Aortic stenosis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Calcific degeneration is the commonest cause in older adults; bicuspid valve disease presents younger and should trigger assessment of the ascending aorta. Progressive obstruction creates LV pressure overload, concentric hypertrophy and eventually impaired coronary reserve and heart failure.

Severity is a synthesis of symptoms, examination and multimodal imaging. Flow-dependent velocity and gradient can appear deceptively modest in low-flow states, while valve area can be affected by measurement error; discordant results should be reviewed by valve-imaging specialists.

Once severe stenosis causes symptoms, LV dysfunction or another high-risk feature, a valve team selects surgical aortic valve replacement or transcatheter implantation. Balloon valvuloplasty is generally a temporary bridge or palliative procedure, not durable routine treatment.

Key points

The classic symptoms are exertional breathlessness, angina and syncope; any symptom attributable to severe stenosis changes prognosis and prompts intervention assessment.
The murmur is harsh, ejection systolic and usually radiates to the carotids; a slow-rising low-volume pulse and soft second heart sound support advanced disease.
Severe high-gradient stenosis is usually Vmax 4.0 m/s or more, mean gradient 40 mmHg or more, or valve area 1.0 cm2 or less, interpreted together rather than in isolation.
A low gradient does not exclude severe stenosis when stroke volume or LVEF is reduced; dobutamine stress echo or CT valve-calcium scoring can resolve discordance.
There is no medicine that relieves the fixed obstruction or improves survival in severe aortic stenosis; definitive treatment is valve replacement.
NICE recommends clinical review and echocardiography every 6–12 months for asymptomatic severe valve disease when intervention would be suitable.
SAVR and TAVI choice belongs to a multidisciplinary valve team and incorporates age, anatomy, surgical risk, frailty, coronary/aortic disease, durability and patient preference.
Very severe asymptomatic disease, an abnormal exercise test or LV systolic impairment can justify intervention before spontaneous symptoms appear.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Calcific degenerative stenosis

Age-related fibrocalcific remodelling progressively stiffens the cusps and is the commonest cause in older adults. Hypertension, chronic kidney disease and other vascular risk factors are associated with calcific disease, but do not by themselves establish its cause or severity.

Bicuspid aortic valve

A congenitally bicuspid valve experiences abnormal mechanical stress and commonly calcifies earlier than a tricuspid valve. Associated ascending-aortic dilatation can influence surveillance and intervention.

Rheumatic valve disease

Post-inflammatory commissural fusion and leaflet thickening can narrow the valve, often alongside aortic regurgitation or mitral disease. The broader valve pattern helps distinguish it from isolated calcific stenosis.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Fixed outflow obstruction
Progressive cusp thickening and restricted opening reduce the effective valve area. The LV must generate a higher systolic pressure to maintain forward flow across the narrowed valve.
2
Concentric hypertrophy
Chronic pressure overload stimulates concentric LV hypertrophy, initially helping to normalise wall stress. The thick ventricle becomes stiff, so filling may increasingly depend on adequate preload and atrial contraction.
3
Coronary and filling-pressure consequences
High myocardial demand, reduced coronary reserve and raised LV filling pressure produce exertional angina and breathlessness even without obstructive coronary disease. Fixed output limits augmentation during exercise.
4
Limited output and decompensation
Fixed obstruction can limit the rise in cardiac output during exercise and contribute to presyncope or syncope. With later fibrosis or contractile failure, stroke volume may fall, causing heart failure and a deceptively low measured gradient despite genuinely severe obstruction.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Effort symptoms

Reduced exercise tolerance, exertional dyspnoea, central chest pressure or exertional presyncope/syncope are the key history; patients may unconsciously reduce activity and deny symptoms.

Typical auscultation

A crescendo–decrescendo ejection systolic murmur at the right upper sternal edge radiates to the neck; later peaking, a quiet A2 and a slow-rising pulse suggest greater severity.

Heart-failure phenotypeRed flag

Orthopnoea, crackles, raised JVP and oedema suggest decompensation and require urgent assessment rather than routine surveillance.

Low-flow severe disease

Symptoms may be disproportionate to a mean gradient below 40 mmHg when LVEF or stroke volume is low; do not dismiss stenosis from the gradient alone.

Bicuspid clues

Younger age, an ejection click or associated aortic dilatation suggests bicuspid valve disease; first-degree relatives may need echocardiographic screening after specialist advice.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Transthoracic echocardiographyFirst step
Why
Define valve anatomy, Vmax, mean gradient, valve area, LVEF, stroke volume, other valves and aortic dimensions.
Interpretation and limitations
Severe high-gradient disease is supported by Vmax at least 4.0 m/s, mean gradient at least 40 mmHg or area at most 1.0 cm2; reconcile discordant measurements and flow state.
02
12-lead ECG
Why
Look for LV hypertrophy, strain, conduction disease, AF or prior infarction.
Interpretation and limitations
ECG supports consequences and procedural planning but a normal tracing does not exclude severe stenosis.
03
Low-dose dobutamine stress echocardiography
Why
Distinguish true-severe from pseudo-severe stenosis in low-flow, low-gradient disease with reduced LVEF.
Interpretation and limitations
A rising gradient with persistently small valve area supports true severe obstruction; increased area with flow suggests pseudo-severe disease.
04
CT aortic-valve calcium and TAVI planning CT
Why
Clarify severity when echo is discordant and map annulus, aorta and vascular access before TAVI.
Interpretation and limitations
Sex-specific calcium thresholds support severe disease; anatomy may favour surgery or make transfemoral TAVI unsuitable.
05
Supervised exercise testing
Why
Unmask symptoms or an abnormal blood-pressure response in apparently asymptomatic severe disease.
Interpretation and limitations
Do not exercise-test a clearly symptomatic patient; provoked symptoms or an abnormal response accelerates valve-team consideration.
06
Coronary assessment
Why
Identify coronary disease before valve intervention using CT coronary angiography or invasive angiography as appropriate.
Interpretation and limitations
Important coronary disease may favour SAVR with CABG over an isolated transcatheter strategy.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Aortic sclerosis

Calcified cusps can produce a similar ejection murmur without important obstruction. Echocardiography shows preserved opening and no severe velocity, gradient or valve-area combination.

Hypertrophic obstructive cardiomyopathy

Dynamic LV outflow obstruction usually becomes louder with standing or Valsalva and lessens with increased preload; echo shows septal hypertrophy and systolic anterior mitral motion.

Mitral regurgitation

The murmur is usually pansystolic, loudest at the apex and radiates towards the axilla rather than the carotids. Echocardiography localises the regurgitant jet and valve lesion.

High-flow systolic murmur

Anaemia, pregnancy or thyrotoxicosis can increase flow and create a soft ejection murmur with brisk pulses. Valve imaging shows no fixed severe obstruction.

Additional chapter-specific clues

Alternative explanations

A flow murmur, aortic sclerosis, hypertrophic cardiomyopathy and other causes of dyspnoea or syncope remain differentials; echo establishes valve anatomy and haemodynamics.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01symptomaticSymptomatic severe aortic stenosisFirst stepSevere stenosis is accompanied by exertional dyspnoea, angina, syncope or heart failure not better explained otherwise.

1Confirm symptom–valve concordance and severity promptly with specialist echocardiography; do not wait for the next surveillance scan.
2Refer to a multidisciplinary heart valve team for intervention assessment and evaluate frailty, comorbidity, coronary/aortic anatomy and procedural risk.
3Offer valve replacement when benefit is expected: SAVR or TAVI according to age, anatomy, durability, access and patient preference; address coronary disease at the same decision.
4DefinitiveIf definitive intervention is temporarily impossible, use cautious symptom treatment and consider balloon valvuloplasty only as a specialist bridge or palliation.

02asymptomaticApparently asymptomatic severe diseaseSevere aortic stenosis is found without volunteered symptoms.

1Check actual activity, repeat expert echo and, if safe, perform supervised exercise testing to reveal symptoms or an abnormal blood-pressure response.
2Refer for intervention if LV systolic dysfunction is attributable to stenosis or exercise testing produces symptoms; discuss very severe Vmax above 5 m/s and other rapid-progression/high-risk findings with the valve team.
3When no intervention trigger exists, give explicit symptom education and review clinically with echocardiography every 6–12 months while intervention remains suitable.
4Advise immediate reassessment rather than waiting for surveillance if breathlessness, chest discomfort, presyncope or exercise decline develops.

03decompensatedAcute pulmonary oedema or shockSevere aortic stenosis presents with hypoxaemia, pulmonary oedema, hypotension or shock.

1Use ABCDE care, continuous ECG and blood-pressure monitoring, IV access and oxygen only for hypoxaemia; call cardiology/critical care and the valve centre urgently.
2Treat congestion cautiously: if fluid overloaded, give a small IV loop-diuretic dose with repeated perfusion and renal assessment; avoid uncontrolled vasodilatation or large preload shifts.
3Identify precipitants such as AF, ischaemia, infection, anaemia or bleeding and treat them without delaying valve evaluation.
4DefinitiveEscalationEscalate for urgent definitive replacement or, in selected unstable patients, balloon valvuloplasty as a bridge decided by the specialist valve team.

04discordantDiscordant low-gradient assessmentValve area suggests severe stenosis but velocity/gradient is lower than expected.

1Recheck Doppler alignment, LV outflow-tract measurement, blood pressure, rhythm and indexed stroke volume.
2If LVEF is reduced, use low-dose dobutamine stress echo to assess flow reserve and projected severity.
3If LVEF is preserved or uncertainty remains, use CT valve-calcium scoring and specialist multimodality review.
4Intervene only after confirming truly severe obstruction and linking it to symptoms or another accepted trigger.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Relieves congestion while urgent valve treatment is arranged; it does not treat the obstruction.

Furosemide

For acute oedema, 20–50 mg IV initially; inject slowly and do not exceed 4 mg/min. Reassess before any repeat dose.

Use especially cautiously in severe aortic stenosis because hypovolaemia and hypotension can reduce coronary perfusion; monitor BP, urine output, renal function, sodium and potassium. The dose is from the SmPC, not a Resuscitation Council peri-arrest regimen.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Left-sided heart failure

Diastolic dysfunction, fibrosis and eventual systolic failure raise pulmonary venous pressure, causing exertional dyspnoea, pulmonary oedema and repeated decompensation if the obstruction remains untreated.

Myocardial ischaemia

Hypertrophied myocardium has increased oxygen demand and reduced subendocardial perfusion reserve. Angina or supply-demand myocardial injury can therefore occur without obstructive coronary disease, while epicardial coronary disease may coexist.

Syncope and sudden death

Fixed cardiac output may not meet vasodilated exercise demand, causing cerebral hypoperfusion. Ventricular arrhythmia or abrupt decompensation can cause sudden death, particularly after symptoms develop.

Pulmonary hypertension and right-heart failure

Persistently raised LV and left-atrial pressure can remodel the pulmonary circulation, increasing RV afterload and eventually producing systemic venous congestion and poorer procedural risk.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

For asymptomatic severe disease suitable for intervention, review symptoms and perform echocardiography every 6–12 months.
For mild aortic stenosis, NICE suggests echocardiography every 3–5 years; individualise shorter intervals for moderate disease, rapid progression or aortic disease.
Track Vmax progression, mean gradient, LVEF, stroke volume and ascending-aortic size using comparable studies.
Ask specifically about walking pace, hills, stairs, chest pressure and presyncope rather than relying on the label asymptomatic.
After SAVR or TAVI, monitor symptoms, prosthetic gradients/regurgitation, conduction disturbance and antithrombotic plan.
During diuresis, monitor perfusion, BP, weight, renal function and electrolytes closely.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

The gradient is flow-dependent

A low mean gradient may reflect low forward flow, not mild disease. Stroke volume, LVEF, dobutamine response and CT calcium prevent a false reassurance.

Symptoms can be hidden

Older adults often reduce activity gradually. Exercise testing in a genuinely asymptomatic, stable patient can reveal the prognostically important symptom.

The murmur can soften late

Low cardiac output may reduce murmur intensity in critical disease; a quiet murmur never overrules severe symptoms and echo findings.

TAVI is not simply the default

Transfemoral feasibility, bicuspid anatomy, aortopathy, coronary disease, future coronary access and lifetime valve durability all influence TAVI versus surgery.

Treat the valve, not just the fluid

Diuretics may buy time in congestion but repeated medical admissions signal the need for urgent definitive assessment.

Balloon valvuloplasty is temporary

Restenosis is common; its main roles are bridge to replacement, urgent stabilisation in selected patients or palliation when replacement is unsuitable.

11Common pitfallsFrequent interpretation and management errors.

01
Calling severe stenosis asymptomatic without asking about self-limited activity or considering supervised exercise testing.
02
Excluding severe disease because the mean gradient is below 40 mmHg despite low flow.
03
Treating pulmonary oedema aggressively without accounting for preload dependence and hypotension.
04
Delaying valve-team referral until LVEF is markedly reduced after symptoms have appeared.
05
Presenting TAVI and SAVR as interchangeable without anatomy, coronary disease, durability and patient preference.