🫀 Aortic Stenosis (AS) = progressive narrowing of the aortic valve, causing obstruction to LV 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).

📖 About

Obstructive lesion at the level of the aortic valve.
Prevalence: ~3% of people >75 years.
In developed countries: calcific degeneration is the most common cause.
In low-income countries: rheumatic disease still important.

🫀 Anatomy

Normal aortic valve has 3 cusps: Left coronary (L), Right coronary (R), Non-coronary (N).
Above them lie the sinuses of Valsalva, filling coronary arteries during diastole.

🔬 Pathology

Calcific (degenerative) → stiffened, thickened cusps; commonest >70 years.
Bicuspid valve → congenital; earlier presentation (40–60s); accelerates calcification.
Rheumatic → leaflet fusion + commissural scarring; often coexists with AR or MS.
Mimics: subvalvular (HOCM, membrane), supravalvular (Williams syndrome).

⚠️ Causes


Type	Cause	Notes
Common	Calcific AS	Elderly; progressive calcification of cusps.
Common	Bicuspid valve	Congenital; premature calcification.
Common	Rheumatic	Post-streptococcal; usually with AR/MV disease.
Rare	Radiation	Valve fibrosis + calcification after chest radiotherapy.
Rare	Williams syndrome	Supravalvular AS; “elfin facies”, hypercalcaemia.
Rare	Endocarditis	Healed vegetations scar the valve.

🩺 Clinical Presentation

Classic triad → Angina 💔, Syncope 💫, Dyspnoea 🫁.
Murmur: harsh ejection systolic, best at right upper sternal edge, radiating to carotids.
Pulses: slow-rising + narrow pulse pressure (pulsus parvus et tardus).
Heaving, non-displaced apex beat (pressure overload).
Late: LV dilatation → displaced apex, heart failure.

📉 Complications

LV failure, pulmonary oedema.
Arrhythmias, sudden cardiac death ⚡.
Stokes–Adams attacks (arrhythmic syncope).
Endocarditis risk.

🧪 Investigations

Bloods: FBC, U&E, CRP, LFTs (esp. if considering endocarditis or TAVI work-up).
ECG: LVH with strain (deep S in V1 + tall R in V5/6; lateral ST depression/T-wave inversion).
CXR: LV enlargement, post-stenotic dilatation of ascending aorta, ± calcified valve.
Echocardiogram = gold standard:
- Severe AS: AVA <1.0 cm²; Mean gradient >40 mmHg; Vmax >4.0 m/s.
- Moderate AS: AVA 1.0–1.5 cm²; Mean gradient 25–40 mmHg.
- Mild AS: AVA >1.5 cm²; Gradient <25 mmHg.

⚡ Management Overview

👀 Watchful waiting: for asymptomatic mild/moderate AS. Annual echo + educate about red-flag symptoms.
💊 Medical therapy: not disease-modifying. – Diuretics for fluid overload (caution – preload dependent). – Treat coexistent HTN, IHD, AF. – Statins ❌ do not slow AS progression.
🔪 Surgical Aortic Valve Replacement (SAVR): gold standard. – Indicated in symptomatic severe AS or asymptomatic with LVEF <50% or undergoing CABG/other valve surgery.
🩻 TAVI/TAVR: less invasive, for older patients or those at high surgical risk.
🎈 Balloon Valvuloplasty (BAV): temporary bridge/palliative option; restenosis common within 6–12 months.

🧾 Surgical Indications (ESC/NICE)

Symptomatic severe AS (angina, syncope, dyspnoea).
Asymptomatic severe AS with:
- LVEF <50%.
- Very severe AS (Vmax ≥5.0 m/s).
- Planned other cardiac surgery.

🏥 Postoperative & Long-Term Care

Mechanical valve: lifelong anticoagulation (INR 2.5–3.5), durable.
Bioprosthetic valve: no lifelong anticoagulation, lifespan 10–15 years.
Ross procedure: pulmonary autograft used in selected young patients.
Endocarditis prophylaxis before high-risk dental work if prosthetic valve.
Lifelong echo follow-up.

📊 Prognosis

Untreated severe symptomatic AS → survival only 2–3 years.
Timely SAVR/TAVI restores near-normal life expectancy if performed before irreversible LV dysfunction.

📚 References

🩺 Case 1 — Classic Symptomatic Triad

A 74-year-old man presents with exertional chest pain and dizziness on climbing stairs. Examination reveals a slow-rising pulse, an ejection systolic murmur loudest at the right upper sternal edge radiating to the carotids, and a soft second heart sound. ECG shows left ventricular hypertrophy — the classic triad of angina, syncope, and heart failure in severe aortic stenosis. Management: 🏥 Urgent cardiology referral, echocardiography to confirm severity, definitive treatment is surgical aortic valve replacement (SAVR) or TAVI if not surgical candidate. Avoid: ❌ Nitrates or vasodilators in severe AS (can drop preload → collapse), and vigorous exercise.

🩺 Case 2 — Incidental Finding

A 68-year-old woman is referred after a systolic murmur is detected at a routine hypertension check. She is asymptomatic with normal exercise tolerance. Echocardiography demonstrates moderate aortic stenosis with preserved left ventricular function, highlighting the importance of surveillance even in asymptomatic cases. Management: 📅 Regular echo follow-up (every 1–2 years for moderate disease), risk factor modification (BP, lipids), patient education on red flag symptoms. Avoid: ❌ Unnecessary intervention if asymptomatic; avoid dehydration and sudden preload reduction.

🩺 Case 3 — Acute Decompensation

An 82-year-old man with known aortic stenosis presents with progressive breathlessness, orthopnoea, and ankle swelling. On exam: bibasal crackles, displaced apex beat, and a harsh ejection systolic murmur. Echo confirms severe aortic stenosis with reduced ejection fraction. He is admitted for optimisation and valve intervention planning. strong>Management: 💊 Diuretics for symptom relief (carefully titrated), oxygen, urgent heart team review for TAVI vs surgery depending on frailty and comorbidity. Avoid: ❌ Excessive diuresis (may drop preload), ACE inhibitors/vasodilators avoided or used with caution, no strenuous exercise. Vasodilators (including ACEIs) can cause precipitous hypotension, syncope, or collapse. Sometimes used if severe LV dysfunction. Avoid hypotension. Great care needed.

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Aortic Stenosis