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Aortic Stenosis

Clinical Subject Page

Aortic Stenosis

Also called

narrowing of the aortic valve

ICD-10

I35.0

Specialty

Cardiology

Onset

chronic

Reviewed

June 2026

On This Page

Overview

Aortic stenosis (AS), commonly known as narrowing of the aortic valve, is a heart valve condition in which the aortic valve becomes narrowed, making it harder for blood to flow from the left ventricle into the aorta. The condition often progresses slowly and may not cause symptoms for years, but it can eventually lead to shortness of breath, chest pain (angina), or fainting (syncope).

Etiology & Risk Factors

Etiology of Aortic Stenosis

The most common causes include:

  • Aortic valve sclerosis (calcification and fibrosis of the aortic valve leaflets) – most common cause
  • Bicuspid aortic valve (BAV) – a congenital abnormality that predisposes the valve to early calcification and degeneration
  • Rheumatic fever – a less common cause in high-income countries but remains important in lower-income countries

Risk Factors

  • Advanced age (risk increases with aging)
  • Bicuspid aortic valve (congenital)
  • Risk factors for atherosclerosis, as aortic valve sclerosis has a similar pathophysiology to atherosclerosis

Pathophysiology

  • Narrowing of the aortic valve during systole obstructs blood flow from the left ventricle (LV) into the aorta.
  • This obstruction causes increased pressure in the LV, leading to concentric left ventricular hypertrophy (thickening of the LV wall).
  • The hypertrophied LV results in:
    • Increased myocardial oxygen demand
    • Impaired ventricular filling during diastole, which can lead to left-sided heart failure
    • Reduced coronary flow reserve
  • Initially, cardiac output is maintained through compensatory mechanisms.
  • As the disease progresses, the LV becomes less compliant, cardiac output decreases, and pressure backs up into the pulmonary veins and capillaries, increasing the workload on the right heart and potentially leading to right-sided heart failure.

Flow summary:
Aortic valve narrowing → LV outflow obstruction → ↑ LV pressure → Concentric LV hypertrophy → ↓ Diastolic filling & ↑ O₂ demand → ↓ Cardiac output → Left heart failure → Pulmonary congestion → Right heart failure (late).

Clinical Presentation

  1. Common symptoms (remember: “SAD”)

    • Syncope (dizziness or fainting)
    • Angina (chest pain)
    • Dyspnea (usually on exertion)

    Physical examination

    • Weak and delayed carotid pulse (pulsus parvus et tardus)
    • Decreased pulse pressure (small blood pressure amplitude)
    • Palpable systolic thrill over the carotids and aorta

    Auscultation findings

    • Harsh crescendo-decrescendo systolic ejection murmur
    • Best heard at the 2nd right intercostal space
    • Murmur radiates to the carotid arteries
    • Soft S2
    • S4 heart sound (due to decreased LV compliance)
    • Early systolic ejection click

History Taking

  • Do you get short of breath when walking or climbing stairs?”
  • “Have you had any chest pain or tightness, especially during activity?”
  • “Have you ever felt dizzy or fainted?”
  • “When did these symptoms start?”
  • “Do your symptoms get worse with exercise?”
  • “Have your symptoms become more frequent or severe?”
  • “Have you ever been told you have a heart murmur or a heart valve problem?”
  • “Do you have a history of rheumatic fever or congenital heart disease?”
  • “Has anyone in your family had heart valve disease?”

Aortic Stenosis Vs Aortic Regurgitation

Valvular Heart Disease · Aortic Stenosis vs Aortic Regurgitation

Aortic Stenosis (AS)
Obstruction to LV outflow → pressure overload → concentric LVH. Most common cause: calcific degeneration in elderly (>65 yrs) or bicuspid aortic valve in younger patients.
Aortic Regurgitation (AR)
Backflow from aorta into LV → volume overload → eccentric LVH + LV dilatation. Causes: aortic root dilatation, bicuspid valve, rheumatic fever, endocarditis, Marfan syndrome.
Parameter Aortic Stenosis Aortic Regurgitation
Pathology Narrowed aortic valve orifice → LV must generate high pressure to eject blood (pressure overload) Incompetent aortic valve → blood regurgitates back into LV during diastole (volume overload)
LV Response Concentric hypertrophy — wall thickens, cavity size normal or reduced Eccentric hypertrophy — wall thickens AND cavity dilates (Laplace law)
Onset Usually chronic & insidious (years of compensated disease before symptoms) Can be chronic (insidious) or acute (endocarditis, aortic dissection — surgical emergency)
Classic Triad / Symptoms
Syncope Angina Dyspnea
SAD triad — appear in this order as severity progresses. Syncope on exertion is a red flag.
Exertional dyspnea Palpitations Angina
Long asymptomatic phase. Symptoms indicate LV decompensation. Acute AR: flash pulmonary edema.
Pulse Pulsus parvus et tardus — small volume, slow-rising, delayed peak Corrigan's (water-hammer) pulse — large volume, bounding, rapid rise and collapse
Blood Pressure Narrow pulse pressure (<40 mmHg); systolic BP may be low in severe AS Wide pulse pressure (>60–80 mmHg); high systolic, low diastolic
Apex Beat Sustained (heaving), non-displaced — pressure-loaded LV Displaced laterally & downward, hyperdynamic — volume-loaded dilated LV
Murmur Type Ejection systolic (crescendo-decrescendo) — heard best at aortic area; radiates to carotids Early diastolic decrescendo — heard best at left sternal border, leaning forward in expiration
Additional Murmurs S4 (stiff LV); paradoxically split S2 (severe); ejection click (bicuspid valve) Austin Flint murmur (low-pitched mid-diastolic rumble at apex); S3 (dilated LV)
ECG Findings LVH with strain pattern (ST depression & T-wave inversion in V5–V6, I, aVL); LV strain LVH (voltage criteria); broad notched P (if LA enlarges); LV volume overload pattern
CXR Findings Normal heart size (concentric LVH); calcified aortic valve; post-stenotic aortic dilatation Cardiomegaly (LV enlargement); prominent aorta; pulmonary edema if decompensated
Echo / Severity Valve area: mild >1.5 cm², moderate 1.0–1.5 cm², severe <1.0 cm²; mean gradient severe >40 mmHg Regurgitant fraction: mild <30%, moderate 30–49%, severe ≥50%; LV end-systolic diameter
Medical Management No effective medical therapy to slow progression. Manage comorbidities (HTN, AF). Avoid vasodilators in severe AS. Vasodilators (nifedipine, ACEi/ARB) to reduce afterload & preload in chronic AR. Bridge to surgery.
Surgical Indications Severe AS + symptoms; severe AS + EF <50%; severe AS undergoing other cardiac surgery Severe AR + symptoms; severe AR + EF <50%; severe AR + LV ESD >50 mm
Intervention Options SAVR TAVR Balloon valvuloplasty (palliation only) SAVR Valve repair (if feasible) — TAVR emerging but less established
Prognosis Untreated symptomatic severe AS: 50% mortality at 2–3 yrs. Rapid decline after symptom onset. Chronic: long compensated phase. Once symptomatic: 10–20% annual mortality without surgery.
Pathophysiology cascade
Aortic Stenosis
1Valve orifice narrows → increased resistance to LV outflow
2LV generates higher systolic pressure → pressure overload
3Concentric LVH (parallel sarcomere addition) — wall:cavity ratio increases
4Diastolic dysfunction → reduced coronary reserve → subendocardial ischaemia
5Decompensation: systolic dysfunction, reduced CO, symptoms (SAD triad)
Aortic Regurgitation
1Valve incompetent → blood regurgitates from aorta into LV during diastole
2LV must handle both forward stroke volume + regurgitant volume → volume overload
3Eccentric LVH (series sarcomere addition) — cavity dilates, wall thickens proportionally
4High diastolic aortic pressure maintained → wide pulse pressure; low LVEDP early
5LV decompensation: EF falls, LVEDP rises, pulmonary hypertension, heart failure
Auscultation findings
Aortic Stenosis
Harsh ejection systolic murmur (crescendo-decrescendo)
Best heard: Right 2nd intercostal space (aortic area)
Radiation: Both carotids — key distinguishing feature
Character: Harsh, rasping; peaks in mid-systole; later peak = more severe
Maneuvers: Louder on squatting (increased preload); softer on standing/Valsalva
S2: Soft or absent A2; paradoxical splitting in severe AS
Extras: Ejection click (bicuspid valve); S4 (non-compliant LV)
Aortic Regurgitation
High-pitched early diastolic decrescendo murmur
Best heard: Left sternal border, 3rd–4th ICS (Erb's point)
Position: Patient leaning forward, end-expiration — brings aorta closer to chest wall
Character: Blowing, high-pitched; begins immediately after S2
Maneuvers: Louder on squatting & handgrip (increased afterload)
Austin Flint murmur: Low-pitched mid-diastolic rumble at apex — regurgitant jet impinges on anterior mitral leaflet
Extras: S3 (dilated LV); wide pulse pressure
Peripheral signs of aortic regurgitation (absent in AS)
Named signs
Corrigan's pulseBounding carotid pulsation — rapid rise & collapse
de Musset's signHead nodding with each heartbeat
Quincke's signVisible nail bed capillary pulsations
Duroziez's signSystolic & diastolic femoral bruits on compression
Traube's sign'Pistol shot' sound over femoral artery
Müller's signVisible uvular pulsation
Key signs in Aortic Stenosis
Pulsus parvus et tardusSlow-rising, small-amplitude carotid pulse — most specific sign of severe AS
Sustained apex beatHeaving, non-displaced — reflects concentric LVH
Systolic thrillPalpable over aortic area in severe AS
Narrow pulse pressureReduced stroke volume → low systolic, near-normal diastolic BP
Absent / soft A2Calcified immobile valve fails to produce closing sound

Investigations

  • Transthoracic echocardiography (TTE) – Gold standard for diagnosis; assesses valve structure, severity of stenosis, pressure gradient, and left ventricular function.
  • Transesophageal echocardiography (TEE) – Used if TTE is inconclusive or for operative planning.
  • ECG – May show left ventricular hypertrophy (LVH) and nonspecific ST-T wave changes.
  • Chest X-ray – May show aortic valve calcification, LV enlargement, pulmonary congestion, or poststenotic dilation of the aorta.
  • Laboratory tests – BNP/NT-proBNP and troponin may be helpful but are not routinely diagnostic.
  • Cardiac catheterization/coronary angiography – Used when noninvasive tests are inconclusive or before valve intervention in selected patients.
  • Cardiac CT or MRI – Used in selected patients for further evaluation and preoperative planning.

Diagnosis

Aortic Stenosis · Diagnostic Criteria & Severity Classification

<1.0
Valve Area (cm²)
Severe AS threshold
>40
Mean Gradient (mmHg)
Severe AS threshold
>4.0
Peak Jet Velocity (m/s)
Severe AS threshold
Modality Finding Notes
History Angina Syncope Dyspnea
SAD triad — mean survival: angina 5 yrs, syncope 3 yrs, dyspnea (HF) 1–2 yrs
 Symptoms appear late. Long asymptomatic compensated phase. Symptom onset = inflection point for prognosis.
Pulse Pulsus parvus et tardus — small volume, slow-rising, delayed peak Best assessed at carotid. Most specific clinical sign of severe AS. May be absent if coexisting AR or hypertension.
Auscultation
Harsh ejection systolic murmur — crescendo-decrescendo, peaks in mid-to-late systole
Best heard: Right 2nd ICS, radiates to carotids
Gallavardin phenomenon: high-frequency component radiates to apex, mimics MR
 Later systolic peak = more severe. Soft or absent A2 (calcified valve). S4 common. Ejection click in bicuspid valve (before calcification).
Maneuvers Louder: squatting, leg raise Softer: standing, Valsalva Contrast with HCM: AS murmur decreases on standing; HCM murmur increases. Valsalva differentiates AS from HCM.
ECG
LVH (Sokolow-Lyon: S in V1 + R in V5/V6 ≥35 mm)
LV strain pattern — ST depression & T-wave inversion in V5–V6, I, aVL
LBBB, AF (late features)
 ECG may be normal even with severe AS. Not used for severity grading. AF carries worse prognosis — loss of atrial kick critical in stiff LV.
Chest X-Ray
Calcified aortic valve (best seen on lateral CXR or fluoroscopy)
Post-stenotic aortic dilatation — dilated proximal ascending aorta
Heart size normal (concentric LVH) unless decompensated; then cardiomegaly + pulmonary edema
 Absence of valve calcification on echo/CT in a patient >65 yrs makes severe AS unlikely. Calcium load correlates with severity.
Echocardiography Transthoracic Echo (TTE) — First-line imaging modality
TOE / TEE — if TTE suboptimal
3D Echo — planimetry of valve area 		TTE is the gold standard for diagnosis and severity grading. Provides valve morphology, gradient, valve area, LV function, and other valve disease.
CT / CMR
CT Aortic Calcium Score (ACS): ≥2000 AU (men) / ≥1200 AU (women) = severe AS
CT Planimetry: direct anatomical valve area measurement
CMR: LV mass, fibrosis (late gadolinium enhancement), flow assessment
 CT calcium scoring used when echo is discordant. CMR useful for detecting myocardial fibrosis — marker of irreversible damage and poor post-op outcome.
Cardiac Catheterization
Gorlin formula: AVA = CO / (SEP × HR × 44.3 × √ΔP)
Direct measurement of transvalvular gradient
 Rarely needed solely for AS diagnosis. Used when echo is non-diagnostic or discordant. Coronary angiography before surgery (if ≥40 yrs or CAD risk factors).
Exercise Testing Symptom-limited treadmill/bicycle stress echo — used in asymptomatic severe AS Contraindicated in symptomatic severe AS. Uncovers occult symptoms, abnormal BP response, and exercise-induced LV dysfunction — guides intervention timing.
Echo severity grading — AHA/ACC & ESC criteria
Mild AS
Vmax: 2.0–2.9 m/s
Mean ΔP: <20 mmHg
AVA: >1.5 cm²
AVAi: >0.85 cm²/m²
VTI ratio: >0.50
Moderate AS
Vmax: 3.0–3.9 m/s
Mean ΔP: 20–39 mmHg
AVA: 1.0–1.5 cm²
AVAi: 0.60–0.85 cm²/m²
VTI ratio: 0.25–0.50
Severe AS
Vmax: ≥4.0 m/s
Mean ΔP: ≥40 mmHg
AVA: <1.0 cm²
AVAi: <0.60 cm²/m²
VTI ratio: <0.25
Very Severe AS
Vmax: ≥5.0 m/s
Mean ΔP: ≥60 mmHg
AVA: <0.6 cm²
AVAi: <0.35 cm²/m²
Independently predicts worse outcomes
Key echocardiographic parameters explained
Peak Jet Velocity (Vmax)
CW Doppler across AV
Highest instantaneous velocity across the stenotic valve. Simple and reproducible. Can be falsely low if poor alignment or low-flow state. Most used single parameter.
Mean Pressure Gradient
ΔP = 4v² (modified Bernoulli)
Average of instantaneous gradients across systole. Flow-dependent — may underestimate severity in low-output states (EF <50% or low SVi <35 mL/m²). More reliable than peak gradient alone.
Aortic Valve Area (AVA)
AVA = (CSAₗǕₒǕₜ × VTIₗǕₒǕₜ) / VTIₐǕǕ
Continuity equation — flow conservation. Gold standard for grading. Errors accumulate: LVOT diameter (squared), LVOT velocity, AV velocity — any one being off skews the result significantly.
Indexed AVA (AVAi)
AVAi = AVA / BSA
Adjusts for body size — useful in small patients where AVA <1.0 cm² may not truly represent severe AS (e.g., BSA <1.6 m²). AVAi <0.60 cm²/m² = severe.
Velocity Ratio (VTI ratio)
VTIₗǕₒǕₜ / VTIₐǕǕ
Dimensionless index — not affected by LVOT diameter error. <0.25 = severe AS. Particularly useful when LVOT measurement is unreliable (e.g., elliptical outflow tract, post-TAVR).
Calcium Score (CT)
Agatston Units (AU)
Men ≥2000 AU / Women ≥1200 AU = severe AS, regardless of gradient. Lower thresholds for women reflect denser leaflet calcification at equivalent stenosis. Used to resolve discordant echo grading.
Low-flow, low-gradient AS — the diagnostic challenge
Classical Low-Flow Low-Gradient (LFLG)
AVA <1.0 cm² + Mean ΔP <40 mmHg + EF <50%
Reduced EF → reduced SV → low gradient despite severe anatomical stenosis. Dobutamine stress echo (DSE) differentiates:
• True severe AS: AVA remains <1.0 cm², gradient increases ≥40 mmHg
• Pseudo-severe AS: AVA normalises >1.0 cm² as flow increases
Paradoxical Low-Flow Low-Gradient
AVA <1.0 cm² + Mean ΔP <40 mmHg + EF ≥50%
Preserved EF but low stroke volume index (SVi <35 mL/m²) — small, hypertrophied, stiff LV. Common in elderly women. Concentric remodeling reduces cavity size.
Use CT calcium scoring (AU) and AVAi to confirm severity. Often missed and undertreated.
Normal-Flow Low-Gradient
AVA <1.0 cm² + Mean ΔP <40 mmHg + SVi ≥35 mL/m²
Often reflects measurement error (LVOT diameter, non-circular LVOT, poor Doppler alignment). Reassess with:
• 3D echo or CT planimetry for true AVA
• CT calcium score
• Velocity ratio (flow-independent)
True moderate AS is also in the differential.
Indications for intervention (AVR/TAVR) — AHA/ACC 2021 & ESC 2021
Class I — Recommended
Symptomatic severe AS (any symptom: angina, syncope, dyspnea) Class I
Severe AS + EF <50% (even if asymptomatic) Class I
Severe AS undergoing other cardiac surgery (CABG, other valve) Class I
Very severe AS (Vmax ≥5 m/s) + low surgical risk — intervention reasonable Class IIa
Class IIa/IIb — Reasonable / May Consider
Asymptomatic severe AS + abnormal exercise test (symptoms, BP drop, complex arrhythmia) Class IIa
Asymptomatic severe AS + rapid progression (Vmax increase ≥0.3 m/s/yr) Class IIa
Moderate AS undergoing other cardiac surgery Class IIb
LFLG severe AS with EF <50% + contractile reserve on DSE Class IIa
Balloon aortic valvuloplasty as bridge to definitive intervention — palliation only Class IIb
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Related Topics

Management

Management of Aortic Stenosis

  • Mild or asymptomatic disease
    • Conservative management with regular monitoring (serial echocardiography).
    • Treat comorbidities (e.g., hypertension, diabetes).
  • Symptomatic or severe aortic stenosis
    • Aortic valve replacement (AVR) is the definitive treatment.
    • Surgical AVR (SAVR): Typically for younger patients with low to moderate surgical risk.
    • Transcatheter AVR (TAVR): Typically for older patients or those at high surgical risk.
  • Acute complications
    • Immediate cardiology/cardiothoracic surgery consultation.
    • Stabilize the patient while expediting definitive valve replacement.

Complications

  • Complications of Aortic Stenosis

    • Left ventricular failure
    • Acute heart failure
    • Cardiogenic shock
    • Atrial fibrillation with rapid ventricular response (may occur in severe disease)

    Complications After Valve Replacement

    • Stroke/thromboembolism
    • Major bleeding
    • Renal failure
    • Arrhythmias (e.g., atrial fibrillation, atrioventricular block)
    • Aortic regurgitation/paravalvular leak
    • Infective endocarditis

Prognosis

  • Asymptomatic patients: Annual mortality is < 1%.
  • Symptomatic patients: If left untreated, > 50% die within 2 years.
  • The worst prognosis is seen in patients with heart failure symptoms, followed by syncope and angina.

Key Points / Clinical Pearls

  • Chronic, progressive narrowing of the aortic valve.
  • Most common cause: Age-related calcific aortic valve sclerosis.
  • Classic symptom triad (SAD): Syncope, Angina, Dyspnea.
  • Classic murmur: Harsh crescendo-decrescendo systolic murmur radiating to the carotids.
  • Gold standard diagnosis: Transthoracic echocardiography (TTE).
  • Definitive treatment: Aortic valve replacement (AVR) (SAVR or TAVR).
  • Once symptoms develop, prompt evaluation for valve replacement is essential because prognosis worsens significantly without treatment.
  •