Lucan · Conditions

Aortic stenosis

Australian guidance: CSANZ Valvular Heart Disease

1. Definition and epidemiology

Aortic stenosis (AS) is obstruction to left ventricular outflow at the level of the aortic valve, most commonly caused by calcific (degenerative) disease of a tricuspid or bicuspid valve. In Australia, calcific AS is the most prevalent form of valvular heart disease in adults, affecting approximately 2 to 5% of people aged over 65 years and rising sharply in prevalence with each decade of life. Bicuspid aortic valve, present in 1 to 2% of the population, predisposes to earlier-onset calcification and is the most common cause of severe AS in patients under 60 years.

2. Pathophysiology

Calcific AS begins with lipid infiltration, macrophage accumulation, and osteoblast-like differentiation of valve interstitial cells in the valve leaflets, mirroring early atherosclerosis but without intimal plaque formation (Robbins Ch 12). Calcium nodules accumulate on the aortic surface of the cusps, progressively restricting leaflet opening and reducing the aortic valve area below the normal 3 to 4 cm squared. The resulting chronic pressure overload across the outflow tract causes concentric left ventricular hypertrophy (LVH) as the myocardium compensates to normalise wall stress. LVH impairs diastolic filling and raises myocardial oxygen demand, eventually exceeding supply via the coronary circulation. Over time, the hypertrophied ventricle decompensates: the ventricle dilates, stroke volume falls, and left ventricular end-diastolic pressure rises, back-propagating to produce pulmonary congestion (Robbins Ch 12). The classic triad of symptoms reflects sequentially worsening haemodynamic compromise: angina from subendocardial ischaemia, syncope from inability to augment cardiac output on effort or from reflex vasodilatation, and dyspnoea from elevated filling pressures and reduced output.

3. Clinical presentation and diagnostic criteria

The classic symptomatic triad of AS is exertional angina, exertional syncope or presyncope, and dyspnoea on exertion (including orthopnoea and paroxysmal nocturnal dyspnoea reflecting late decompensation). Once any of these symptoms develop, median survival without intervention is 2 to 3 years for angina and syncope, and under 18 months for dyspnoea and heart failure. On examination, the cardinal sign is an ejection systolic murmur loudest at the right upper sternal border radiating to the carotid arteries, often accompanied by a slow-rising and low-volume carotid pulse (pulsus parvus et tardus), a soft or absent aortic second heart sound, a sustained and undisplaced apex beat reflecting concentric hypertrophy, and a fourth heart sound. Severe disease is suggested by late peaking of the systolic murmur, loss of the second heart sound, and a narrow pulse pressure. An early systolic ejection click implies a mobile bicuspid valve and is absent in heavily calcified leaflets.

4. Investigations and AU-specific cutoffs

Transthoracic echocardiography (TTE) is the cornerstone investigation and is indicated whenever AS is clinically suspected. TTE determines valve morphology (tricuspid vs bicuspid), quantifies the mean pressure gradient and peak velocity across the valve, calculates the aortic valve area by continuity equation, and assesses LV function including LVEF and the degree of LVH. Echocardiographic severity thresholds aligned with CSANZ and international (ESC/AHA) guidance are: severe AS when peak aortic jet velocity is 4.0 m/s or greater, mean gradient is 40 mmHg or greater, and aortic valve area (AVA) is 1.0 cm squared or less (indexed AVA 0.6 cm squared per metre squared body surface area or less). Very severe AS is defined by peak velocity above 5.0 m/s or mean gradient above 60 mmHg. A 12-lead ECG is performed to identify LVH, left bundle branch block, or AF that may influence pacing or surgical risk decisions. Chest X-ray may show a boot-shaped heart or aortic valve calcification on lateral view. Coronary angiography is recommended before valve intervention in all patients above 40 years and in younger patients with cardiovascular risk factors, to identify coexisting coronary artery disease requiring concurrent revascularisation. Cardiac CT calcium scoring of the aortic valve (Agatston score above 1600 AU in men, above 800 AU in women) is used when echo findings are discordant to confirm haemodynamically severe AS.

5. Management

Asymptomatic severe AS with preserved LVEF (50% or greater) is managed with clinical and echocardiographic surveillance every six to twelve months. Intervention is indicated in symptomatic severe AS, in asymptomatic severe AS with LVEF below 50%, and in very severe AS with peak velocity above 5 m/s even without symptoms, given the high rate of rapid symptom onset and sudden death in this subset. The two options for aortic valve replacement are surgical aortic valve replacement (SAVR) and transcatheter aortic valve implantation (TAVI). TAVI is the preferred approach for patients who are inoperable, at high surgical risk, or at intermediate surgical risk in older adults (typically above 75 years), while SAVR remains the standard for low-surgical-risk patients below 65 years, particularly if a bioprosthetic SAVR offers equivalent durability to a TAVI prosthesis over a longer life expectancy. Multidisciplinary heart team assessment integrating surgical risk score (EuroSCORE II, STS-PROM), frailty assessment, anatomical suitability for TAVI, and patient preference guides the choice between SAVR and TAVI. There is no effective pharmacological therapy proven to slow the progression of calcific AS or to replace valve intervention once the haemodynamic threshold is met. Patients with coexisting AF require anticoagulation per AF management guidelines. Transcatheter balloon aortic valvuloplasty is reserved as a temporising bridge to definitive intervention in haemodynamically unstable patients or where palliative goals are unclear.

6. Pharmacology and AU PBS notes

No pharmacological therapy modifies the natural history of calcific AS or is recommended as disease-modifying therapy. Statin therapy, once hypothesised to retard calcification, did not reduce progression in randomised trials and is not indicated for AS progression alone, though it may be continued if indicated for coexisting dyslipidaemia under Heart Foundation guidelines. Vasodilators including ACE inhibitors, ARBs, and dihydropyridine calcium channel blockers must be used cautiously in severe AS, as the fixed outflow obstruction prevents the compensatory increase in cardiac output needed to maintain blood pressure, risking severe hypotension. Nitrates carry a similar risk and should be avoided or used only at very low doses if angina is present. If concomitant heart failure due to reduced LVEF develops before intervention is possible, cautious low-dose loop diuretics (frusemide, typically 20 to 40 mg oral daily) may be used to reduce congestion without compromising preload excessively. Beta blockers are relatively contraindicated in decompensated AS with low-flow, low-gradient physiology. Following TAVI, dual antiplatelet therapy with aspirin 100 mg daily plus clopidogrel 75 mg daily for three to six months is typically prescribed, followed by single antiplatelet therapy; specific regimens depend on bleeding risk and any indication for anticoagulation. No PBS streamlined codes apply to disease-specific AS pharmacotherapy. PBS listing applies to anticoagulation agents (apixaban, rivaroxaban, warfarin) for AF management in patients with AS who develop this complication.

7. Complications and monitoring

Major complications include sudden cardiac death (annual risk 1% in asymptomatic severe AS, rising sharply once symptoms develop), decompensated heart failure with pulmonary oedema, syncope and related injury, and infective endocarditis. Post-TAVI specific complications include cerebrovascular events (stroke or transient ischaemic attack from embolic debris during valve deployment), new left bundle branch block requiring permanent pacemaker implantation (in up to 15 to 30% of TAVI cases depending on prosthesis type), paravalvular aortic regurgitation, and prosthetic valve endocarditis. Patients who have undergone TAVI do not have a sternotomy scar, which is a key clinical examination finding to recognise valve status. Infective endocarditis rates after TAVI are similar to after SAVR overall, but outcomes of prosthetic valve endocarditis are worse for TAVI patients, partly confounded by older age at implantation. Surveillance echocardiography in asymptomatic severe AS is recommended every six to twelve months. After successful SAVR or TAVI, echocardiography is performed at 30 days and then annually to assess prosthesis function and detect structural valve deterioration. Patients with bicuspid aortic valve require periodic aortic root and ascending aorta surveillance by CT or cardiac MRI given associated aortopathy risk.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.