Aortic Stenosis

A 72-year-old man presents with progressive exertional dyspnea, episodes of chest pain, and a recent episode of syncope while climbing stairs. He has a history of hypertension and hyperlipidemia. On examination, his pulse is low amplitude and delayed. Blood pressure is 130/85 mmHg. Cardiac auscultation reveals a harsh crescendo-decrescendo systolic ejection murmur best heard at the right upper sternal border, radiating to the carotids. The second heart sound is soft, and an S4 gallop is present. Echocardiography shows an aortic valve area of 0.8 cm², peak aortic jet velocity of 4.5 m/s, and mean transvalvular gradient of 50 mmHg, with preserved LVEF. Diagnosis?

Diagnosis is symptomatic severe high-gradient aortic stenosis.

The combination of exertional dyspnea, angina, exertional syncope, pulsus parvus et tardus, a systolic ejection murmur radiating to the carotids, and concordant severe echocardiographic findings is characteristic of severe aortic stenosis.

1. Definition

Aortic stenosis is progressive narrowing of the aortic valve that produces left ventricular outflow obstruction and chronic pressure overload.

Consequences include:

1.      Concentric LV hypertrophy

2.      Diastolic dysfunction

3.      Increased myocardial oxygen demand

4.      Elevated LV filling pressures

5.      Reduced cardiac output in advanced disease

6.      Heart failure

2. Etiology

Major causes include:

1.      Degenerative calcific aortic stenosis

1.      Most common in older adults

2.      Progressive leaflet calcification and restriction

2.      Bicuspid aortic valve

1.      Congenital abnormality

2.      Produces stenosis at a younger age

3.      May be associated with ascending aortic disease

3.      Rheumatic valve disease

1.      Causes commissural fusion

2.      Often occurs with concomitant mitral valve disease

3. Pathophysiology

1.      Progressive valve narrowing causes a fixed obstruction to LV outflow.

2.      The LV generates higher systolic pressure to maintain forward flow.

3.      Chronic pressure overload produces concentric LV hypertrophy.

4.      LV hypertrophy causes:

1.      Reduced ventricular compliance

2.      Diastolic dysfunction

3.      Increased LV filling pressure

4.      Increased myocardial oxygen demand

5.      Reduced coronary perfusion reserve and increased oxygen demand can cause angina even without obstructive coronary artery disease.

6.      Elevated LV filling pressures cause pulmonary venous hypertension and exertional dyspnea.

7.      During exercise, the fixed obstruction limits the ability to increase cardiac output, contributing to exertional presyncope or syncope.

4. Clinical Features

The classic symptomatic manifestations are:

1.      Exertional dyspnea

2.      Angina

3.      Exertional syncope or presyncope

Other features include:

1.      Fatigue

2.      Reduced exercise tolerance

3.      Heart failure symptoms in advanced disease

The development of symptoms in severe AS is clinically important because untreated symptomatic severe AS has an unfavorable prognosis.

5. Physical Examination

5.1 Murmur

1.      Harsh crescendo-decrescendo systolic ejection murmur

2.      Best heard at the right upper sternal border

3.      Typically radiates to the carotid arteries

5.2 Pulse

Pulsus parvus et tardus:

1.      Low-amplitude carotid pulse

2.      Delayed systolic upstroke

This is a classic finding in hemodynamically significant AS.

5.3 Heart Sounds

1.      Soft or absent A2 may occur in severe calcific AS.

2.      S4 may occur because atrial contraction occurs against a stiff, hypertrophied LV.

3.      Paradoxical splitting of S2 can occur in advanced disease because of prolonged LV ejection.

5.4 Dynamic Maneuvers

The murmur generally:

1.      Becomes louder with increased venous return and stroke volume, such as with squatting.

2.      Becomes softer with reduced preload, such as during the strain phase of Valsalva or standing.

6. Heyde Syndrome

Heyde syndrome is the association of:

1.      Aortic stenosis

2.      Gastrointestinal bleeding, commonly from angiodysplasia

3.      Acquired von Willebrand syndrome

High shear stress across the stenotic valve causes loss of high-molecular-weight von Willebrand factor multimers, producing an acquired bleeding tendency.

7. Diagnosis

7.1 Transthoracic Echocardiography

Transthoracic echocardiography is the first-line diagnostic test.

It assesses:

1.      Valve morphology and calcification

2.      Peak aortic jet velocity

3.      Mean transvalvular gradient

4.      Aortic valve area

5.      Stroke volume

6.      LVEF

7.      LV hypertrophy and remodeling

8.      Associated valve disease

Severity should be assessed using an integrated approach, not a single measurement.

7.2 Severe High-Gradient Aortic Stenosis

Findings supporting severe high-gradient AS include:

1.      Peak aortic jet velocity ≥4.0 m/s

2.      Mean gradient ≥40 mmHg

3.      Aortic valve area ≤1.0 cm²

4.      Indexed AVA ≤0.6 cm²/m² also supports severe AS

This patient has:

1.      AVA 0.8 cm²

2.      Peak velocity 4.5 m/s

3.      Mean gradient 50 mmHg

These are concordant findings of severe high-gradient AS.

7.3 Very Severe Aortic Stenosis

Very severe AS is characterized by:

1.      Peak velocity >5.0 m/s

2.      And/or mean gradient ≥60 mmHg

8. Low-Gradient Aortic Stenosis

8.1 Classical Low-Flow, Low-Gradient AS

Typical findings:

1.      AVA ≤1.0 cm²

2.      Mean gradient <40 mmHg

3.      Peak velocity <4.0 m/s

4.      LVEF <50%

5.      Stroke volume index ≤35 mL/m²

Low-dose dobutamine stress echocardiography can help distinguish true severe AS from pseudo-severe AS.

8.2 Paradoxical Low-Flow, Low-Gradient AS

Typical findings:

1.      AVA ≤1.0 cm²

2.      Mean gradient <40 mmHg

3.      LVEF ≥50%

4.      Stroke volume index ≤35 mL/m²

These patients often have a small, concentrically remodeled LV with significant diastolic dysfunction.

8.3 Normal-Flow, Low-Gradient AS

Typical findings:

1.      AVA ≤1.0 cm²

2.      Mean gradient <40 mmHg

3.      LVEF ≥50%

4.      Stroke volume index >35 mL/m²

This discordant pattern requires reassessment of measurement accuracy, blood pressure, flow conditions, and true stenosis severity.

9. Additional Investigations

9.1 ECG

May show:

1.      LV hypertrophy

2.      LV strain pattern

3.      Left atrial enlargement

4.      Conduction abnormalities

9.2 Chest X-Ray

May show:

1.      Aortic valve calcification

2.      Post-stenotic ascending aortic dilation

3.      Cardiomegaly in advanced disease

4.      Pulmonary congestion in heart failure

9.3 Cardiac CT

Cardiac CT is useful for:

1.      TAVI procedural planning

2.      Annular sizing

3.      Assessment of aortic root and vascular anatomy

4.      Coronary ostial assessment

5.      Aortic valve calcium scoring when echocardiographic findings are discordant

CT calcium scores supporting severe AS are approximately:

1.      >2000 Agatston units in men

2.      >1200 Agatston units in women

These thresholds are particularly useful in low-gradient or discordant AS.

9.4 Coronary Assessment

Coronary anatomy should be assessed before valve intervention when clinically appropriate.

Assessment may include:

1.      CT coronary angiography in suitable patients

2.      Invasive coronary angiography when significant CAD is suspected or CT assessment is inadequate

Invasive cardiac catheterization is not routinely required solely to diagnose AS when echocardiographic findings are conclusive.

10. Management

10.1 Medical Therapy

No medication has been proven to reverse severe AS or reliably halt progression of calcific valve obstruction.

1.      Hypertension should be treated with careful blood pressure monitoring.

2.      Diuretics may be used cautiously for congestion.

3.      Statins should be prescribed for standard cardiovascular indications, not specifically to slow AS progression.

4.      Medical treatment should not delay valve intervention in symptomatic severe AS.

10.2 Definitive Treatment

Aortic valve replacement is the definitive treatment for symptomatic severe AS.

Intervention is recommended for eligible patients with symptomatic severe high-gradient AS.

This patient has:

1.      Severe high-gradient AS

2.      Exertional dyspnea

3.      Angina

4.      Exertional syncope

5.      Preserved LVEF

He therefore has a clear indication for prompt Heart Team evaluation and aortic valve replacement.

11. TAVI Versus SAVR

The choice between TAVI/TAVR and SAVR should be individualized by a multidisciplinary Heart Team.

Important factors include:

1.      Age

2.      Life expectancy

3.      Surgical risk

4.      Frailty

5.      Valve anatomy

6.      Vascular access

7.      Coronary anatomy

8.      Need for CABG or other cardiac surgery

9.      Aortic root or ascending aortic disease

10.  Valve durability and lifetime management

11.  Patient preference

According to the 2025 ESC/EACTS guideline:

1.      TAVI is recommended in patients aged ≥70 years with tricuspid AS when anatomy is suitable, particularly when transfemoral access is feasible.

2.      SAVR is recommended in patients <70 years when surgical risk is low.

3.      For other patients, TAVI or SAVR is selected according to individualized Heart Team assessment.

According to the 2020 ACC/AHA guideline, both transfemoral TAVR and SAVR are appropriate options for many patients aged 65 to 80 years, with individualized shared decision-making.

Therefore, in this 72-year-old patient, TAVI would generally be favored under current ESC/EACTS guidance if:

1.      The valve is tricuspid

2.      Anatomy is suitable

3.      Transfemoral access is feasible

4.      There is no need for concomitant CABG, ascending aortic surgery, or another operation favoring SAVR

12. Other Important Indications for Intervention

Valve intervention is also recommended or considered in selected patients with severe AS, including:

1.      LVEF <50% without another cause

2.      Symptoms demonstrated during exercise testing

3.      Selected asymptomatic severe high-gradient AS at low procedural risk

4.      Very severe AS

5.      Rapid hemodynamic progression

6.      Markedly elevated BNP or NT-proBNP without another explanation

7.      Abnormal blood pressure response during exercise testing

13. Complications

Untreated severe AS may cause:

1.      Heart failure

2.      Pulmonary hypertension

3.      Atrial fibrillation

4.      Ventricular arrhythmias

5.      Myocardial ischemia

6.      Syncope

7.      Progressive LV systolic dysfunction

8.      Sudden cardiac death

14. Prognosis

1.      AS may remain asymptomatic for years.

2.      Prognosis worsens significantly once severe AS becomes symptomatic.

3.      Historical fixed survival estimates such as 5 years after angina, 3 years after syncope, and 2 years after heart failure are oversimplified and should not be used as precise modern prognostic estimates.

4.      Timely aortic valve replacement improves symptoms and survival in appropriately selected patients with symptomatic severe AS.

15. Key Clinical Insight

Exertional dyspnea, angina, or syncope in an older adult with a harsh systolic ejection murmur radiating to the carotids and pulsus parvus et tardus should strongly suggest aortic stenosis.

For this patient:

AVA 0.8 cm² + Vmax 4.5 m/s + mean gradient 50 mmHg + exertional symptoms = symptomatic severe high-gradient aortic stenosis.

This is a clear indication for prompt evaluation for aortic valve replacement.

References

1.      Praz F, Borger MA, Lanz J, et al. 2025 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2025;46(44):4635-4736. doi:10.1093/eurheartj/ehaf194.

2.      Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation. 2021;143(5):e72-e227. doi:10.1161/CIR.0000000000000923.

3.      Desai MY, Braunwald E. The Pathophysiologic Basis and Management of Calcific Aortic Valve Stenosis: JACC State-of-the-Art Review. J Am Coll Cardiol. 2025;86(9):659-672. doi:10.1016/j.jacc.2025.06.049.