Aortic Stenosis

One of the most common valvular heart diseases — narrowing of the aortic valve orifice, obstructing left ventricular outflow. Usually from degenerative calcification (elderly), but also congenital bicuspid valve (younger patients), rheumatic heart disease, or radiation-induced injury. Australian prevalence of severe AS: ~1.5% of those aged >55, 3.5% of those aged >75, with an incidence of 1.8 per 1000/year. Untreated symptomatic severe AS carries a 2-year mortality of 30–50% — early detection and referral matter.

Clinical features

Exertional dyspnoea or reduced exercise tolerance is the most common initial symptom. Cardinal symptoms: dyspnoea, heart failure, angina, and syncope. As AS progresses, LV hypertrophy increases myocardial oxygen demand and can compress intramural coronary arteries, causing angina even without coronary artery disease; severe AS prevents cardiac output from rising normally with exercise, which can cause exertional hypotension and syncope.

Examination: an ejection systolic (mid-systolic) murmur in the right 2nd intercostal space, radiating to the neck — becomes softer on hand grip (increased afterload). Also: low-volume pulse, systolic thrill, reduced pulse pressure, an apex that isn’t displaced, a soft second heart sound. ECG frequently shows LVH.

Differentiating a systolic murmur

Cause	Site/radiation	Dynamic manoeuvre	Other features
Aortic stenosis	Right 2nd ICS, radiates to neck	Softer with hand grip	Low-volume pulse, systolic thrill, reduced pulse pressure, soft S2
Hypertrophic cardiomyopathy	Left lower sternal border ± pansystolic (MR)	Louder with Valsalva/standing, softer with squatting	Sharp/jerky carotid pulse, double apical impulse, prominent JVP ‘a’ waves
Mitral regurgitation	Apex, radiates to axilla	Louder with hand grip	Displaced/forceful apex, soft S1, S3 common
Tricuspid regurgitation	Left lower sternal border	Louder on inspiration	Large JVP V waves
Pulmonary stenosis	Left 2nd ICS	Best on inspiration	Giant JVP ‘a’ waves, no radiation to neck
Ventricular septal defect	Left lower sternal area	Louder on expiration	Thrill at left sternal edge

A detailed exam can be helpful but doesn’t reliably diagnose or grade severity on its own. Baseline work-up: ECG (rhythm, LVH) and CXR (heart size, pulmonary congestion).

Severity assessment

Transthoracic echocardiography is the first and most useful investigation. Four broad echocardiographic categories:

1. High-gradient AS — mean gradient ≥40mmHg, peak velocity ≥4.0m/s, valve area ≤1cm² (or ≤0.6cm²/m²). The classic severe-AS picture.
2. Low-flow, low-gradient AS with reduced EF — mean gradient <40mmHg, valve area ≤1cm², LVEF <50%, stroke volume index ≤35mL/m². Low-dose dobutamine stress echocardiography distinguishes true-severe from pseudo-severe AS.
3. Low-flow, low-gradient AS with preserved EF — same gradient/area/SVi criteria but LVEF ≥50%; typically hypertensive elderly patients with a small, markedly hypertrophied LV. Aortic valve calcium scoring on CT (Agatston score ≥1200 AU women / ≥2000 AU men) corroborates true severe disease when dobutamine echo isn’t feasible/conclusive.
4. Normal-flow, low-gradient AS with preserved EF — SVi >35mL/m²; usually only moderate AS.

Asymptomatic severe AS with normal LV systolic function has a similar survival to age-matched controls, with sudden death risk < 1%/year. Recommended surveillance: echo every 3–5 years for mild disease, 1–2 years for moderate, 6–12 months for severe. Exercise testing (by an experienced operator) can add prognostic value in asymptomatic severe AS, verifying the absence of symptoms — but should not be performed in symptomatic patients, given the risk of adverse outcomes.

Management

Aortic valve replacement is the only treatment that improves mortality in symptomatic severe AS — medical therapy does not alter disease progression. Treating at the onset of mild symptoms can prevent heart failure, syncope, or angina.

Symptomatic patients with severe high-gradient AS (mean gradient >40mmHg, peak velocity >4.0m/s, valve area <1.0cm² or <0.6cm²/m²) should be evaluated for valve replacement. Risk scores (EuroSCORE, STS score) aid prognosis and treatment decisions alongside symptoms/exam findings; earlier intervention may be considered with abnormal exercise testing, elevated biomarkers, rapid progression, or very severe stenosis.

TAVI vs surgical AVR (SAVR): decided via a multidisciplinary “heart team” (cardiologist, cardiothoracic surgeon, geriatrician, and others) based on clinical, anatomical, and procedural factors — TAVI is often preferred for patients over 75, or those at high perioperative risk. Patients who undergo TAVI without a pre-existing indication for oral anticoagulation should get lifelong single antiplatelet therapy.

Medical management alongside valve assessment: treat hypertension (~40% of AS patients) and hyperlipidaemia. Start antihypertensives at low doses, up-titrating gradually — ACE inhibitors are safe and well tolerated in symptomatic severe AS, improving haemodynamics, effort tolerance, and dyspnoea.

Perioperative risk (non-cardiac surgery)

AS increases perioperative complication risk during non-cardiac surgery, depending on stenosis severity, symptom status, and co-existing cardiac disease. Severe symptomatic AS is a significant risk factor for perioperative MI, heart failure, and mortality — for elective intermediate/high-risk non-cardiac surgery, valve replacement is recommended first. Asymptomatic severe AS with normal LVEF can safely undergo low-to-intermediate-risk surgery if it doesn’t involve large volume shifts. Consider antibiotic prophylaxis for high-risk procedures in patients with prosthetic valves (including transcatheter valves) or a history of infective endocarditis — see Infective & Inflammatory Heart Disease.