumatic MS): in patients considered for percutaneous mitral balloon commissurotomy (PMBC), TEE should be performed to assess the presence or absence of LA thrombus and to evaluate the severity of MR.[3]
  • ACC/AHA 2020, COR 1, LOE C-LD: in rheumatic MS with a discrepancy between resting echocardiographic findings and clinical symptoms, exercise testing with Doppler or invasive haemodynamic assessment is recommended to evaluate symptomatic response, exercise capacity, and the response of the mean mitral gradient and pulmonary artery pressure.[3]

Rheumatic MS measurement points

  • Planimetry (ACC/AHA 2020): the parasternal long-axis window can identify the characteristic diastolic doming; short-axis scanning will demonstrate commissural fusion and allow planimetry of the mitral orifice; 3D echocardiography (TTE or TEE) provides greater accuracy of MVA measurement.[3]
  • Heart rate (ACC/AHA 2020): mean transvalvular gradients should always be reported with heart rate, because a high heart rate will result in overestimation of stenosis severity.[3]
  • Pressure half-time (ACC/AHA 2020): additional assessment of rheumatic MS includes the mitral pressure half-time, with acknowledgement that this parameter is also affected by LA and LV compliance.[3]
  • Mismatch (ACC/AHA 2020): if the mean gradient does not match the valve area, other methods, such as the continuity equation, should be considered.[3]
  • RV systolic pressure (ACC/AHA 2020): estimated from the TR velocity.[3]
  • MR before PMBC (ACC/AHA 2020): TEE is useful because LA shadowing on TTE may underestimate MR severity; MR that is more than mild is a contraindication to PMBC.[3]
  • TOE (ESC/EACTS 2025): should be systematically performed in PMC candidates to exclude LA thrombus or after an embolic episode, and may play an essential role for procedural guidance.[1]
  • Exercise (ESC/EACTS 2025): exercise testing is indicated in asymptomatic patients or when symptoms are equivocal or discordant with stenosis severity; exercise echocardiography is preferred over DSE, especially when there are contraindications to dobutamine.[1]
  • Wedge pressure (ACC/AHA 2020): the mean wedge pressure is an acceptable substitute for mean LA pressure, but the LV–to–wedge gradient will overestimate the true transmitral gradient because of phase delay and delayed transmission of pressure changes.[3]

Degenerative MS with mitral annular calcification

  • Shadowing (ESC/EACTS 2025): echocardiography is used for initial evaluation but is frequently limited by acoustic shadowing due to severe calcification.[1]
  • Planimetry (ESC/EACTS 2025): less reliable than in rheumatic MS, so TOE should be used liberally.[1]
  • Gradient (ESC/EACTS 2025): mean transmitral gradient has been associated with increased mortality irrespective of MR severity.[1]
  • CT (ESC/EACTS 2025): ECG-gated CCT is necessary to assess the degree and locations of calcifications, especially if an intervention is planned.[1]

Tricuspid regurgitation

ESC/EACTS 2025 says assessment of TR severity should ideally be performed in euvolaemic status, with optimised pulmonary and systemic pressures, using an integrative approach of multiple qualitative and quantitative parameters.[1] TTE provides sufficient diagnostic information in most patients.[1]

ACC/AHA 2020 Table 20. Stages of TR (the table prints Stages B to D)

StageDefinitionValve haemodynamicsHaemodynamic consequencesClinical symptoms and presentation
BProgressive TRCentral jet <50% RA; vena contracta width <0.7 cm; ERO <0.40 cm²; regurgitant volume <45 mLNoneNone
CAsymptomatic severe TRCentral jet ≥50% RA; vena contracta width ≥0.7 cm; ERO ≥0.40 cm²; regurgitant volume ≥45 mL; dense continuous wave signal with triangular shape; hepatic vein systolic flow reversalDilated RV and RA; elevated RA with "c-V" waveElevated venous pressure; no symptoms
DSymptomatic severe TRCentral jet ≥50% RA; vena contracta width ≥0.7 cm; ERO ≥0.40 cm²; regurgitant volume ≥45 mL; dense continuous wave signal with triangular shape; hepatic vein systolic flow reversalDilated RV and RA; elevated RA with "c-V" waveElevated venous pressure; dyspnoea on exertion, fatigue, ascites, oedema
[2]

ACC/AHA 2020 adds that the severity of TR can be dynamic and dependent on changes in preload and pulmonary pressure.[2] The ACC/AHA 2020 supportive text says characterisation of TR severity relies on an integrative assessment of multiple parameters, but many limitations remain.[3]

  • ACC/AHA 2020, COR 1, LOE C-LD: in TR, TTE is indicated to evaluate the presence and severity of TR, determine the aetiology, measure right-sided chambers and the inferior vena cava, assess RV systolic function, estimate pulmonary artery systolic pressure and characterise any associated left-sided heart disease.[3]
  • ACC/AHA 2020, COR 2a, LOE C-LD: invasive measurement of cardiac index, right-sided diastolic pressures, pulmonary artery pressures and pulmonary vascular resistance, as well as right ventriculography, can be useful when clinical and non-invasive data are discordant or inadequate.[3]

TR measurement points

  • What the echo covers (ESC/EACTS 2025): evaluation of severity and aetiology (including characterisation of left-sided heart disease and, if applicable, CIED lead location and interaction with the valve apparatus), the impact of TR on the right-sided chambers (RV and RA size and function), and assessment of central venous (inferior vena cava) and pulmonary pressures.[1]
  • Beyond severe (ESC/EACTS 2025): a grading scheme including "massive" and "torrential" grades has been proposed to refine TR reduction assessment after transcatheter interventions and has been used in several studies.[1]
  • When to act (ESC/EACTS 2025): although this five-grade scale may be associated with a proportional increase in symptoms and event risk, an intervention should be considered without delay as soon as TR is severe, with the aim of reducing TR to moderate or less.[1]
  • Pulmonary pressure (ESC/EACTS 2025): echocardiography often underestimates pulmonary pressures in cases of severe TR, so right heart catheterisation is recommended in all candidates for an intervention to assess the haemodynamic consequences of TR on the RA and venous circulation (e.g. ventricularisation of the RA pressure curves), measure end-diastolic RV pressure and document volume overload.[1]
  • Pulmonary pressure (ACC/AHA 2020): PASP is estimated from maximal TR velocity; a weak TR signal or severe TR may result in underestimation, and direct invasive measurement can resolve this uncertainty.[3]
  • RV function (ESC/EACTS 2025): in severe TR, RV function is often overestimated, so the most conservative thresholds are suggested to identify RV dysfunction at the earliest stage possible; CMR should be used when accurate RV measurements are necessary for decision-making.[1]
  • Normal RV systolic function (ACC/AHA 2020): defined by several parameters, including TAPSE >16 mm, tricuspid valve systolic annular velocity >10.0 cm/s, and RV end-systolic area <20.0 cm² or fractional area change >35%.[3]
  • Annulus (ACC/AHA 2020): in TR undergoing left-sided valve surgery, an annular diastolic diameter >40 mm (or >21 mm/m²) indicates an increased risk of persistent or progressive TR after isolated mitral valve surgery.[3]
  • Cardiac output (ACC/AHA 2020): thermodilution measurements may be inaccurate with severe TR, so a Fick cardiac output should be used to calculate pulmonary resistance.[3]

Mixed and multiple valve disease

ACC/AHA 2020 says Doppler haemodynamics have been validated for single-valve disease but have not necessarily been studied in multivalve disease.[3] ESC/EACTS 2025 says haemodynamic interdependence between multiple valve defects alters loading and flow conditions, limiting the diagnostic validity of measures established to grade single valve defects.[1]

  • Low flow (ESC/EACTS 2025): in the presence of multiple VHD, low-flow states are frequent.[1]
  • Continuity and PHT (ESC/EACTS 2025): the continuity equation becomes erroneous if transvalvular flows are unequal, and PHT-derived methods are inaccurate if ventricular compliance or filling is altered.[1]
  • Valve areas (ACC/AHA 2020): limitations exist for calculations such as valve areas because of differential flows with multivalve disease.[3]
  • TOE (ESC/EACTS 2025): can provide important detailed anatomical and mechanistic flow-independent information.[1]
  • CMR (ESC/EACTS 2025): enables independent assessment of valvular regurgitation using volumetric methods or direct flow quantification.[1]
  • Calcium (ESC/EACTS 2025): AV calcium scoring confirms the diagnosis of true severe AS under low-flow conditions.[1]
  • Invasive output (ESC/EACTS 2025): cardiac output by thermodilution or the Fick equation using estimated oxygen uptake is inaccurate in low-flow conditions or severe TR, commonly present in multiple VHD.[1]

Mixed aortic valve disease

ESC/EACTS 2025 says the severity of mixed AV disease is often underestimated, and patients with balanced moderate AR and AS show adverse event rates comparable to severe isolated AS.[1] Transvalvular gradients measured by Doppler reflect the overall haemodynamic burden of both regurgitation and stenosis, and are strongly associated with adverse outcomes.[1] So high gradients justify intervention in moderate mixed AV disease even if regurgitation is graded moderate and the calculated or planimetric AVA is >1 cm².[1]

  • ESC/EACTS 2025 Recommendation Table 12 (recommendations on indications for intervention in patients with mixed moderate aortic stenosis and moderate aortic regurgitation), Class I, Level B: intervention is recommended in symptomatic patients with mixed moderate AV stenosis (footnote c: AVA >1 cm²) and moderate regurgitation, and a mean gradient ≥40 mmHg or Vmax ≥4.0 m/s.[1]
  • ESC/EACTS 2025 Recommendation Table 12 (same table), Class I, Level C: intervention is recommended in asymptomatic patients with mixed moderate AV stenosis (AVA >1 cm²) and moderate regurgitation with Vmax ≥4.0 m/s, and LVEF <50% not attributable to other cardiac disease.[1]
  • ACC/AHA 2020, COR 1, LOE B-NR: in symptomatic patients with combined AS and AR and a peak transvalvular jet velocity of at least 4.0 m/s or a mean transvalvular gradient of at least 40 mm Hg, AVR is recommended.[3]
  • ACC/AHA 2020, COR 1, LOE C-EO: in asymptomatic patients with combined AS and AR who have a jet velocity of ≥4.0 m/s with an LVEF <50%, SAVR is recommended.[3]

Mixed mitral and multiple valve disease

  • Mixed MV disease (ESC/EACTS 2025): usually present with rheumatic valve disease or MAC; if MVA is ≤1.5 cm², recommendations for isolated MS apply.[1]
  • ACC/AHA 2020, COR 1, LOE C-EO: for mixed valve disease, TTE is recommended to assess the aetiology, severity and pathophysiological impact.[3]
  • ACC/AHA 2020, COR 2a, LOE C-EO: with ambiguous symptoms suspected to be attributable to mixed mitral valve disease, further assessment of filling pressure using biomarkers or invasive haemodynamic measurements at rest or with exercise is reasonable.[3]

Prosthetic valves

Read a prosthetic gradient against that valve's own baseline.[3] ACC/AHA 2020 says TTE after valve implantation or repair assesses the procedural result and is the baseline against which any change can be compared.[3] Normal transvalvular velocities and gradients vary across types and sizes of prosthetic valves and are also affected by patient-specific factors, including body size and cardiac output.[3] ESC/EACTS 2025 says all patients with prosthetic valves require lifelong clinical and echocardiographic follow-up.[1]

  • When to scan a biological valve (ESC/EACTS 2025): serial TTE measurements of transprosthetic gradients, the effective valve area and leaflet motion and morphology should be performed within 3 months after implantation, again at 1 year, and annually thereafter, or sooner if new cardiovascular symptoms occur.[1]
  • ACC/AHA 2020, COR 1, LOE B-NR: after a surgical or transcatheter prosthetic valve or valve repair, an initial postprocedural TTE is recommended for evaluation of valve haemodynamics and ventricular function.[3]
  • ACC/AHA 2020, COR 1, LOE C-EO: with a prosthetic valve or prior repair and a change in clinical symptoms or signs suggesting valve dysfunction, repeat TTE is recommended.[3]
  • ACC/AHA 2020, COR 1, LOE C-LD: with a prosthetic valve replacement or prior valve repair and clinical symptoms or signs that suggest prosthetic valve dysfunction, additional imaging with TEE, gated cardiac CT or fluoroscopy is recommended, even if TTE does not show valve dysfunction.[3]
  • ACC/AHA 2020, COR 2a, LOE C-LD: with a bioprosthetic surgical valve, TTE at 5 and 10 years and then annually after implantation is reasonable, even in the absence of a change in clinical status.[3]
  • ACC/AHA 2020, COR 2a, LOE C-LD: with a bioprosthetic TAVI, TTE annually is reasonable.[3]
  • Mechanical valves (ACC/AHA 2020 text): routine annual TTE is not needed if the postoperative baseline study is normal and no clinical change is apparent.[3]

Grading haemodynamic deterioration of a biological valve

ESC/EACTS 2025 says that to ensure timely diagnosis of structural valve deterioration, serial measurements should be compared with the TTE performed at discharge, or within 1–3 months after implantation.[1] ESC/EACTS 2025 Table 12 gives the criteria; each valve row applies to SVD or non-structural valve dysfunction (except PVL or PPM), thrombosis, or endocarditis, with footnote ᵃ (aortic) or ᵇ (mitral) printed after the closing parenthesis and given below the table.[1]

ESC/EACTS 2025 Table 12. Criteria for the diagnosis of moderate or severe aortic and mitral haemodynamic valve deterioration

Valve and criterionModerateSevere
Aortic BHV (SVD or non-structural valve dysfunction (except PVL or PPM)ᵃ, thrombosis, or endocarditis)Increase in mean transvalvular gradient ≥10 mmHg resulting in mean gradient ≥20 mmHgIncrease in mean transvalvular gradient ≥20 mmHg resulting in mean gradient ≥30 mmHg
ANDAND
Decrease in EOA ≥0.3 cm² or ≥25%, and/or decrease in DVI ≥0.1 or ≥20%, compared with echocardiographic assessment performed 1–3 months post-procedureDecrease in EOA ≥0.6 cm² or ≥50%, and/or decrease in DVI ≥0.2 or ≥40%, compared with echocardiographic assessment performed 1–3 months post-procedure
OROR
New occurrence or increase of ≥1 grade of intraprosthetic AR resulting in ≥ moderate ARNew occurrence or increase of ≥2 grades of intraprosthetic AR resulting in ≥ moderate-to-severe AR
Mitral BHV (SVD or non-structural valve dysfunction (except PVL or PPM)ᵇ, thrombosis, or endocarditis)Increase in DVI ≥0.4 or ≥20%, resulting in DVI ≥2.2, or decrease in EOA ≥0.5 cm² or ≥25%, resulting in EOA <1.5 cm², usually associated with increase of transmitral gradient ≥5 mmHgIncrease in DVI ≥0.8 or ≥40%, resulting in DVI ≥2.7, or decrease in EOA ≥1.0 cm² or ≥50%, resulting in EOA <1 cm², usually associated with increase of transmitral gradient ≥10 mmHg
OROR
New occurrence or increase of ≥1 grade of intraprosthetic MR resulting in ≥moderate MRNew occurrence or increase of ≥2 grades of intraprosthetic MR resulting in ≥moderate-to-severe MR
[1]

Table 12 footnotes: ᵃobstruction by pannus, dilatation of the aortic root after stentless BHV, or AV-sparing operations; ᵇleaflet entrapment by pannus, chordae, or suture.[1] In this rendering, the AND and OR connectors and the rows that follow them sit under the Moderate and Severe columns; the source prints those rows without a first-column label.[1]

[1]
  • After the diagnosis (ESC/EACTS 2025): moderate or severe haemodynamic deterioration should prompt referral to an experienced Heart Valve Centre and exclusion of all causes of non-structural valve dysfunction, particularly PVL or PPM, as well as thrombosis and endocarditis.[1]
  • Advanced imaging (ESC/EACTS 2025): this step requires TOE, CCT and/or PET-CT to document SVD-related morphological changes and elucidate the mechanism.[1]
  • Failure (ESC/EACTS 2025): SVD with corresponding clinical criteria (e.g. new or worsening symptoms, LV or RV dilation/dysfunction, or PH) indicates BHV failure with potential need for reintervention.[1]
  • Dysfunction types (ESC/EACTS 2025): prosthetic valve dysfunction can be intrinsic permanent change to the prosthesis (SVD) or non-structural valve dysfunction from any abnormality not intrinsic to the prosthesis itself.[1]
  • Ten-year figure (ACC/AHA 2020): studies based on TTE follow-up estimate that approximately 30% of patients with a surgical aortic bioprosthesis develop evidence of valve dysfunction over the 10 years after implantation (defined as an increase in mean gradient of ≥10 mm Hg or worsening of transprosthetic regurgitation from mild to moderate or from moderate to severe).[3]

High gradient: stenosis, mismatch or pannus?

  • Mismatch (ACC/AHA 2020): in some patients the orifice area of the implanted prosthesis may be inadequate to meet the cardiac output demands of the patient, even when the valve is functioning normally; this patient–prosthesis mismatch is associated with a high transvalvular gradient, persistent LV hypertrophy and an increased rate of cardiac events after valve replacement.[3]

  • Telling them apart (ACC/AHA 2020): prosthetic valve stenosis is distinguished from mismatch by comparison with the early postoperative baseline study and by visualisation of the appearance and motion of the leaflets.[3]

  • Stenosis course (ACC/AHA 2020): a progressive increase in transvalvular velocity and pressure gradient with abnormal thickened/calcified leaflets (bioprosthetic) or evidence of pannus (mechanical).[3]

  • Bileaflet mechanical valves (ACC/AHA 2020): non-laminar flow with significant pressure recovery means a high velocity in the central narrow slit-like orifice may not correlate with prosthetic stenosis or mismatch.[3]

  • Leaflet motion (ACC/AHA 2020): mechanical leaflets are best evaluated with fluoroscopy or cine-CT because strong reflections obscure motion on echo in most patients; excessive gradients with normal leaflet motion and no thrombus mean mismatch or pannus (or both).[3]

  • Mismatch outcomes (ESC/EACTS 2025): in the aortic position, severe PPM is associated with decreased quality of life, more rehospitalisation and reintervention and possibly reduced long-term survival, although findings are not consistent throughout all studies; moderate PPM is more common but seems to have a limited impact on outcomes.[1]

  • Mitral and tricuspid mismatch (ESC/EACTS 2025): less is known about its prevalence and consequences, and established definitions are lacking.[1]

  • ACC/AHA 2020, COR 1, LOE B-NR: in suspected mechanical or bioprosthetic valve stenosis, TTE and TEE are recommended to diagnose the cause and severity of obstruction, assess ventricular function and estimate pulmonary artery systolic pressure.[3]

  • ACC/AHA 2020, COR 1, LOE C-EO: in mechanical valve stenosis, fluoroscopy or cine-CT is recommended to assess motion of the mechanical valve leaflets.[3]

  • ACC/AHA 2020, COR 2a, LOE C-LD: in bioprosthetic valve stenosis, 3D TEE or 4D CT imaging can be useful to rule out leaflet thrombosis.[3]

Prosthetic regurgitation and thrombosis

  • ACC/AHA 2020, COR 1, LOE B-NR: in suspected mechanical or bioprosthetic valve regurgitation, TTE and TEE are recommended to determine the cause and severity of the leak, assess ventricular function and estimate pulmonary artery systolic pressure.[3]
  • Mitral prostheses (ACC/AHA 2020): the LA side is obscured by acoustic shadowing from the TTE approach; TTE is inadequate for prosthetic mitral valves and TEE is needed when prosthetic MR is a concern.[3]
  • Aortic prostheses (ACC/AHA 2020): both TTE and TEE are needed, as the posterior aspect is shadowed on TTE and the anterior aspect on TEE; acoustic shadowing may affect detection of a paravalvular leak by either approach, with TTE suboptimal for posterior and TEE for anterior defects.[3]
  • Where is the leak? (ACC/AHA 2020): a critical step is to distinguish transvalvular from paravalvular leak, which also requires TEE in addition to TTE; VARC has suggested an approach to paravalvular leak severity with a 5-class grading scheme.[3]
  • PVL (ESC/EACTS 2025): the diagnosis of PVL requires systematic TOE, because TTE may be inconclusive; TOE is recommended in all cases of suspected prosthetic valve dysfunction or endocarditis.[1]
  • Suspect thrombosis (ESC/EACTS 2025): obstructive valve thrombosis should be suspected with any prosthesis and new dyspnoea or HF symptoms, an embolic event or an unexpected increase in transvalvular gradients; if TTE is uncertain, confirm by TOE and/or CCT to distinguish thrombus, pannus and degeneration.[1]
  • ESC/EACTS 2025 Recommendation Table 17 (recommendations for the management of prosthetic valve dysfunction), group "Valve thrombosis", Class I, Level C: TOE and/or 4D-CT are recommended in patients with suspected valve thrombosis to confirm the diagnosis.[1]
  • Cinefluoroscopy (ESC/EACTS 2025): can detect impaired MHV leaflet motion and reduced opening angles; with CCT it provides useful additional information if valve thrombus or pannus is suspected.[1]
  • HALT (ESC/EACTS 2025): detected by CCT in 10%–30% of aortic BHVs depending on antithrombotic management, definition, timepoint and valve type; routine use of CCT to detect HALT is not indicated.[1]

When the echo and the patient disagree

Discordance between the scan and the story is a recognised trigger for more testing.[1][3] ESC/EACTS 2025 says right heart catheterisation should be performed in patients with equivocal echocardiographic findings, particularly those with MV disease, as well as in all candidates for treatment of severe TR.[1] ESC/EACTS 2025 warns that the pulmonary capillary wedge pressure v-wave can inform about MR severity but is neither sensitive nor specific.[1] The v-wave may also be increased with reduced LA compliance or diastolic LV dysfunction, as in MS or chronic HF.[1]

  • Serial imaging (ESC/EACTS 2025): studies to detect changes over time, or variability due to haemodynamic conditions or initiation/up-titration of medical therapy, are of utmost importance to guide decisions.[1]
  • Exercise echo (ESC/EACTS 2025): helps to identify the cause of dyspnoea, unveil symptoms in apparently asymptomatic patients and identify dynamic changes of VHD severity, and can contribute to refinement of the indication for an intervention, especially for AS and MR.[1]
  • What exercise echo measures (ESC/EACTS 2025): LV global and segmental function, pulmonary artery pressure, and aortic and mitral pressure gradients; it also documents exercise-induced increase of MR and TR severity, especially in secondary disease.[1]

Pitfalls

Measurement traps the guidelines name
  • Grading AS during hypertension: ACC/AHA 2020 says it may underestimate or, less often, overestimate stenosis severity, and recommends optimising blood pressure control before measuring suspected Stage D3 AS (COR 1, LOE B-NR).[3]
  • Poor alignment: ACC/AHA 2020 says AS severity may be underestimated without a parallel intercept angle between the beam and the aortic jet.[3]
  • Trusting AVA alone: ESC/EACTS 2025 says that although AVA is theoretically the ideal parameter for assessing severity, there are numerous technical limitations associated with its calculation.[1]
  • Calling small-AVA, low-gradient AS with preserved LVEF severe too soon: footnote c of ESC/EACTS 2025 Recommendation Table 4 (recommendations on indications for intervention in symptomatic and asymptomatic severe aortic stenosis) says explanations other than severe AS (such as measurement errors, uncontrolled blood pressure, and conditions lowering the stroke volume) are frequent and must be carefully excluded.[1]
  • Reading a low calcium score as mild disease: ESC/EACTS 2025 says cautious interpretation is required in patients who can develop severe AS without pronounced AV calcification, such as in BAV, concomitant amyloidosis, and predominantly fibrotic stenosis associated with post-rheumatic, radiation-induced and inflammatory disease.[1]
  • Overgrading primary MR with colour: in its primary MR section, ESC/EACTS 2025 says accurate colour flow settings must be used; ACC/AHA 2020 says colour on a single frame may overestimate non-holosystolic prolapse MR.[1][3]
  • Trusting PISA by 2D TTE in secondary MR: the † footnote of ACC/AHA 2020 Table 18 (Stages of Secondary MR) says it underestimates the true ERO because of the crescentic shape of the proximal convergence.[2]
  • Grading SMR before treatment: ESC/EACTS 2025 says SMR assessment should be performed after optimisation of medical therapy and in a euvolaemic and normotensive state.[1]
  • Reporting a rheumatic MS gradient without heart rate: in its rheumatic MS diagnostic text, ACC/AHA 2020 says a high heart rate will result in overestimation of stenosis severity.[3]
  • Trusting continuity or PHT in multiple valve disease: ESC/EACTS 2025 says the continuity equation becomes erroneous if transvalvular flows are unequal, and PHT-derived methods are inaccurate if the ventricular compliance or filling is altered.[1]
  • Calling AR severe on Doppler alone: ACC/AHA 2020 Table 15 (Stages of Chronic AR) says, in Stages C and D, that diagnosis of chronic severe AR requires evidence of LV dilation.[2]
  • Treating a high bileaflet mechanical valve velocity as stenosis: ACC/AHA 2020 says it may not correlate with stenosis or mismatch because of pressure recovery.[3]

Special populations

  • Women with AS (ESC/EACTS 2025): the pathophysiology of AS seems to differ by sex, with women having less calcium and more fibrosis.[1]
  • Small ventricles (ESC/EACTS 2025): concentric hypertrophy and remodelling are more frequent in women, giving higher LVEF but smaller LV cavity and stroke volume; paradoxical low-flow, low-gradient constellations are frequent and may contribute to underdiagnosis of severe AS in women and delay an intervention.[1]
  • Sex-specific flow and calcium (ESC/EACTS 2025): sex-specific thresholds to define flow limitation (<40 mL/m² for men and <32 mL/m² for women) have been suggested, and CCT calcium scoring should be performed in women with discordant echocardiographic parameters.[1]
  • Calcium thresholds by sex (ACC/AHA 2020): sex-specific Agatston unit thresholds for diagnosis of severe AS are 1300 in women and 2000 in men, reflecting the contribution of leaflet fibrosis, in addition to calcification, to increased leaflet stiffness in women.[3]
  • Older patients with AS (ESC/EACTS 2025): transthyretin cardiac amyloidosis may coexist with AS in elderly patients and the two conditions may causally interrelate.[1]
  • Pregnancy (ESC 2025 pregnancy, Recommendation Table 2, Class I, Level C): TTE is recommended as first-line imaging tool in any pregnant woman with unexplained or new cardiovascular signs or symptoms.[6]
  • Gradients in pregnancy (ESC 2025 pregnancy): in stenotic native valve lesions, serial TTE will usually demonstrate an increase in valve gradient of up to 50% due to the normal pregnancy-related increase in cardiac output.[6]
  • Stress testing in pregnancy (ESC 2025 pregnancy): stress echocardiography using bicycle ergometry may improve diagnostic specificity, and pharmacologic stress agents (e.g. dobutamine) should be avoided.[6]
  • Under anaesthesia (ACC/AHA 2020, chronic primary MR section): intraoperative TEE is the standard for imaging during MR surgery, and because anaesthesia lessens afterload, preload and mitral valve closing force, decisions about MR severity should be made at the same loading conditions as in the awake state.[3]

Evidence, guidelines and regional differences

Most grading numbers are shared, but a few differ by body and should be quoted with their source.[1][3]

ESC/EACTS 2025

Europe

  • Calcium score indicating severe AS: >2000 AU in men, >1200 AU in women (high sensitivity and specificity, ∼85%)
  • Velocity ratio: may assist evaluation when other parameters are equivocal (<0.25 suggests that severe AS is highly likely)
  • Secondary MR: EROA ≥30 mm² and/or RVol ≥45 mL identified as having a significant impact on outcomes
  • Biological valve TTE: within 3 months, at 1 year, then annually, or sooner if new cardiovascular symptoms occur

ACC/AHA 2020

United States

  • Calcium score for severe AS: 2000 in men, 1300 in women
  • Velocity ratio: ≤0.25 is consistent with severe AS
  • Secondary MR: severe defined as ERO ≥40 mm² (Table 18: ERO ≥0.40 cm²†; †PISA by 2D TTE underestimates the true ERO)
  • Surgical bioprosthesis TTE: at 5 and 10 years and then annually after implantation, even without a change in clinical status (COR 2a, LOE C-LD); bioprosthetic TAVI: annually (COR 2a, LOE C-LD)
[1] [3] [2]

In Australia and New Zealand

The 2024 CSANZ position statement on structural and valvular heart disease with TTE says TTE is the most widely available and utilised modality for screening, diagnosis and serial monitoring of cardiac structure and function.[4] The CSANZ statement gives its objectives as a guiding framework of acceptable indications for initial and serial TTE, and the minimum required standard for TTE examinations and reporting.[4] Only its abstract is held for this topic, so none of its grading thresholds are quoted here.

Guidelines checked for this topic

Rows on this page come from the 2025 ESC/EACTS and 2020 ACC/AHA valvular heart disease guidelines, each the newest of its body among the guidelines checked for this topic (census 2026-10-09).[1][3] The 2026 ESC HF row and the 2025 ESC pregnancy rows are quoted for their own populations.[5][6] The 2021 ESC/EACTS valvular heart disease guideline (PMID 34453165) is superseded by the 2025 edition and is not used. The ASE and EACVI valve quantitation documents (2017 to 2025) are not held as text for this topic, so none of their numbers are used. The British Society of Echocardiography valve guidelines are not held as text for this topic either.

Exam pearls

  • Severe AS by velocity or gradient (ACC/AHA 2020 Table 13, Stages of AS, Stages C1, C2 and D1): Vmax ≥4 m/s or mean ΔP ≥40 mm Hg; very severe AS (Stage C1 cell) is Vmax ≥5 m/s or mean P ≥60 mm Hg.[2]
  • Most robust AS parameter (ESC/EACTS 2025): the mean pressure gradient.[1]
  • Low flow (ESC/EACTS 2025): SVi 35 mL/m² is conventionally accepted, although sex-specific thresholds have been proposed; flow reserve is a ≥20% increase in stroke volume with low-dose dobutamine, and with a 10%–20% change a projected AVA is calculated.[1]
  • True severe AS on dobutamine (ACC/AHA 2020): fixed valve area, velocity ≥4 m/s (mean gradient ≥40 mm Hg) at any flow rate, valve area still ≤1.0 cm².[3]
  • Severe AR (ACC/AHA 2020 Table 15, Stages of Chronic AR, Stages C and D): diagnosis of chronic severe AR requires evidence of LV dilation as well as the severe haemodynamic criteria.[2]
  • Primary MR (ACC/AHA 2020 Table 17, Stages of Chronic Primary MR): severe criteria are central jet MR >40% LA or holosystolic eccentric jet MR, vena contracta ≥0.7 cm, regurgitant volume ≥60 mL, regurgitant fraction ≥50%, ERO ≥0.40 cm² and angiographic grade 3+ to 4+, and the table footnote says not all criteria for each category will be present in each patient; Stage C2 is LVEF ≤60% and/or LVESD ≥40 mm.[2]
  • TR (ACC/AHA 2020 Table 20, Stages of TR): severe criteria are central jet ≥50% RA, vena contracta width ≥0.7 cm, ERO ≥0.40 cm², regurgitant volume ≥45 mL, a dense continuous wave signal with triangular shape and hepatic vein systolic flow reversal.[2]
  • MS (ACC/AHA 2020 Table 16, Stages of MS): severe stages have mitral valve area ≤1.5 cm² and diastolic pressure half-time ≥150 ms; the mean gradient (usually >5 mm Hg to 10 mm Hg in severe MS) is not a severity criterion because it varies with heart rate and flow.[2]
  • Prosthetic aortic BHV, severe haemodynamic deterioration (ESC/EACTS 2025 Table 12, criteria for the diagnosis of moderate or severe aortic and mitral haemodynamic valve deterioration; SVD or non-structural valve dysfunction (except PVL or PPM)ᵃ, thrombosis, or endocarditis; ᵃobstruction by pannus; dilatation of the aortic root after stentless BHV; or AV-sparing operations): increase in mean transvalvular gradient ≥20 mmHg resulting in mean gradient ≥30 mmHg, AND decrease in EOA ≥0.6 cm² or ≥50% and/or decrease in DVI ≥0.2 or ≥40% versus the echo 1–3 months post-procedure; OR new occurrence or increase of ≥2 grades of intraprosthetic AR resulting in ≥ moderate-to-severe AR.[1]
Say it this way at the viva
  • "I grade on integrated, quantitative data checked for consistency, as ESC/EACTS 2025 asks; when the numbers disagree in AS, flow state may be further categorised by SVi, and in low-flow, low-gradient AS with reduced LVEF I use dobutamine stress echo and the CT calcium score as complementary tests, quoting the calcium thresholds by body."[1][3]
References6ShowHide
  1. [1]Praz F, et al. 2025 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J, 2025.PMID 40878295
  2. [2]Otto CM, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 2021.PMID 33332150
  3. [3]Otto CM, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2021.PMID 33342586
  4. [4]Chong A, et al. 2024 CSANZ Position Statement on Indications, Assessment and Monitoring of Structural and Valvular Heart Disease With Transthoracic Echocardiography in Adults. Heart Lung Circ, 2024.PMID 38749800
  5. [5]Køber L, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
  6. [6]De Backer J, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294

Test yourself

Practise what you just read

  • SAQ
  • Case
PreviousECG rhythm recognition and conduction blocksimaging-noninvasiveNextEchocardiography: EF quantitation and diastology basicsimaging-noninvasive