Aortic Stenosis

A progressive valvular lesion that obstructs outflow from the left ventricle.

• The most common primary valve disease in Europe and North America.

On echo, by integrating peak velocity, mean gradient and valve area against BSE thresholds — never one number in isolation.

Common and strongly age-related — predominantly a disease of the elderly.

• ≈2% at 65 years.
• ≈4% at 85 years.
• The commonest indication for valve replacement.

A long asymptomatic phase, then rapid decline once symptoms appear.

• Asymptomatic disease: risk of sudden death ~1%.
• Symptomatic without replacement: average survival 2–5 years, ~2% monthly mortality, ~50% sudden death.

Mostly degenerative calcification of an elderly valve; the rest is largely congenital (bicuspid) or rheumatic.

Progressive fibrosis and calcification of the valve — now the commonest cause of AS in the UK.

• Driven by chronic inflammation and mechanical stress — an active, atherosclerosis-like process, not passive wear.
• Begins as valve sclerosis — irregular leaflet thickening without obstruction to flow.

The same risk factors as atherosclerotic disease.

• Hypertension.
• Smoking.
• Diabetes.
• Hypercholesterolaemia.
• Chronic renal failure.

A common congenital valve with two functioning leaflets instead of three.

• Turbulent flow promotes fibrosis and earlier calcification.
• Present in 1–2% of the population; autosomal dominant inheritance.

A narrowing valve forces the LV to generate higher systolic pressure; it compensates with concentric hypertrophy, which eventually becomes harmful.

• Normal valve area is 2.6–3.5 cm²; significant obstruction occurs as the AVA approaches 1.0 cm².
• Diastolic dysfunction: the stiff ventricle becomes filling-dependent on atrial contraction (40–50% vs the usual ~20%) — so sinus rhythm matters.
• Oxygen supply–demand mismatch: greater muscle mass plus low aortic and high LV wall pressures cause subendocardial hypoperfusion and angina.

• LV pressure is higher during ejection, due to the resistance from outflow obstruction.
• There is an increase in end-systolic volume and a rightward shift of the loop.

The classic symptom triad is angina, exertional syncope and dyspnoea; signs centre on an ejection systolic murmur and a slow-rising, low-volume pulse.

• [@portabletext/react] Unknown block type "span", specify a component for it in the `components.types` propAngina — can occur with normal coronaries (↑ demand from LVH, ↓ supply).
• Syncope — exertional; fixed output cannot meet demand.
• Dyspnoea — pulmonary congestion; usually a late feature.
• Ejection systolic murmur — harsh, crescendo–decrescendo, loudest in the aortic area, radiates to the carotids; softens as severity rises and output falls.
• Slow-rising pulse; low and narrow pulse pressure; heaving apex beat; precordial/carotid thrill.
• Ejection click preceding the murmur; soft or absent S2.

Coronary perfusion falls even with normal arteries, while myocardial demand rises.

• AS raises LVEDP and lowers mean aortic pressure — both cut coronary blood flow.
• LV hypertrophy increases muscle mass and oxygen demand.
• Concomitant coronary atherosclerosis may also coexist.

• Sudden death (asymptomatic ~1%; symptomatic ~50%).
• Left ventricular failure.
• Arrhythmias — ventricular (more common) and supraventricular.
• Heart block (calcification of the conduction system).
• Infective endocarditis.
• Embolic phenomena (valve or aortic atheroma).
• Acquired von Willebrand syndrome with lower-GI bleeding from angiodysplasia (Heyde syndrome), and mechanical haemolytic anaemia.

Red cells are mechanically sheared as they cross the stenotic, calcified valve at high velocity, producing a microangiopathic (mechanical) haemolytic anaemia.

Echocardiography is the core test — it confirms the diagnosis, grades severity and shows the consequences; everything else is supporting.

Any one of three measurements, ideally concordant, plus the downstream consequences.

• Peak (jet) velocity ≥4 m/s.
• Mean gradient ≥40 mmHg.
• Valve area <1.0 cm² (or indexed AVA <0.6 cm²/m²).
• Plus consequences of severe AS, e.g. impaired LV function or dilatation.

Continuous-wave Doppler captures the peak transaortic velocity, which is converted to a pressure gradient by the simplified Bernoulli equation.

• Left ventricular hypertrophy (present in ~85%).
• LV strain pattern — T-wave inversion and ST depression in the inferior and lateral leads.
• AV nodal block (calcification of the conduction system).
• Longstanding disease: left anterior hemiblock, poor R-wave progression, LBBB or complete heart block.

Usually normal until LV failure develops; then non-specific changes appear.

• Post-stenotic dilatation of the ascending aorta (right mediastinum).
• Valvular calcification.
• Cardiomegaly and features of cardiac failure.

Full, slow, sinus, tight — maintain preload, a slow sinus rhythm, contractility and a high-normal SVR/coronary perfusion pressure.

• The disease is progressive and refractory to medical management.
• The only definitive treatment for severe disease is valve replacement.

Intervene for symptomatic severe AS, and for asymptomatic severe AS with adverse markers.

• Symptomatic severe aortic stenosis.
• Asymptomatic severe AS with: LVEF <50% (no other cause); abnormal exercise test; markedly raised BNP; or severe pulmonary hypertension without other explanation.
• Moderate AS when undergoing other cardiac surgery (Heart Team decision).
• Avoid intervention where survival/quality of life is unlikely to improve (e.g. severe comorbidity, survival <1 year).

Three options for severe symptomatic AS, chosen by the Heart Team on individual risk and anatomy.

By the multidisciplinary Heart Team, weighing surgical risk (e.g. EuroSCORE II), anatomy/technical suitability, comorbidities and patient preference — lower-risk patients generally toward SAVR, higher-risk toward TAVI, with BAV as a bridge or palliation.

The European System for Cardiac Operative Risk Evaluation — an operative mortality score validated for cardiac surgery.

• Patient factors: age, sex, renal impairment, mobility, lung disease, arteriopathy, diabetes, preoperative state, endocarditis.
• Cardiac factors: NYHA class, CCS angina class, LV function, recent MI, pulmonary hypertension.
• Operation factors: urgency, aortic surgery, operation weight.
• Less reliable in high-risk or elderly patients.

(Placeholder — answer to be written: indications and timing of AVR/TAVI, including symptom onset, very severe AS, LV dysfunction and rapid progression.)

A fixed-output state poorly tolerant of falls in SVR, tachycardia and loss of sinus rhythm — anaesthesia must defend preload, rhythm, contractility and coronary perfusion pressure.

It depends on symptoms, candidacy for valve replacement, and the risk of the planned surgery.

AS is a fixed-output state: stroke volume cannot rise to compensate for falls in SVR or preload, and tachycardia worsens supply–demand — so protect each haemodynamic variable.

• Preload — maintain; avoid hypovolaemia.
• Contractility — maintain; titrate myocardial depressants carefully.
• Afterload — avoid SVR drops; treat hypotension aggressively with vasoconstrictors to pre-anaesthetic pressure.
• Rate/rhythm — maintain sinus rhythm; avoid tachycardia; keep potassium normal.

Classically avoided in severe AS, but not absolutely contraindicated — a carefully titrated catheter technique can be used.

• Single-shot spinal is hazardous: rapid sympathectomy drops SVR, the fixed valve cannot compensate, and a spiral of hypotension, ischaemia and death can follow.
• Continuous spinal or combined spinal–epidural (catheter) allows slow titration with vasopressor support — most appropriate in mild-to-moderate disease.