aortic stenosis

Imagine trying to force a garden hose's worth of water through a pinched nozzle: the pump behind it has to push much harder, and the stream that comes out is fast and narrow. In aortic stenosis the aortic valve — the door between the left ventricle and the aorta — becomes stiff and narrowed, so the left ventricle must generate far higher pressure to eject blood into the body.

Over time the left ventricle responds to this pressure overload by thickening its walls (hypertrophy). This helps for a while but eventually the muscle stiffens and the heart's reserve runs out. The classic symptom triad is exertional breathlessness, chest pain resembling angina, and fainting or near-fainting (syncope), reflecting the heart's inability to raise output when demand rises.

The most common cause in older adults is gradual calcium build-up on a previously normal valve; in younger patients it is often a congenitally bicuspid valve, and worldwide rheumatic disease remains important. Severity is judged on echocardiography by the jet velocity across the valve, the pressure gradient, and the calculated valve area. Once severe stenosis causes symptoms, valve replacement — surgical or transcatheter — is the definitive treatment.

Symptomatic severe aortic stenosis carries a serious prognosis without intervention, but this is a reference description, not a substitute for individual cardiology assessment.