Aortic Stenosis

Definition

Aortic stenosis (AS) is narrowing of the aortic valve orifice that obstructs the ejection of blood from the left ventricle into the aorta during systole. It is the most common valvular heart lesion requiring intervention in high-income countries, and its prevalence rises steeply with age.¹

Pathophysiology

The narrowed valve creates a fixed obstruction to left-ventricular outflow. To maintain stroke volume against the high pressure gradient, the left ventricle undergoes concentric hypertrophy. Over time this produces impaired relaxation and diastolic dysfunction, raised filling pressures and pulmonary congestion, and eventually systolic impairment. The thickened myocardium has higher oxygen demand and reduced coronary flow reserve, causing angina even without coronary disease. Because cardiac output cannot rise normally on exertion, systemic vasodilation during exercise can precipitate exertional syncope.¹

Calcific AS is not a passive wear-and-tear process. It begins with endothelial injury and lipid deposition, progresses through chronic inflammation and fibrosis, and ends in osteoblast-like differentiation of valve interstitial cells with active bone-matrix formation — which is why the valve calcifies rather than simply thickens, and why lipid-lowering therapy does not halt it once established.

Co-morbidities

Aortic stenosis shares risk factors with, and frequently coexists with, coronary artery disease — around half of patients undergoing valve replacement have significant coronary disease requiring concurrent bypass grafting or stenting. Hypertension compounds the afterload the hypertrophied ventricle must overcome and is common in this largely elderly population. Chronic kidney disease and diabetes accelerate valve calcification and raise procedural risk. Atrial fibrillation can appear as left atrial pressure rises, and the loss of atrial contraction it causes is poorly tolerated in a stiff, hypertrophied ventricle. Frailty and sarcopenia are common in the older AS population and are actively assessed when planning surgical (SAVR) versus transcatheter (TAVI) valve replacement.²

Prevalence

Aortic sclerosis (valve thickening without obstruction) affects around a quarter of adults over 65. Significant aortic stenosis is present in roughly 2–4% of adults over 65 and becomes more common with each decade, making it an increasingly frequent problem in an ageing population. Bicuspid valve disease presents a generation earlier, typically between 40 and 60 years.

Causes and risk factors

• Calcific (degenerative) AS — the most common cause, typically over the age of 70; an active process of valve fibrosis and calcification sharing risk factors with atherosclerosis.
• Congenital bicuspid aortic valve — the leading cause in younger adults, present in around 1–2% of the population and often accompanied by aortopathy that needs its own surveillance.
• Rheumatic heart disease — now uncommon in high-income settings and almost always accompanied by mitral valve involvement; still important in First Nations and lower-income populations.
• Accelerating factors — chronic kidney disease and dialysis, prior chest radiotherapy, and metabolic syndrome all shorten the time from sclerosis to severe stenosis.¹

Symptoms

The classic triad

AS is typically silent for years. The onset of the classic symptom triad marks a critical turning point:

• Exertional breathlessness and, later, heart-failure symptoms
• Angina (exertional chest tightness), often in the absence of coronary disease
• Syncope or pre-syncope, characteristically on exertion

Why symptoms appear so late

The hypertrophied ventricle compensates efficiently, so the valve area can halve before anything is felt. Many people also attribute early breathlessness to age or deconditioning and reduce their activity without noticing — meaning a patient who reports "no symptoms" may simply have stopped doing whatever would produce them. Asking specifically what the person has given up is more revealing than asking whether they are breathless.

Recognising deterioration

Any new exertional chest tightness, light-headedness, blackout or a clear fall in exercise tolerance in known AS is a change in disease state, not a bad day. Once symptoms appear in severe AS, average survival without valve replacement is around two to three years, so symptomatic severe AS is treated promptly.³

Diagnosis

Why diagnosis matters

Grading severity and detecting the transition to symptoms are what determine timing of intervention — the single decision that changes outcome in this condition. Asymptomatic severe AS under structured surveillance carries a low annual risk of sudden death, so accurate staging allows watchful waiting to be safe rather than merely hopeful.⁴

How is it diagnosed?

Examination may reveal an ejection systolic murmur radiating to the carotids, a slow-rising (parvus et tardus) pulse and a soft or absent second heart sound. In the elderly these signs are less reliable, and the murmur may be the only clue. Diagnosis and grading are confirmed with transthoracic echocardiography.^1,2

Echocardiography and severity grading

Severity rests on three measurements taken together — peak jet velocity, mean gradient and calculated valve area — because any one alone can mislead in the presence of altered flow.⁵

Low-flow, low-gradient aortic stenosis

Where symptoms and valve area appear discordant with a low gradient — often with reduced ejection fraction, or a small, stiff ventricle with preserved ejection fraction — dobutamine stress echocardiography or a CT aortic-valve calcium score is used to confirm true severity. This pattern is easy to under-call, and under-calling it withholds the only effective treatment.⁵

Investigations for related conditions

Coronary assessment before intervention, renal function, and screening for atrial fibrillation and pulmonary hypertension all form part of the workup, because each alters procedural risk and the choice between SAVR and TAVI.²

Management

Management and goals

There is no medical therapy proven to slow the progression of AS. The goals are therefore to time valve replacement correctly, to keep the person safely active while waiting, and to manage the conditions that share its risk profile.¹

Treatment options

• Asymptomatic AS — periodic surveillance echocardiography (interval set by severity), cardiovascular risk-factor management, and education about the symptoms that warrant urgent review.
• Symptomatic severe AS — aortic valve replacement is the definitive treatment. A multidisciplinary Heart Team chooses the approach based on age, surgical risk, anatomy and patient preference.
• Medical care — cautious treatment of coexisting heart failure and hypertension, and careful use of vasodilators, which can be poorly tolerated in severe AS.²

Surgical versus transcatheter replacement

Transcatheter aortic valve implantation (TAVI) was first established in patients too high-risk for surgery, but randomised trials in low-risk patients found it non-inferior or superior to surgery for death, stroke and rehospitalisation at one year.^6,7 TAVI is now used across the risk spectrum, with the choice turning increasingly on age, valve durability expectations, anatomy and the need for concomitant procedures rather than on operative risk alone. Practically, TAVI means a shorter admission, no sternotomy and faster mobilisation; SAVR means a sternotomy with its precautions and a longer rehabilitation arc.

Identifying deterioration

Between reviews, the events that matter are the triad symptoms and any unexplained fall in exercise capacity. Syncope on exertion in known AS is an emergency, not a faint to be observed at home.³

Action plan

1. Know the three symptoms that change management: exertional breathlessness, chest tightness, dizziness or blackout.
2. Report any of them to the cardiology team promptly, without waiting for the next scheduled echocardiogram.
3. Seek urgent care for blackout on exertion, chest pain at rest, or breathlessness that stops you lying flat.
4. Attend surveillance echocardiograms even when feeling well — the interval is set by valve severity, not by symptoms.
5. Keep dental health under active review, and tell any dentist or proceduralist about the valve.

Medications

Medications in aortic stenosis

No drug slows valve calcification; statins were tested for this purpose and did not work. Medication therefore treats the accompanying conditions — antihypertensives, heart-failure therapy, rate or rhythm control and anticoagulation for atrial fibrillation, and secondary prevention for coexisting coronary disease.¹

Medicines to use with care

In severe AS the ventricle depends on adequate preload and afterload to maintain a workable gradient. Nitrates, high-dose diuretics and rapid up-titration of vasodilators can therefore cause abrupt hypotension or syncope. They are not forbidden, but they are started low and titrated slowly under supervision — a point worth knowing before assuming a dizzy patient has simply progressed.²

After valve replacement

Mechanical valves require lifelong warfarin with a target INR set by valve type and position; bioprosthetic valves and TAVI generally require antiplatelet therapy, with anticoagulation reserved for another indication such as atrial fibrillation. Endocarditis-prevention advice applies to all prosthetic valves.

Multi-system manifestations

Acquired von Willebrand syndrome and gastrointestinal bleeding

High shear stress across the stenotic valve cleaves the largest von Willebrand factor multimers, producing a mild acquired bleeding tendency. Combined with intestinal angiodysplasia, this causes the recurrent gastrointestinal bleeding known as Heyde syndrome, which typically resolves after valve replacement.⁸ Unexplained iron-deficiency anaemia in severe AS should raise it.

Pulmonary circulation

Chronically raised left atrial pressure transmits back to the pulmonary circulation, producing post-capillary pulmonary hypertension. It is a marker of more advanced disease, worsens procedural risk, and often improves — though not always fully — after the valve is treated.

Kidneys

Reduced cardiac output and shared vascular risk factors make chronic kidney disease common, and it both accelerates valve calcification and raises the risk of contrast-associated injury around imaging and intervention.

Conduction system

Calcification extending from the valve annulus into the adjacent conduction tissue causes left bundle branch block and heart block. This is also the commonest complication of TAVI, and a proportion of patients need a permanent pacemaker afterwards — relevant to physiotherapy because it affects early mobilisation and monitoring.

Living with aortic stenosis

Activity and exercise

Regular moderate activity is safe and encouraged in mild to moderate asymptomatic disease. In severe or symptomatic AS, activity stays light and symptom-limited until the valve is treated. Guidance is graded by severity rather than applied uniformly, and it is worth having explicitly, because vague advice to "take it easy" causes avoidable deconditioning in people whose valve does not require it.⁹

Surveillance and what to report

Most people attend surveillance echocardiography every six months to three years depending on severity. Recognising the cardinal symptoms and reporting them promptly is the single most important step a person with AS can take, because symptom onset is what triggers referral for valve replacement.⁴

Dental care and endocarditis prevention

A damaged or prosthetic valve is a target for infection. Regular dental care matters, and specified high-risk groups are advised antibiotic prophylaxis before certain dental procedures per current guidance.²

Travel and altitude

Commercial air travel is generally tolerated in asymptomatic disease. Severe symptomatic AS, recent syncope or decompensated heart failure warrant medical advice before flying, and high-altitude travel is best discussed with the cardiology team.

After valve replacement

Most people return to previous activities within weeks (TAVI) to a few months (SAVR). Exercise-based cardiac rehabilitation after valve surgery improves exercise capacity and is safe.¹⁰

Prognosis

Asymptomatic severe AS carries a relatively low annual risk of sudden death, and watchful waiting with structured surveillance is appropriate.⁴ Once symptoms appear the prognosis changes sharply, with average survival without valve replacement of around two to three years.³ Following successful SAVR or TAVI, survival and quality of life improve substantially and approach those of an age-matched population without AS. The main avoidable harms are late presentation and unrecognised low-gradient severe disease.

Role of the physiotherapist

Exercise advice depends closely on severity and symptoms:

• Mild–moderate, asymptomatic AS — regular moderate-intensity aerobic activity is safe and encouraged. Very heavy resistance work, maximal isometric effort and breath-holding (Valsalva) are best avoided because of the large blood-pressure swings they cause.⁹
• Severe or symptomatic AS — vigorous and competitive exercise, and formal maximal exercise testing, are contraindicated until the valve is treated, because of the risk of syncope, arrhythmia and sudden death. Activity should stay light and symptom-limited.
• Around valve replacement — supervised prehabilitation before SAVR/TAVI and cardiac rehabilitation afterwards are safe and improve functional capacity, confidence and quality of life.^10,11

The physiotherapist is also often the clinician who sees the patient most frequently between cardiology reviews, and so is well placed to detect the symptom transition that changes management — a fall in exercise tolerance recorded objectively is more useful to the Heart Team than a subjective report months later.

Physiotherapy red flags — stop and escalate: exertional chest pain, light-headedness or blackout, or new/worsening breathlessness during activity. Anyone with known or suspected aortic stenosis who experiences these should seek urgent medical care.

Warning signs

Part 1 · References

1. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease. Circulation 2021;143(5):e72–e227.
2. Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS guidelines for the management of valvular heart disease. Eur Heart J 2022;43(7):561–632.
3. Ross J Jr, Braunwald E. Aortic stenosis. Circulation 1968;38(1 Suppl):61–67.
4. Pellikka PA, Sarano ME, Nishimura RA, et al. Outcome of 622 adults with asymptomatic, haemodynamically significant aortic stenosis during prolonged follow-up. Circulation 2005;111(24):3290–3295.
5. Baumgartner H, Hung J, Bermejo J, et al. Recommendations on the echocardiographic assessment of aortic valve stenosis: a focused update from the EACVI and the ASE. Eur Heart J Cardiovasc Imaging 2017;18(3):254–275.
6. Mack MJ, Leon MB, Thourani VH, et al; PARTNER 3 Investigators. Transcatheter aortic-valve replacement with a balloon-expandable valve in low-risk patients. N Engl J Med 2019;380(18):1695–1705.
7. Popma JJ, Deeb GM, Yakubov SJ, et al; Evolut Low Risk Trial Investigators. Transcatheter aortic-valve replacement with a self-expanding valve in low-risk patients. N Engl J Med 2019;380(18):1706–1715.
8. Vincentelli A, Susen S, Le Tourneau T, et al. Acquired von Willebrand syndrome in aortic stenosis. N Engl J Med 2003;349(4):343–349.
9. Pelliccia A, Sharma S, Gati S, et al. 2020 ESC guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J 2021;42(1):17–96.
10. Sibilitz KL, Berg SK, Tang LH, et al. Exercise-based cardiac rehabilitation for adults after heart valve surgery. Cochrane Database Syst Rev 2016;(3):CD010876.
11. Ribeiro GS, Melo RD, Deresz LF, Dal Lago P, Pontes MR, Karsten M. Cardiac rehabilitation programme after transcatheter aortic valve implantation versus surgical aortic valve replacement: systematic review and meta-analysis. Eur J Prev Cardiol 2017;24(7):688–697.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.