Aortic Stenosis
On this page
Direct answer
Exertional angina, syncope or dyspnoea in a patient with a harsh crescendo-decrescendo systolic murmur at the right upper sternal edge radiating to the carotids, a slow-rising low-volume pulse (parvus et tardus) and a soft or absent aortic component of the second heart sound means severe aortic stenosis — and symptom onset is everything, with classical untreated survivals of roughly five years for angina, three for syncope and two for heart failure. Severity is echocardiographic: valve area below 1 square centimetre (indexed below 0.6), mean gradient 40 mmHg or more, or peak velocity 4 m/s or more. Intervention — surgical replacement or transcatheter aortic valve implantation — follows symptoms, left ventricular dysfunction or asymptomatic high-risk criteria; no drug slows progression.
What you must remember
- Causes by clock: degenerative calcific tricuspid disease in the elderly (the commonest in an ageing India), bicuspid valve presenting in the fifth-sixth decade, rheumatic stenosis younger with mitral involvement and commissural fusion.
- Symptom triad with survival arithmetic: angina about five years, syncope about three, dyspnoea or heart failure about two — the numbers that frame urgency once symptoms begin.
- Examination package: crescendo-decrescendo murmur right upper sternal border radiating to carotids, parvus et tardus carotid upstroke, soft or absent A2 with paradoxical splitting, fourth heart sound, systolic thrill; the murmur lengthens and grows with severity while A2 fades.
- Severity thresholds: peak velocity 4 m/s or more, mean gradient 40 mmHg or more, area below 1 square centimetre or indexed below 0.6 square centimetre per square metre; very severe means velocity 5 m/s or more or gradient 60 mmHg or more.
- Low-flow low-gradient states: depressed ejection fraction with small stroke volume — dobutamine stress echocardiography demonstrates contractile reserve and true severity; paradoxical low-flow with normal ejection fraction needs indexed stroke volume calculation.
- Intervention logic: symptoms with severe stenosis mandate intervention regardless of ejection fraction; asymptomatic triggers include ejection fraction below 50 percent, very severe stenosis with rapid progression, and abnormal exercise response — debated and individualised.
- TAVI versus surgery: transcatheter implantation favours elderly, frail or high operative-risk patients with femoral access; surgery favours the young and low-risk, bicuspid anatomy and coexistent lesions; balloon valvuloplasty is only a palliative bridge.
- Pharmacological caution: nitrates and other vasodilators, and aggressive diuresis can precipitate collapse in severe stenosis — a preload-dependent circulation; treat angina cautiously with beta-blockers and pursue definitive therapy.
Numbers that change management
A 74-year-old has exertional syncope and the murmur above; echo shows peak velocity 4.4 m/s, mean gradient 45 mmHg, valve area 0.8 square centimetres and ejection fraction 50 percent. The reasoning runs: symptoms plus severe high-gradient stenosis equals mechanical relief, and the route follows the patient — age, frailty, iliofemoral anatomy and operative risk tilt toward transcatheter implantation here, with coronary assessment beforehand. Post-procedure care covers pacemaker risk (especially with pre-existing conduction disease) and antithrombotic plans.
Contrast two clinic decisions with the same valve numbers but no symptoms: a fit 60-year-old with severe stenosis and a normal exercise test is watched — intervention before symptoms buys no mortality benefit in the standard-risk patient; and a patient with low ejection fraction and a gradient of only 28 mmHg is not "moderate" by gradient alone — dobutamine stress separates true severe stenosis with reserve (benefits from replacement) from contractile failure (does not).
The Indian reality
Three patterns cross Indian practice. Rheumatic aortic stenosis arrives young, fused alongside a mitral valve that needs attention in the same sitting, pushing decisions toward surgery rather than percutaneous routes. Bicuspid disease presents in the forties-to-sixties with calcific degeneration decades ahead of the tricuspid population — listen for it in younger adults and follow serially. And access economics shape the route: transcatheter implantation remains concentrated in metro centres at substantial out-of-pocket cost, while surgical replacement is covered under government insurance schemes — so the heart-team conversation in India includes finance, not just anatomy. Late presentation with decompensated failure is commoner than in Western clinics, making the vasodilator warning practical: the stenotic valve converts the circulation into a preload-dependent circuit, and liberal vasodilators or over-diuresis precipitate collapse.
Frequently asked questions
What classical survival is quoted for the aortic stenosis symptom triad?
Approximately five years for angina, three for syncope and two for heart failure without intervention.
Which echo parameters define severe aortic stenosis?
Peak velocity 4 m/s or more, mean gradient 40 mmHg or more, or valve area below 1 square centimetre (indexed below 0.6 square centimetre per square metre).
Why are vasodilators dangerous in severe aortic stenosis?
The fixed orifice makes cardiac output preload-dependent; dropping systemic resistance or venous return cannot be matched by flow across the valve.
How is low-flow low-gradient aortic stenosis evaluated?
Dobutamine stress echocardiography (with depressed ejection fraction) or indexed stroke volume assessment (with normal ejection fraction) to separate true severe stenosis from low-flow states.
How are TAVI and surgical replacement chosen?
Transcatheter implantation for elderly, frail or high surgical risk patients with suitable access; surgery for younger low-risk patients, bicuspid anatomy or coexistent lesions — a heart-team decision.