Pathophysiology
Endothelial injury and lipid infiltration on the valve leaflets trigger inflammation, osteogenic differentiation of valvular interstitial cells and calcium deposition. Reduced effective orifice area increases LV afterload -> concentric hypertrophy -> diastolic dysfunction.
Sources: ACC/AHA 2020 Valvular Heart Disease Guideline (Circulation 2021;143:e72); ESC/EACTS 2021 Valvular Heart Disease Guidelines (Eur Heart J 2022;43:561)
Clinical presentation
Classic triad: exertional angina, syncope, dyspnoea/heart failure. Crescendo-decrescendo systolic ejection murmur at right upper sternal border radiating to carotids; delayed and diminished carotid upstroke (pulsus parvus et tardus); soft/absent S2.
Sources: ACC/AHA 2020 Valvular Heart Disease Guideline (Circulation 2021;143:e72); ESC/EACTS 2021 Valvular Heart Disease Guidelines (Eur Heart J 2022;43:561)
Diagnosis
Transthoracic echocardiography quantifies aortic-jet velocity, mean gradient and valve area. Severe AS: peak velocity >4 m/s, mean gradient >40 mmHg, area <1.0 cm^2. CT for valve calcium score and TAVI planning; coronary angiography pre-procedure.
Sources: ACC/AHA 2020 Valvular Heart Disease Guideline (Circulation 2021;143:e72); ESC/EACTS 2021 Valvular Heart Disease Guidelines (Eur Heart J 2022;43:561)
Management
Symptomatic severe AS mandates valve replacement - TAVI now first-line for intermediate/high-risk and increasingly for low-risk elderly; SAVR for younger patients, bicuspid morphology with aortopathy, or unfavourable TAVI anatomy. Avoid vasodilators in severe AS.
Sources: ACC/AHA 2020 Valvular Heart Disease Guideline (Circulation 2021;143:e72); ESC/EACTS 2021 Valvular Heart Disease Guidelines (Eur Heart J 2022;43:561)







