TextbookCardiologyAortic Stenosis

Aortic Stenosis

Progressive narrowing of the aortic valve orifice causing left ventricular outflow obstruction. Most commonly caused by degenerative calcification in the elderly or bicuspid aortic valve in younger patients.

Key Facts

Classic triad: exertional angina, syncope, and heart failure — onset of symptoms indicates poor prognosis without intervention Murmur: ejection systolic murmur, best heard at right upper sternal edge, radiating to carotids; slow-rising pulse Severe AS criteria: valve area <1.0 cm², mean gradient >40 mmHg, peak velocity >4 m/s Aortic valve replacement (surgical AVR or TAVI) is the definitive treatment for symptomatic severe AS TAVI (transcatheter aortic valve implantation) is standard for inoperable/high-risk patients and increasingly used in intermediate/low risk Prognosis without intervention: median survival ~2-3 years from symptom onset (angina 5 yrs, syncope 3 yrs, heart failure 2 yrs) Most common valvular heart disease in the developed world; prevalence ~3% over age 75 NICE NG208 recommends echocardiography for all patients with a cardiac murmur and symptoms

Overview

Key Facts

Aortic stenosis (AS) is the most common acquired valvular heart disease in developed countries. It involves progressive narrowing and calcification of the aortic valve, leading to obstruction of left ventricular outflow.

Epidemiology

  • Prevalence: ~2-3% in adults >65 years; ~5% in >75 years
  • Most common indication for valve replacement surgery
  • Male:female ratio ~2:1 for calcific AS
  • Bicuspid aortic valve affects ~1-2% of the population

Aetiology

  • Degenerative calcification (senile/calcific AS): most common in developed countries (>65 years)
  • Bicuspid aortic valve: most common cause in <65 years; presents 10-20 years earlier than tricuspid valve AS
  • Rheumatic heart disease: common in developing countries; commissural fusion
  • Rare: congenital, radiation-induced, post-endocarditis

Pathophysiology

  • Progressive narrowing of the aortic valve orifice increases LV afterload
  • LV undergoes concentric hypertrophy to maintain cardiac output (compensated phase)
  • Eventually, LV compliance falls, diastolic function impairs, and LV dilatation occurs (decompensated)
  • Fixed cardiac output leads to exertional symptoms: reduced coronary perfusion (angina), impaired cerebral perfusion (syncope), and pulmonary congestion (dyspnoea/heart failure)
  • Severe AS reduces coronary flow reserve even without coronary disease

Clinical Presentation

Classical Symptom Triad

  • Exertional angina: even with normal coronary arteries (supply-demand mismatch from LVH)
  • Exertional syncope: failure to augment cardiac output; also vasodepressor mechanism
  • Heart failure: late symptom; indicates decompensation — dyspnoea, orthopnoea, PND

Examination Findings

  • Ejection systolic murmur: crescendo-decrescendo, best at right upper sternal edge, radiates to carotids
  • Slow-rising, low-volume pulse (pulsus parvus et tardus)
  • Narrow pulse pressure
  • Soft or absent S2 (calcified immobile valve)
  • Late-peaking murmur indicates more severe stenosis
  • Heaving, non-displaced apex (concentric LVH); displaced if decompensated

Red Flags

  • Onset of any symptom in triad (angina, syncope, HF) — indicates need for urgent valve intervention
  • Severe AS with new symptoms: median survival <2-3 years without surgery
  • Sudden cardiac death (rare but occurs)
  • Severe AS requiring non-cardiac surgery: high perioperative risk

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Hypertrophic cardiomyopathyEjection systolic murmur at LLSE, increases with ValsalvaEchocardiography
Aortic sclerosisSystolic murmur without haemodynamic obstruction, normal pulseEchocardiography
Mitral regurgitationPansystolic murmur at apex, radiates to axillaEchocardiography
Pulmonary stenosisESM at left upper sternal edge, wide split S2Echocardiography
Subaortic membraneFixed subaortic stenosis, young patientEchocardiography
Supravalvular ASWilliams syndrome, elfin faciesEchocardiography, genetics

Diagnosis / Investigation

Bedside

  • ECG: LVH (Sokolow-Lyon criteria: SV1 + RV5 >35 mm), left axis deviation, P mitrale, strain pattern (ST depression + T-wave inversion in lateral leads)

Bloods

  • BNP/NT-proBNP: elevated in decompensated AS; prognostic value
  • FBC, U&Es, LFTs: preoperative assessment
  • Coagulation: if planning intervention

Imaging

  • Transthoracic echocardiography (TTE): diagnostic gold standard
    • Valve area, peak velocity, mean gradient
    • LV function, wall thickness, dimensions
    • Assess for concomitant AR, MR
  • CT aorta/aortic root: pre-TAVI assessment for sizing
  • Cardiac catheterisation/coronary angiography: assess coronary arteries pre-intervention
  • Cardiac MRI: myocardial fibrosis assessment, valve assessment

Special Tests

  • Dobutamine stress echo: assess severity in low-flow, low-gradient AS with reduced LV function (assess contractile reserve)
  • CT calcium scoring: aortic valve calcium score can help confirm severe AS in equivocal cases

Severity Grading

ParameterMildModerateSevere
Peak velocity (m/s)<3.03.0-4.0>4.0
Mean gradient (mmHg)<2525-40>40
Valve area (cm²)>1.51.0-1.5<1.0

Management

Non-pharmacological

  • Symptom surveillance: serial echocardiography (6-12 monthly for moderate, annually for mild)
  • Avoid strenuous exercise in severe AS
  • Dental hygiene (endocarditis prophylaxis no longer routinely recommended by NICE)

Pharmacological

  • No medical therapy slows AS progression
  • Heart failure management: cautious use of diuretics for congestion; avoid vasodilators if possible (risk of hypotension)
  • Statins: do not slow AS progression (SEAS, SALTIRE trials negative)
  • ACEi/ARBs: traditionally avoided but increasingly used cautiously in AS with HF or hypertension
  • Avoid excessive preload reduction (diuretics) or afterload reduction (GTN, vasodilators) — may cause profound hypotension

Surgical/Interventional

  • Surgical aortic valve replacement (SAVR): gold standard for symptomatic severe AS
    • Mechanical valve: younger patients (<60-65); requires lifelong warfarin
    • Bioprosthetic valve: older patients (>65-70); avoids anticoagulation but limited durability (10-20 years)
    • Operative mortality: ~1-3% in low-risk patients
  • TAVI (transcatheter aortic valve implantation):
    • Standard for high-risk/inoperable patients; increasingly used in intermediate and low-risk
    • PARTNER and CoreValve trials demonstrate non-inferiority or superiority to SAVR in certain populations
    • Complications: paravalvular leak, conduction disturbance (LBBB/pacemaker ~10-20%), stroke, vascular access complications
  • Balloon aortic valvuloplasty: temporising bridge to definitive treatment; not durable

Referral Criteria

  • All symptomatic severe AS: urgent referral for valve intervention assessment
  • Asymptomatic severe AS with LV dysfunction (EF <50%): referral for intervention
  • Moderate AS with symptoms: cardiology assessment for monitoring and planning

Prognosis

  • Asymptomatic severe AS: relatively good prognosis; annual risk of sudden death ~1%
  • Symptomatic severe AS without intervention: median survival:
    • Angina: ~5 years
    • Syncope: ~3 years
    • Heart failure: ~2 years
  • Post-SAVR: 10-year survival ~60-70%
  • Post-TAVI: 5-year survival ~50-60% (patient population generally older/higher risk)
  • Operative mortality SAVR: ~1-3% (low risk); TAVI: ~2-5% (procedural + 30-day)
  • Bioprosthetic valve degeneration: ~10-20% at 15-20 years

Other Relevant Information

Severity Classification Summary

ParameterMildModerateSevere
Peak velocity<3.0 m/s3.0-4.0 m/s>4.0 m/s
Mean gradient<25 mmHg25-40 mmHg>40 mmHg
Valve area>1.5 cm²1.0-1.5 cm²<1.0 cm²
Indexed AVA>0.85 cm²/m²0.6-0.85 cm²/m²<0.6 cm²/m²

Indications for Intervention (ESC/ACC)

IndicationClass
Symptomatic severe ASClass I
Severe AS + LVEF <50%Class I
Severe AS + positive exercise testClass I
Severe AS + undergoing other cardiac surgeryClass I
Asymptomatic very severe AS (Vmax >5.5 m/s)Class IIa