Asymptomatic severe aortic stenosis: exercise testing and surgery triggers

This page is about the patient with severe aortic stenosis (AS) who reports no symptoms, a group that ESC/EACTS 2025 says makes up to 40% of patients with severe AS at diagnosis.^[1] It covers how severe AS is defined, how exercise testing unmasks symptoms, the asymptomatic intervention rows, surveillance intervals, and pointers on TAVI versus SAVR. The full TAVI-versus-SAVR evidence and symptomatic AS are covered in Severe aortic stenosis: TAVI versus surgical valve replacement. Valve choice and antithrombotic therapy after replacement are covered in Prosthetic heart valves: choice, anticoagulation and thrombosis.

Why the asymptomatic patient is a problem

ESC/EACTS 2025 says up to 40% of patients with severe AS do not report symptoms at the time of diagnosis.^[1] In its general section on exercise testing in valve disease, ESC/EACTS 2025 notes that because valve lesions progress slowly, patients may gradually limit their activity over several years and deny actual symptoms that exercise testing can unmask.^[1] It says this is particularly important in AS, because once symptoms occur there is a sharp increase in the risk of sudden cardiac death unless a valve intervention is performed.^[1]

ACC/AHA 2020 puts numbers on the asymptomatic phase.^[3] It says event-free survival at 2 years is about 75% to 80% with a jet velocity below 3.0 m/s, compared with only 30% to 50% with a jet velocity of 4.0 m/s or more.^[3] In asymptomatic severe AS with normal LV systolic function, it says survival during the asymptomatic phase is similar to age-matched controls.^[3] The risk of sudden death is low (below 1% per year) when patients are followed prospectively and promptly report symptom onset.^[3]

ACC/AHA 2020 adds that periodic monitoring is needed in asymptomatic severe AS because symptom onset is insidious and may not be recognised by the patient.^[3] It says the most common initial symptom of AS is exertional dyspnoea or decreased exercise tolerance.^[3] ESC/EACTS 2025 says AS evolves slowly from mild to severe obstruction through increasing valve fibrosis and calcification, although progression accelerates as haemodynamic severity increases.^[1]

Defining severe AS and its haemodynamic grades

ESC/EACTS 2025 calls echocardiography key to confirming the diagnosis and assessing the anatomy and severity of stenosis.^[1] European grading rests on the mean pressure gradient (the most robust parameter), the peak transvalvular velocity (Vmax) and the effective aortic valve area (AVA).^[1] The guideline adds that AVA is theoretically the ideal parameter, but there are numerous technical limitations in calculating it.^[1]

When these echo parameters disagree, ESC/EACTS 2025 says AS may be further categorised by flow state using stroke volume index (SVi).^[1] A threshold of 35 mL/m² is conventionally accepted to separate low from normal flow, although sex-specific thresholds have been proposed.^[1]

ESC/EACTS 2025: concordant and discordant echo criteria in AS (guideline text; no class or level given)

^[1]

In low-flow, low-gradient AS, ESC/EACTS 2025 says cardiac CT (CCT) calcium scoring of the aortic valve provides important adjunctive information, because it correlates with haemodynamic severity, progression and clinical outcomes.^[1] It says values above 2000 Agatston units (AU) in men and above 1200 AU in women indicate severe AS with high sensitivity and specificity (about 85%).^[1] It asks for cautious interpretation when severe AS can develop without pronounced valve calcification.^[1] Its examples are bicuspid valves, concomitant amyloidosis, and predominantly fibrotic stenosis associated with post-rheumatic, radiation-induced and inflammatory disease.^[1]

ACC/AHA 2020 stages

ACC/AHA 2020 Table 13 stages AS from patients at risk (Stage A) and progressive obstruction (Stage B) to severe asymptomatic (Stage C) and symptomatic AS (Stage D).^[3][2] It says haemodynamic severity is best characterised by the transaortic maximum velocity (or mean pressure gradient) when the transaortic volume flow rate is normal.^[3]

ACC/AHA 2020 Table 13 (Stages of AS): selected rows, Stages B, C1 and C2

^{[2] [3]}

The ACC/AHA 2020 supportive text adds that in very severe AS (aortic velocity 5.0 m/s or more or mean pressure gradient 60 mm Hg or more), the rate of symptom onset is approximately 50% at 2 years.^[3][2]

^{[2] [1] [3]}

Unmasking symptoms with exercise testing

Exercise testing is the tool for unmasking symptoms in a patient who reports none.^[1] ESC/EACTS 2025 says exercise testing can unmask symptoms and haemodynamic intolerance (fall in BP above 20 mm Hg) and is recommended for risk stratification in asymptomatic patients with severe AS.^[1] That sentence is in the guideline text (no class or level given).^[1] In roughly one-third of patients with severe AS who report no symptoms, the guideline says exercise testing can uncover symptoms or reduced exercise capacity attributable to AS, and such patients should be treated as symptomatic.^[1]

ESC/EACTS 2025 also lists limits.^[1] Exercise testing is not always feasible because of frailty or impaired mobility.^[1] Misconceptions about its risk and tolerability contribute to its overall underuse in valve disease, despite data confirming its safety in most asymptomatic patients.^[1]

• What it adds (ESC/EACTS 2025 text). Exercise testing may provide additional information about the haemodynamic severity of valve disease and help determine the risk and optimal timing of intervention by objectively evaluating functional capacity.^[1]
• Exercise echocardiography (ESC/EACTS 2025 text). It may provide additional prognostic information by assessing the increase in mean pressure gradient and change in LV function.^[1]
• Cardiopulmonary exercise testing (ESC/EACTS 2025 text). Eventually complemented by echocardiography, it can help to uncover cardiac dysfunction in asymptomatic patients, discriminate cardiac from pulmonary limitation or deconditioning in patients with non-specific symptoms, and inform risk stratification.^[1]

ACC/AHA 2020: recommendations for exercise testing in patients with AS (both rows)

^[3]

The ACC/AHA 2020 supportive text sets the conditions.^[3] Performed under the direct supervision of an experienced clinician, with close monitoring of blood pressure and ECG, exercise testing in asymptomatic patients is relatively safe.^[3] It may provide information not evident during the initial clinical evaluation, particularly when the patient's functional capacity is unclear.^[3] As reported in several prospective and retrospective studies, the risk of exercise testing is low in asymptomatic patients with AS.^[3] It is avoided in symptomatic AS because of a high risk of complications, including syncope, ventricular tachycardia and death.^[3]

^{[3] [1]}

Reading the test

• Provoked symptoms (ACC/AHA 2020). Patients with symptoms provoked by exercise testing should be considered symptomatic, even if the clinical history is equivocal.^[3]
• Which symptoms (ACC/AHA 2020). Separating normal exercise limits from AS symptoms can be challenging, particularly in elderly sedentary patients; exercise-induced angina, excessive dyspnoea early in exercise, dizziness and syncope are consistent with symptoms of AS.^[3]
• Beyond symptoms (ACC/AHA 2020). Exercise testing can also identify a limited exercise capacity or an abnormal blood pressure response.^[3]
• Exercise haemodynamics (ACC/AHA 2020). Recording aortic valve haemodynamics with exercise is of limited value and does not show additive value for predicting clinical outcome when baseline measures of haemodynamic severity and functional status are considered.^[3]
• What follows (ACC/AHA 2020). When symptoms are provoked by exercise testing, the patient is considered symptomatic and meets a COR 1 recommendation for AVR.^[3]
• A blood pressure fall (ACC/AHA 2020). The rate of symptom onset within 1 to 2 years is high (about 60% to 80%) in patients without overt symptoms who show a systolic fall of 10 mm Hg or more from baseline to peak exercise, or a significant decrease in exercise tolerance compared with age and sex normal standards.^[3]
• A flat blood pressure response (ACC/AHA 2020). Management of patients with a lack of appropriate rise in BP with exercise is less clear; decisions about elective AVR include surgical risk, patient preferences and clinical factors such as age and comorbid conditions.^[3]

Newer trial data on treadmill testing

The EARLY TAVR treadmill registry is a prespecified, registry-based follow-up of the EARLY TAVR randomised trial, at 75 clinical sites across the US.^[9] Between July 2017 and December 2021, apparently asymptomatic patients with severe AS underwent standardised treadmill stress testing (TST).^[9] Those with a normal TST were randomised to TAVI or clinical surveillance; those with a positive TST were invited into a prospective registry and followed through 2 years.^[9]

Of 1250 patients screened, 962 met trial criteria: 816 (84.8%) had a normal TST and 146 (15.2%) a positive one.^[9] Of these, 105 consented to enrol in the registry.^[9] TST was found to be safe, with no reported deaths, syncope or cardioversions.^[9] Among patients with a positive TST, rates of AVR were 79.9% at 1 year and 85.9% at 2 years.^[9] The authors concluded that 20% of these patients remained untreated at 1 year despite having an indication for prompt treatment.^[9]

Rates of mortality and AVR were similar for patients with a class I indication (symptoms during testing) and those with a class IIa indication (drop in systolic blood pressure).^[9] Multivariable baseline predictors of a positive TST were higher peak velocity, lower ejection fraction, prior coronary artery bypass and prior stroke.^[9]

Natriuretic peptides and imaging markers

ESC/EACTS 2025 says biomarkers of cardiac wall stress, such as BNP, or of myocardial damage, such as troponin, may help to monitor valve disease and determine the most appropriate timing of intervention.^[1] In valve disease, the natriuretic peptide ratio (measured BNP or NT-proBNP over the upper limit of normal for age, sex and assay) has been shown to be a powerful, independent and incremental predictor of mortality.^[1] In AS, the guideline says natriuretic peptides can help to identify high-risk asymptomatic patients who may benefit from early intervention.^[1] They can also be used to arbitrate the source of symptoms in patients with several potential causes.^[1]

ACC/AHA 2020 calls an elevated serum BNP a marker of subclinical heart failure and LV decompensation.^[3] It reports a cohort of 387 asymptomatic adults with severe AS in which a BNP above 300 pg/mL (3 times normal) carried a hazard ratio of 7.38 for AS-related events over 5 years.^[3] It adds that serum BNP levels are also predictive of symptom onset during follow-up and of persistent symptoms after AVR.^[3]

A 2025 analysis of the EARLY TAVR trial looked at single biomarker measurements.^[10] A core laboratory measured NT-proBNP and high-sensitivity troponin T in 798 of the 901 patients randomised in EARLY TAVR (89%).^[10] Higher levels were broadly associated with higher event rates in asymptomatic severe high-gradient AS.^[10] Yet the relative benefit of early TAVI was consistent regardless of baseline biomarker levels, and tended to be more pronounced at the lowest levels.^[10] The authors suggest limited value for single measurements of these biomarkers to guide the timing of TAVI in asymptomatic patients.^[10]

• Global longitudinal strain (ESC/EACTS 2025 text). Assessment of GLS can be useful for risk stratification and evaluation of extravalvular cardiac damage; a threshold of −15% may contribute to identifying patients with severe asymptomatic AS at increased risk of clinical deterioration or premature mortality.^[1]
• Cardiac magnetic resonance (ESC/EACTS 2025 text). It is used to identify altered global LV geometry due to remodelling and to quantify myocardial scarring and diffuse fibrosis, which are associated with the occurrence of adverse events.^[1]
• Fibrosis and early intervention (EVOLVED post hoc analysis). In a post hoc analysis of the trial, in 224 asymptomatic participants with severe AS and midwall fibrosis on cardiac magnetic resonance, followed for a median of 42 months, fibrosis burden (per 1% increase) was associated with an increase in the primary end point (HR 1.23) but not with all-cause death.^[12]
• No interaction (EVOLVED post hoc analysis). There was no interaction between randomisation arm and midwall fibrosis burden for the primary (P for interaction = .39) or secondary end points.^[12]

When to intervene: the asymptomatic rows

ESC/EACTS 2025 says intervention is recommended in asymptomatic patients with severe AS and an LVEF below 50% without another cause.^[1] For severe high-gradient AS without adverse prognostic features, it says close active clinical surveillance, so-called watchful waiting, has previously been the default management strategy.^[1] It says four RCTs comparing early intervention with clinical surveillance suggest that early intervention should be considered as an alternative in patients at low procedural risk.^[1]

That approach is reinforced if adverse prognostic features are present.^[1] The guideline's list is very high Vmax, elevated natriuretic peptides, severe valve calcification, rapid Vmax progression, or LVEF below 55%.^[1] Restricted local resources (that may impede close surveillance) or long waiting lists (that preclude prompt treatment when symptoms develop) are further arguments favouring early intervention.^[1]

ESC/EACTS 2025 Recommendation Table 4: selected rows (all four asymptomatic rows)

^[1]

In ESC/EACTS 2025 Figure 7 (management of patients with severe aortic stenosis), footnotes c and d qualify two items of a list headed "presence of one or more of the following", and footnote e qualifies close active surveillance.^[1] The item for severe valve calcification and Vmax progression of 0.3 m/s/year or more carries footnote c: an aortic valve calcium score above 2000 in men and above 1200 in women.^[1] The item for elevated BNP or NT-proBNP levels attributable to AS carries footnote d: more than three times the age- and sex-corrected normal range.^[1] Close active surveillance carries footnote e: educate the patient and reassess at least every 6 months, or promptly if symptoms occur.^[1]

Once symptoms appear, the symptomatic rows apply.^[1] ESC/EACTS 2025 recommends intervention 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) (Class I, Level B).^[1] Its text adds that early intervention is strongly recommended in all symptomatic patients with an estimated life expectancy exceeding 1 year.^[1]

^{[3] [1]}

ACC/AHA 2020 timing rows

ACC/AHA 2020 says its timing recommendations apply to both SAVR and TAVI.^[3] Its Figure 2 legend says periodic monitoring is indicated for all patients in whom AVR is not yet indicated, including asymptomatic (Stage C) patients.^[3]

ACC/AHA 2020 Recommendations for Timing of Intervention of AS: selected rows (rows 1-3 and 6-11; rows 4 and 5, for symptomatic low-flow, low-gradient severe AS, Stages D2 and D3, are omitted)

^[3]

The ACC/AHA 2020 supportive text explains the thresholds.^[3] In very severe AS (aortic velocity 5.0 m/s or more, or mean gradient 60 mm Hg or more), the rate of symptom onset is approximately 50% at 2 years.^[3] On multivariable analysis of a large cohort of adults with asymptomatic AS (more than 500 patients), an aortic velocity of 5 m/s or more was associated with a more than 6-fold increased risk of cardiovascular mortality.^[3] In very severe asymptomatic AS with low surgical risk, the decision between AVR and watchful waiting takes into account patient age, avoidance of patient–prosthesis mismatch, anticoagulation issues and patient preferences.^[3]

On progression, ACC/AHA 2020 says the average rate for calcific stenosis of a trileaflet valve is a rise in aortic velocity of about 0.3 m/s per year, with marked variability between patients.^[3] Predictors of rapid progression include older age, more severe valve calcification and a faster rate of haemodynamic progression on serial studies.^[3] On LVEF, it says an aortic velocity of 5 m/s or more or an LVEF below 60% are each associated with higher all-cause and cardiovascular mortality rates in the absence of AVR.^[3] Requiring at least 3 serial imaging studies showing a consistent decline in LVEF ensures that the changes are not simply due to recording, measurement or physiological variability.^[3]

For the LVEF-below-50% row (Stage C2), ACC/AHA 2020 says survival is better with AVR than with medical treatment in patients with a low LVEF and severe AS.^[3] It explains that the depressed LVEF in many patients is caused by excessive afterload (afterload mismatch), and LV function improves after AVR in such patients.^[3]

How the two guidelines line up

^{[1] [3]}

The randomised trials of early intervention

ESC/EACTS 2025 describes four RCTs comparing early intervention with clinical surveillance: EARLY TAVR, EVOLVED, RECOVERY and AVATAR.^[1] The summaries below come from each trial report's own abstract, with ESC/EACTS 2025 readings marked as such; RECOVERY has a 2020 report and a 10-year report (2026).^[4][16]

^{[4] [1] [16] [5] [7] [8]}

More from the trial reports

• RECOVERY, 2020 report. Death from any cause during follow-up (the major secondary end point) occurred in 7% of the early-surgery group and 21% of the conservative-care group (HR 0.33); ESC/EACTS 2025 reports that RECOVERY showed a reduction in all-cause mortality following early SAVR over a mean follow-up of 6.2 years. In the conservative-care group, the cumulative incidence of sudden death was 4% at 4 years and 14% at 8 years.^[4][1]
• RECOVERY, 10-year report (2026). Among the 145 randomised asymptomatic patients with very severe AS, death from any cause occurred in 11 patients (15%) with early surgery and 23 (32%) with conservative care (HR 0.42, 95% CI 0.21–0.86). The authors conclude that early surgery led to a lower risk of the composite of operative mortality or cardiovascular death than conservative care at 10 years.^[16]
• AVATAR, operative data. In the early-surgery group, 72 patients (92.3%) underwent SAVR, with an operative mortality of 1.4%.^[5]
• AVATAR, long-term follow-up. In 157 low-risk patients (mean STS score 1.7%), all with negative exercise stress testing, the primary composite occurred in 23.1% with early surgery and 46.8% with conservative treatment after a median of 63 months (HR 0.42; P = .002).^[6]
• AVATAR, components. Kaplan-Meier estimates of all-cause death (HR 0.44) and heart failure hospitalisation (HR 0.21) were significantly lower with early surgery than with conservative treatment.^[6]
• EARLY TAVR, components. Death occurred in 8.4% with TAVI and 9.2% with surveillance, stroke in 4.2% and 6.7%, and unplanned cardiovascular hospitalisation in 20.9% and 41.7%.^[7]
• EARLY TAVR, crossover. During a median follow-up of 3.8 years, 87.0% of the clinical surveillance group underwent aortic valve replacement.^[7]
• EVOLVED. In the trial conducted August 2017 to October 2022, with final follow-up on July 26, 2024, unplanned AS-related hospitalisation was 6% with early intervention and 17% with conservative management (HR 0.37); the authors note a wide 95% CI around the primary end point, with further research needed.^[8]

How ESC/EACTS 2025 reads the trials

• EARLY TAVR. ESC/EACTS 2025 reports that the trial showed a 50% reduction in its primary composite with pre-emptive intervention, driven by the 26.2% of the surveillance group who converted to TAVI within 6 months of randomisation because of symptoms or adverse prognostic factors.^[1]
• EARLY TAVR, hard end points. The guideline reports no significant difference in strokes and all-cause mortality over 5-year follow-up.^[1]
• EVOLVED. ESC/EACTS 2025 reports that early intervention failed to reduce all-cause death or unplanned AS-related hospitalisation compared with clinical surveillance, and notes that the study was underpowered and the median time to intervention was prolonged to 5 months.^[1]
• RECOVERY and AVATAR. The guideline reports a reduction in all-cause mortality after early SAVR in RECOVERY over a mean follow-up of 6.2 years. In AVATAR it reports a reduction in the composite primary end point after a mean of 2.5 years, with a significant reduction in heart failure hospitalisations and mortality at long-term follow-up.^[1]
• Limits of the surgical trials. ESC/EACTS 2025 lists small sample sizes, selected young populations at low surgical risk (mean ages 64 and 67 years) and mostly very severe AS.^[1]
• Pooled evidence. The guideline reports a meta-analysis of the four RCTs in which early intervention was associated with a significant reduction in unplanned cardiovascular or heart failure hospitalisation and stroke, but not all-cause or cardiovascular mortality. It lists trial heterogeneity and the study-level analysis as limitations.^[1]
• More trials coming. ESC/EACTS 2025 says additional RCTs (NCT04204915 and NCT03972644) will further inform the management of severe asymptomatic AS.^[1]

What happens to the surveillance arm

A 2025 analysis of the EARLY TAVR valve implant population compared patients who had early TAVI with surveillance patients who had delayed AVR.^[11] Delayed AVR was classed by presentation as a progressive valve syndrome (for example NYHA class II) or an acute valve syndrome (for example NYHA class III or IV, or syncope).^[11] Through 5 years, 87.0% of surveillance patients (388 of 446) underwent delayed AVR; 39.2% presented with an acute valve syndrome, and median time to delayed AVR was 11.1 months.^[11]

For the composite of death, stroke or heart failure hospitalisation at 2 years after the procedure, early TAVI was better than delayed AVR (adjusted HR 0.61).^[11] Delayed AVR with an acute valve syndrome was associated with worse outcomes than early TAVI (adjusted HR 2.12), driven largely by stroke.^[11]

EARLY TAVR analyses published in 2026

A 2026 analysis stratified the EARLY TAVR trial population into four age groups: 65 to 69 years (n=141), 70 to 74 years (n=263), 75 to 79 years (n=250) and 80 years or older (n=247).^[17] No interaction was detected between age and the treatment effect of early TAVI versus clinical surveillance for the composites or individual outcomes.^[17] At 2 years, the absolute difference in heart failure hospitalisation between the early TAVI and surveillance arms was greatest in the oldest patients.^[17] It was 9.1% at 80 years or older, 5.9% at 75 to 79, 5.1% at 70 to 74 and 4.4% at 65 to 69.^[17] In the surveillance group, time to conversion to AVR was similar across all age groups (median 11 months).^[17] The authors write that these data suggest early TAVI should be considered in all age groups above 65 years.^[17]

A second 2026 analysis, of the 901 patients randomised at 75 centres in the United States and Canada, looked at integrated LV health.^[18] The protocol defined it as absolute LV global longitudinal strain of 15% or more, LV mass index below 115 g/m² in men or below 95 g/m² in women, and left atrial volume index of 34 mL/m² or less.^[18] Benefit of early TAVI over clinical surveillance was seen whether LV health was normal or not; because LV health was not prespecified as a stratification variable, these analyses are exploratory.^[18] In the intention-to-treat population, normal integrated LV health at 2 years was less frequent in the surveillance group than in those treated early (35.9% versus 48.1%; P < 0.001).^[18] The authors conclude that these exploratory findings suggest limited value for measures of LV health to guide the timing of TAVI in asymptomatic patients.^[18]

Surveillance: intervals and what to watch

ESC/EACTS 2025 says the rate of progression of AS varies widely, and that asymptomatic patients, their family and medical caregivers need careful education.^[1] It puts particular emphasis on regular follow-up (ideally at a Heart Valve Centre) and prompt reporting of symptoms.^[1]

Surveillance intervals by AS severity

^{[1] [2]}

• Shorten the interval as AS worsens (ESC/EACTS 2025). With increasing stenosis severity, progression accelerates and follow-up intervals should be gradually reduced.^[1]
• Moderate AS (ESC/EACTS 2025). Several studies suggest the prognosis of moderate degenerative AS is worse than previously considered, particularly with significant valve calcification.^[1]
• Natriuretic peptides (ESC/EACTS 2025). Serial measurements can provide additional useful information on the timing of treatment.^[1]
• Table 5 footnotes (ACC/AHA 2020). The AS column (headed Aortic Stenosis with an asterisk) applies with normal stroke volume; patients with mixed valve disease may need serial evaluations at shorter intervals than single-valve lesions.^[2]
• What the ACC/AHA intervals are not (ACC/AHA 2020). The Table 5 intervals apply to most patients with each lesion and do not take into consideration the aetiology of the valve disease.^[2]
• Individual timing (ACC/AHA 2020). Timing of periodic clinical evaluation in asymptomatic severe AS depends on comorbidities and patient-specific factors, as well as AS severity.^[3]

ACC/AHA 2020 also lists triggers for an earlier echo.^[3] In known AS, repeat TTE is prudent when the murmur becomes louder or peaks later in systole, A2 is diminished or absent, or symptoms occur that might be attributable to AS.^[3] It is also appropriate with increased haemodynamic demands, either elective, such as non-cardiac surgery or pregnancy, or acute, such as systemic infection, anaemia or gastrointestinal bleeding.^[3]

For moderate AS, ACC/AHA 2020 gives an average annual progression of a 0.3 m/s rise in velocity, a 7 mm Hg rise in mean gradient and a 0.1 cm² fall in valve area.^[3] It notes marked individual variability, with faster progression in older patients and with more severe leaflet calcification.^[3]

APRAISE-AS (2026), a 12-month open-label, two-arm, parallel-group randomised controlled pilot trial in two tertiary cardiac centres, assigned 38 participants with asymptomatic severe AS to standard care (n=19) or standard care plus the APRAISE-AS remote-monitoring intervention (n=19).^[19] The trial evaluated the utility of remote monitoring, incorporating a symptom tracker, frailty assessment and quality of life score, to pre-empt or detect a change in clinical status and inform patient management.^[19] The authors conclude that remote monitoring of severe asymptomatic AS can be safely delivered in practice; although the pilot did not recruit to target, a digitally enabled clinical pathway was acceptable to clinicians and patients.^[19]

^{[2] [1]}

Medical therapy while waiting

• No drug changes the valve (ESC/EACTS 2025 text). No medical therapies have been shown to influence the natural history of AS to date.^[1]
• Statins (ACC/AHA 2020). In calcific AS (Stages B and C), statin therapy is not indicated for prevention of haemodynamic progression of AS (COR 3: No Benefit, LOE A).^[3]
• Hypertension (ESC/EACTS 2025 text). Coexistent hypertension should be treated to avoid additional afterload, preferably with renin-angiotensin system blockers, although careful titration is required to avoid symptomatic hypotension.^[1]
• Hypertension (ACC/AHA 2020). In asymptomatic AS (Stages B and C), hypertension should be treated according to standard GDMT, started at a low dose and gradually titrated upward as needed, with appropriate clinical monitoring (COR 1, LOE B-NR).^[3]

TAVI or SAVR when an asymptomatic patient needs a valve

This section gives pointers only; the trials and anatomy behind the choice are covered in Severe aortic stenosis: TAVI versus surgical valve replacement. ESC/EACTS 2025 says the mode of intervention depends on estimated life expectancy, expected prosthesis durability, patient preference and the trade-offs of each option.^[1]

ESC/EACTS 2025 Recommendation Table 4: selected rows (mode of intervention; the non-transfemoral TAVI, bicuspid TAVI and balloon valvotomy rows are omitted)

^[1]

The ESC/EACTS 2025 asymptomatic rows do not name a mode of intervention; the mode-of-intervention rows sit in the same Recommendation Table 4, whose title covers both symptomatic and asymptomatic severe AS.^[1] EARLY TAVR tested transfemoral TAVI with a balloon-expandable valve, while RECOVERY and AVATAR tested early surgery.^[7][4][5]

ACC/AHA 2020 Section 3.2.4.2: selected rows (rows 1-6)

^[3]

The ACC/AHA 2020 supportive text explains its row 5.^[3] It says published RCTs comparing TAVI and SAVR included only patients with symptoms attributable to severe AS.^[3] Asymptomatic patients with COR 2a indications for AVR should either undergo SAVR or wait until a COR 1 indication is present before intervention.^[3] An LVEF below 50% in a patient with severe AS is a COR 1 indication for AVR, so the choice of TAVI versus SAVR then follows the same considerations as in patients with symptoms attributable to severe AS.^[3] ACC/AHA 2020 says its age breakpoints serve as the starting point for shared decision-making, not as absolute values for chronological age.^[3]

^{[3] [1]}

Special situations

Other cardiac surgery

ESC/EACTS 2025 recommends SAVR in symptomatic and asymptomatic patients with severe AS undergoing CABG or surgical intervention on the ascending aorta (Class I, Level C).^[1] ACC/AHA 2020 says AVR is indicated in asymptomatic patients with severe AS (Stage C1) who are undergoing cardiac surgery for other indications (COR 1, LOE B-NR).^[3] Its supportive text says the added risk of AVR at the time of other cardiac surgery is less than the risk of reoperation within 5 years.^[3]

For moderate AS, ESC/EACTS 2025 says SAVR should be considered in symptomatic and asymptomatic patients undergoing CABG or surgical intervention on the ascending aorta (Class IIa, Level C).^[1] Its footnote defines moderate AS as an AVA of 1.0–1.5 cm² (or mean aortic gradient of 25–40 mmHg) in normal-flow conditions, and says clinical assessment is essential to determine whether SAVR is appropriate for an individual patient.^[1] ACC/AHA 2020 says AVR may be considered in moderate AS (Stage B) in patients undergoing cardiac surgery for other indications (COR 2b, LOE C-EO).^[3]

Women contemplating pregnancy

The 2025 ESC guideline on cardiovascular disease and pregnancy has three severe aortic stenosis rows in its Recommendation Table 18 (native valve disease and pregnancy).^[15] Intervention should be considered before pregnancy in those with asymptomatic severe aortic stenosis after counselling on the risks and benefits (ESC 2025, Class IIa, Level C).^[15] Intervention is recommended before pregnancy in symptomatic patients with severe aortic stenosis (ESC 2025, Class I, Level C).^[15] In very selected symptomatic pregnant women with severe aortic stenosis not responding to medical therapy, non-surgical options such as balloon valvuloplasty or TAVI may be considered (ESC 2025, Class IIb, Level C).^[15] The ESC/EACTS 2025 valve guideline lists, among conditions that should be corrected prior to considering pregnancy, severe symptomatic AS, or asymptomatic patients with impaired LV function or a pathological exercise test (no class or level given).^[1]

Patients who cannot exercise

ESC/EACTS 2025 says exercise testing is not always feasible because of frailty or impaired mobility.^[1] Its Class IIa, Level A row (severe, high-gradient AS, LVEF of 50% or more, low procedural risk) asks for absence of symptoms to be confirmed by a normal exercise test, if feasible.^[1]

Pitfalls

• Do not call AS moderate on a low gradient alone. ESC/EACTS 2025 separates low-flow, low-gradient AS (SVi ≤35 mL/m²) from normal-flow, low-gradient AS (SVi above 35 mL/m²); patients with the normal-flow pattern usually have moderate stenosis.^[1]
• Do not skip the cause of a low LVEF. Both ESC/EACTS 2025 LVEF triggers require that there is no other cause: LVEF below 50% (Class I, Level B), and LVEF below 55% as a parameter of the Class IIa, Level B row for LVEF of 50% or more with low procedural risk.^[1]
• Do not act on one BNP. The ESC/EACTS 2025 BNP parameter needs levels more than three times the age- and sex-corrected normal range, confirmed on repeated measurement without other explanation.^[1]
• Do not forget the procedural risk. Every ESC/EACTS 2025 Class IIa asymptomatic row with LVEF of 50% or more requires low procedural risk, and the ACC/AHA 2020 COR 2a rows for AVR in asymptomatic severe AS (Stage C1) require low surgical risk.^[1][3]

Evidence, guidelines and regional differences

ANZ practice

No NHFA or CSANZ guideline on aortic stenosis or on the timing of intervention was found in the guidelines checked for this topic, so the ESC/EACTS and ACC/AHA rows above apply. The 2024 CSANZ position statement covers transthoracic echocardiography (TTE) in structural and valvular heart disease in adults.^[13] It aims to give clinicians a framework of acceptable indications for initial and serial TTE in commonly encountered adult conditions, and sets the minimum required standard for TTE examinations and reporting.^[13] Its abstract lists valvular heart diseases among the areas covered.^[13] Only its abstract is held for this topic, so its surveillance intervals are not quoted here.

The 2021 CSANZ and ANZSCTS position statement sets the minimum standard for accreditation of TAVI institutions and operators in Australia.^[14] It states that it is not a guideline statement.^[14] EVOLVED recruited at 24 cardiac centres across the UK and Australia.^[8]

Guidelines checked

A row called the newer one, or said to apply, is so among the guidelines checked for this topic:

• Sources of the rows and statements used: ESC/EACTS valvular heart disease (2025; Recommendation Tables 4 and 5 from the version-of-record PDF, narrative from the journal text); ESC cardiovascular disease and pregnancy (2025; Recommendation Table 18); ACC/AHA valvular heart disease (2020; rows and supportive text from the JACC co-publication, Tables 5 and 13 from Circulation); trial reports, abstracts only; and the 2024 CSANZ TTE and 2021 CSANZ/ANZSCTS TAVI statements, abstracts only.^{[1][15][3][2][7][13][14]}
• Also swept for same-month or newer rows on aortic stenosis: every held guideline published in the same month as, or after, the guideline that owns each row; for the ACC/AHA 2020 rows that is every held ESC and ACC/AHA guideline from 2021 on, including the 2026 ESC heart failure and cardiac rehabilitation guidelines.
• Not held as text for this topic: the 2025 ACC/AHA/HRS/ISACHD/SCAI adult congenital heart disease guideline and the 2026 AHA/ACC multisociety perioperative guideline.
• Superseded and not used as a source for this topic: the 2021 ESC/EACTS valvular heart disease guideline, replaced by the 2025 edition.

Exam pearls

• ESC/EACTS 2025: LVEF below 50% without another cause, intervention recommended (Class I, Level B); severe high-gradient AS with LVEF of 50% or more, low procedural risk and a normal exercise test if feasible, intervention should be considered as an alternative to close active surveillance (Class IIa, Level A).^[1]
• ESC/EACTS 2025 Class IIa, Level B parameters (LVEF of 50% or more, low procedural risk): mean gradient ≥60 mmHg or Vmax above 5.0 m/s; severe calcification plus Vmax progression ≥0.3 m/s/year; BNP/NT-proBNP more than three times the age- and sex-corrected normal range, confirmed on repeat without other explanation; LVEF below 55% without another cause.^[1]
• Exercise BP: ESC/EACTS 2025 uses a sustained fall above 20 mmHg (Class IIa, Level C); ACC/AHA 2020 (apparently asymptomatic severe AS, Stage C1, low surgical risk) uses a systolic fall of 10 mm Hg or more from baseline to peak exercise, or decreased exercise tolerance normalised for age and sex (COR 2a, LOE B-NR).^[1][3]
• Very severe AS: ESC/EACTS 2025 defines it as a mean gradient ≥60 mmHg or Vmax above 5.0 m/s; the ACC/AHA 2020 row for asymptomatic very severe AS (aortic velocity of 5 m/s or more) with low surgical risk is COR 2a, LOE B-R.^[1][3]
• Surveillance of severe asymptomatic AS: at least every 6 months (ESC/EACTS 2025 text); echo every 6–12 months (ACC/AHA 2020 Table 5).^[1][2]
• ACC/AHA 2020 prefers SAVR to TAVI for asymptomatic patients with COR 2a indications (abnormal exercise test, very severe AS, rapid progression or elevated BNP) (COR 1, LOE B-NR).^[3]

References19ShowHide

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]Kang DH, et al. Early Surgery or Conservative Care for Asymptomatic Aortic Stenosis. N Engl J Med, 2020.PMID 31733181
5. [5]Banovic M, et al. Aortic Valve Replacement Versus Conservative Treatment in Asymptomatic Severe Aortic Stenosis: The AVATAR Trial. Circulation, 2022.PMID 34779220
6. [6]Banovic M, et al. Aortic valve replacement vs. conservative treatment in asymptomatic severe aortic stenosis: long-term follow-up of the AVATAR trial. Eur Heart J, 2024.PMID 39217448
7. [7]Généreux P, et al. Transcatheter Aortic-Valve Replacement for Asymptomatic Severe Aortic Stenosis. N Engl J Med, 2025.PMID 39466903
8. [8]Loganath K, et al. Early Intervention in Patients With Asymptomatic Severe Aortic Stenosis and Myocardial Fibrosis: The EVOLVED Randomized Clinical Trial. JAMA, 2025.PMID 39466640
9. [9]Généreux P, et al. Treadmill Stress Test in Patients With Asymptomatic Severe Aortic Stenosis: A Prespecified Registry-Based Follow-Up of the EARLY TAVR Randomized Clinical Trial. JAMA Cardiol, 2026.PMID 42485012
10. [10]Lindman BR, et al. Cardiac Biomarkers in Patients With Asymptomatic Severe Aortic Stenosis: Analysis From the EARLY TAVR Trial. Circulation, 2025.PMID 40163596
11. [11]Généreux P, et al. Outcomes of Early vs Delayed Aortic Valve Replacement: Analysis of the EARLY TAVR Valve Implant Population. JACC Cardiovasc Interv, 2025.PMID 41297989
12. [12]Craig NJ, et al. Myocardial Fibrosis and Early Intervention in Asymptomatic Patients With Severe Aortic Stenosis: Insights From the EVOLVED Randomized Clinical Trial. JAMA Cardiol, 2026.PMID 41984459
13. [13]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
14. [14]Bennetts J, et al. 2021 CSANZ and ANZSCTS Position Statement on the Operator and Institutional Requirements for a Transcatheter Aortic Valve Implantation (TAVI) Program in Australia. Heart Lung Circ, 2021.PMID 34483050
15. [15]De Backer J, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294
16. [16]Kang DH, et al. Early Surgery or Conservative Care for Asymptomatic Aortic Stenosis at 10 Years. N Engl J Med, 2026.PMID 41880613
17. [17]Goel K, et al. Age and Procedural Timing for Asymptomatic Severe Aortic Stenosis: Analysis From the EARLY TAVR Trial. Circ Cardiovasc Interv, 2026.PMID 42233211
18. [18]Lindman BR, et al. Left Ventricular Health and TAVR Timing in Asymptomatic Severe Aortic Stenosis: Analysis From the EARLY TAVR Trial. J Am Coll Cardiol, 2026.PMID 41128701
19. [19]Khan N, et al. Evaluating the use of proactive surveillance and remote patient monitoring to guide the timing of valve intervention in patients with severe asymptomatic aortic stenosis (APRAISE-AS): results of a pilot randomised controlled trial. Heart, 2026.PMID 42642075