Friday, April 3, 2026

Aortic Stenosis

A 72 year old male 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 mm Hg. 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 aortic valve area of 0.8 cm², peak velocity of 4.5 m/s, and mean gradient of 50 mmHg, with preserved LVEF. Diagnosis?

Diagnosis is Symptomatic Severe Aortic Stenosis.

1. Definition

Aortic stenosis is a valvular disorder characterized by progressive narrowing of the aortic valve, resulting in obstruction to left ventricular outflow, causing pressure overload, concentric left ventricular hypertrophy, and eventual heart failure.

2. Etiology

  1. Degenerative calcific AS (most common in elderly)
    • Progressive leaflet calcification and reduced mobility
    • Risk factors overlap with atherosclerosis
  2. Bicuspid aortic valve
    • Congenital abnormality leading to early calcification
    • Presents earlier, often in middle age
  3. Rheumatic heart disease
    • Commissural fusion, often with concomitant mitral disease

3. Pathophysiology

  1. Fixed obstruction increases afterload → concentric LV hypertrophy
  2. LVH leads to:
    • Increased oxygen demand
    • Reduced subendocardial perfusion
  3. Results in myocardial ischemia even without CAD
  4. Diastolic dysfunction develops due to stiff ventricle
  5. Advanced disease leads to:
    • Reduced stroke volume
    • Decreased cardiac output
    • Pulmonary congestion and heart failure

4. Clinical Features

4.1 Classic Triad

  1. Angina
    • Due to supply-demand mismatch
  2. Dyspnea
    • Due to elevated LV filling pressures
  3. Syncope (exertional)
    • Due to inability to augment cardiac output during vasodilation

4.2 Additional Features

  1. Fatigue and reduced exercise tolerance
  2. Presyncope or dizziness
  3. Signs of heart failure in advanced disease

5. Special Association

Heyde Syndrome

  1. Aortic stenosis + GI bleeding from angiodysplasia
  2. Mechanism:
    • High shear stress across valve → degradation of von Willebrand factor
    • Leads to acquired bleeding tendency

6. Physical Examination

  1. Murmur
    • Harsh crescendo–decrescendo systolic murmur
    • Best heard at right upper sternal border
    • Radiates to carotids
    • May radiate to apex
  2. Carotid pulse
    • Pulsus parvus et tardus
  3. Heart sounds
    • Soft or absent A2
    • Paradoxical splitting of S2
    • S4 gallop
  4. Pulse pressure
    • Often narrow
  5. Dynamic maneuvers
    • Increases with squatting
    • Decreases with Valsalva

7. Diagnosis

7.1 Transthoracic Echocardiography (Gold Standard)

Evaluates:

  1. Valve anatomy and calcification
  2. Aortic valve area (AVA)
  3. Peak velocity
  4. Mean gradient
  5. Left ventricular function

Severity must be assessed using multiple parameters.

7.2 Additional Investigations

  1. ECG
    • LVH, left atrial enlargement
  2. Chest X-ray
    • LV enlargement
    • Aortic valve calcification
    • Post-stenotic dilation
  3. Cardiac catheterization
    • Used when noninvasive data are discordant
    • Required before intervention

8. Severity Classification

Severity

AVA (cm²)

Velocity (m/s)

Gradient (mmHg)

Mild

>1.5

<3

<20

Moderate

1.0–1.5

3–4

20–40

Severe

≤1.0

≥4

≥40

9. Hemodynamic Subtypes

9.1 Classical Low-Flow Low-Gradient

  • LVEF <50%
  • Reduced stroke volume
  • Requires dobutamine stress echo

9.2 Paradoxical Low-Flow Low-Gradient

  • LVEF ≥50%
  • Small, stiff LV
  • Reduced stroke volume

9.3 Normal-Flow Low-Gradient

  • Discordant findings
  • Requires careful reassessment

10. Management

10.1 Medical Therapy

  1. Symptomatic relief only
  2. Diuretics for congestion, used cautiously
  3. Treat hypertension carefully, including ACE inhibitors or ARBs
  4. Maintain adequate preload

Medical therapy does not halt disease progression.

10.2 Definitive Treatment

Valve replacement is the only curative therapy

SAVR

  • Preferred in younger patients
  • Bicuspid valve
  • Concomitant surgery needed

TAVR

  • Preferred in older patients or high-risk individuals
  • Decision based on age, anatomy, and comorbidities

11. Indications for Valve Replacement

  1. Symptomatic severe AS
  2. Severe AS with LVEF <50%
  3. Selected asymptomatic patients with:
    • Very severe AS
    • Abnormal exercise test
    • Rapid progression
    • Elevated BNP

12. Complications

  1. Heart failure
  2. Arrhythmias
  3. Sudden cardiac death
  4. Pulmonary hypertension

13. Prognosis

  1. Long asymptomatic phase
  2. Once symptoms develop:
    • Angina → ~5 year survival
    • Syncope → ~3 year survival
    • Heart failure → ~2 year survival

14. Key Clinical Insight

Aortic stenosis should be suspected in elderly patients with exertional syncope, angina, or dyspnea and a systolic murmur radiating to the carotids. Once symptoms develop, mortality increases sharply without valve replacement, making early recognition and timely intervention critical.

Triad of angina, syncope, and dyspnea = symptomatic severe aortic stenosis → urgent valve replacement

15. Exam Pearls

  1. Triad: angina, syncope, dyspnea
  2. Murmur radiates to carotids
  3. Pulsus parvus et tardus is hallmark
  4. Echo is diagnostic
  5. Low-flow low-gradient AS requires careful evaluation
  6. Valve replacement is definitive treatment
  7. Do not delay intervention once symptoms appear

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