Aortic Stenosis ✅

Related Subjects: |Aortic Anatomy |Acute Coronary Syndrome (ACS) General |Aortic Dissection |Acute Heart Failure and Pulmonary Oedema |Aortic Regurgitation (Incompetence) |Aortic Stenosis |Aortic Sclerosis |Transcatheter aortic valve implantation (TAVI) |Infective Endocarditis

🫀 Aortic Stenosis (AS) = progressive narrowing of the aortic valve, causing obstruction to left ventricular outflow. 💡 Most common valvular lesion in the UK, particularly in elderly men. ⏳ Once symptoms develop, untreated AS carries a poor prognosis (average survival 2–3 years).

📖 Overview

• Obstructive lesion at the level of the aortic valve.
• Prevalence: ~3% of people >75 years.
• In developed countries: calcific degeneration is most common.
• In low-income countries: rheumatic disease remains relevant.
• Progression is gradual; LV adapts via concentric hypertrophy to maintain cardiac output until late stages.
• Complications arise from chronic pressure overload → LV hypertrophy, diastolic dysfunction, eventually systolic failure.

🫀 Anatomy & Valve Morphology

• Normal aortic valve has 3 cusps: Left (L), Right (R), Non-coronary (N).
• Above the cusps lie the sinuses of Valsalva, which fill the coronary arteries during diastole.
• LV outflow tract adapts by concentric hypertrophy in response to chronic obstruction.
• Bicuspid aortic valves (1–2% population) predispose to earlier stenosis and ascending aortic aneurysm.

🔬 Pathophysiology

• Calcific AS: Age-related deposition of calcium on valve leaflets → stiffening and obstruction, most common >70 years.
• Bicuspid valve: Congenital anomaly; stenosis presents 40–60s; accelerated calcification.
• Rheumatic: Leaflet thickening, commissural fusion, often coexisting with AR or MS.
• LV adapts by concentric hypertrophy → increased diastolic pressure, preserved systolic function initially.
• Long-standing obstruction → myocardial fibrosis → arrhythmias, sudden cardiac death.
• Mimics include subvalvular (HOCM, membranous obstruction) and supravalvular AS (Williams syndrome).

⚠️ Causes

🩺 Clinical Presentation

• Classic triad: Angina 💔, Syncope 💫, Dyspnoea 🫁.
• Murmur: harsh ejection systolic, RUSB, radiating to carotids; crescendo-decrescendo.
• Pulses: slow-rising, narrow pulse pressure (pulsus parvus et tardus).
• LV heave due to hypertrophy; later apex displaced with LV dilation.
• Symptoms progress with severity; early stages may be asymptomatic.
• Arrhythmias: AF common in advanced disease; risk of sudden cardiac death increases with LV dysfunction.

📉 Complications

• LV failure, pulmonary oedema.
• Arrhythmias, sudden cardiac death ⚡.
• Stokes–Adams attacks (due to high-grade AV block or arrhythmias).
• Infective endocarditis, especially on calcified or prosthetic valves.
• Ascending aortic dilatation in bicuspid valves → risk of dissection.

🧪 Investigations

• Bloods: FBC, U&E, CRP, LFTs (for pre-op assessment, endocarditis work-up).
• ECG: LVH with strain pattern: deep S in V1, tall R in V5/V6, lateral ST depression/T-wave inversion.
• CXR: LV enlargement, post-stenotic ascending aorta dilatation, calcified aortic valve.
• Echocardiography = gold standard:
  • Severe AS: AVA <1.0 cm², mean gradient >40 mmHg, Vmax >4 m/s.
  • Moderate AS: AVA 1.0–1.5 cm², mean gradient 25–40 mmHg.
  • Mild AS: AVA >1.5 cm², gradient <25 mmHg.
  • Assess LV function, wall thickness, aortic root diameter, and concomitant valve lesions.
• Cardiac CT / MRI: Assess annulus size for TAVI, aortic root pathology, coronary anatomy.
• Coronary angiography: Pre-op for patients >40 years or with CAD risk factors.
• Exercise testing: Only if asymptomatic and unclear clinical status; detect latent symptoms.

⚡ Management Overview (NICE/ESC compliant)

• 👀 Watchful waiting: Asymptomatic mild/moderate AS, annual echo, educate on red-flag symptoms.
• 💊 Medical therapy: Not disease-modifying. Diuretics cautiously for fluid overload. Treat coexistent HTN, IHD, AF. Statins do NOT slow progression.
• 🔪 Surgical Aortic Valve Replacement (SAVR): Gold standard; symptomatic severe AS, LVEF <50%, or concurrent cardiac surgery.
• 🩻 TAVI/TAVR: High surgical risk, elderly; less invasive, similar outcomes in appropriate candidates.
• 🎈 Balloon Valvuloplasty (BAV): Temporary relief in palliative or bridge-to-SAVR situations; restenosis common within 6–12 months.
• 💉 Anticoagulation: Only if mechanical prosthesis placed; avoid in native valve unless other indications (AF).

🧾 Surgical Indications (ESC/NICE)

📊 Prognosis

• Untreated severe symptomatic AS → survival 2–3 years.
• Timely SAVR/TAVI restores near-normal life expectancy if performed before irreversible LV dysfunction.
• Post-TAVI or SAVR LV mass regression occurs over 6–12 months, improving symptoms and survival.

🩺 Case Examples

Case 1 – Classic Triad: 74-year-old man with exertional chest pain, dizziness. Murmur: ejection systolic RUSB radiating to carotids. ECG: LVH. Management: Urgent echo → severe AS confirmed; refer for SAVR/TAVI. Avoid: Nitrates or vigorous exercise due to preload dependence.

Case 2 – Incidental AS: 68-year-old woman, asymptomatic, murmur on routine check. Echo: moderate AS, preserved LV function. Management: Annual echo, patient education, risk factor control.

Case 3 – Acute Decompensation: 82-year-old man with breathlessness, ankle swelling. Echo: severe AS with reduced EF. Management: Careful diuretics, oxygen, urgent heart-team review for valve intervention. Avoid excessive preload reduction.

📚 References

• 2017 ESC/EACTS Guidelines on Valvular Heart Disease
• NICE NG208: Heart Valve Disease (2021)