6th May 2025

Aortic Stenosis

Pathology and Epidemiology

The aortic valve is, in normal physiology, a tri-leaflet valve separating the left ventricle from the aortic root and the systemic circulation. Aortic stenosis (AS) thus refers to narrowing of the aortic valve. When the effective orifice area of the valve becomes significantly reduced, a greater force is required by the left ventricle to expel adequate blood volume through the aortic valve during systole. This leads to increased wall stress and compensatory hypertrophy of the left ventricular myocardium, a combination of which leads to the signs and symptoms of AS. 

AS typically occurs due to calcific degeneration of the valve over time, and is thus more common in the elderly population, with prevalence at 10% >80 years. If stenosis is found in younger populations, this is often in the context of a congenitally abnormal valve, such as a bicuspid valve. When found, patients with bicuspid valves should undergo assessment for associated abnormalities which typically involves cross sectional imaging of the heart and aorta, as bicuspid valves are associated with aortic root dilation and aortic coarctation. Rheumatic AS, though a possible cause, is no longer common in developed countries.

In rarer cases it can also occur due to subvalvular or supravalvular stenoses seen in the left ventricular outflow tract and aorta but these will not be covered here.

The natural history of AS is normally benign until it becomes severe. When severe and symptomatic, 5 year survival is between 15-50% and patients are at risk of sudden cardiac death.

Presentation – Symptoms

Patients can be entirely unaware of their valve disease, which may be picked up due to detection of a murmur on routine auscultation leading to further screening. Otherwise, if symptomatic the patient may present with a typical combination of shortness of breath on exertion, anginal chest pain, syncope or pre-syncope, dizziness or new heart failure. The anginal type chest pain can occur due to a combination of reduced outflow leading to impaired coronary perfusion, but also increased demand from a hypertrophied ventricle.

The difference in presentation is important as, in current guidelines, asymptomatic patients are typically not considered for interventional management unless in the presence of other significant findings, or undergoing surgery for an alternative pathology. Once patients become symptomatic, they have a poor prognosis if left untreated and thus will at least require consideration of workup for intervention.

Presentation – Signs

On basic examination one is likely to find a number of typical signs. These include:

• Slow-rising pulse
• Narrow pulse pressure
• Ejection systolic murmur loudest in the aortic region radiating to the carotids
• Soft A2

In addition, if the patient has developed heart failure as a result of their AS, they may have developed typical signs of heart failure with congestion such as peripheral oedema, bilateral crepitations on auscultation of the lungs and an elevated jugular venous pressure.

Diagnosis and Investigations

AS should be considered as a differential diagnosis with the above history. Confirmatory testing is typically with echocardiography, given that echo is relatively cheap, quick and is available every day of the week in many hospitals, and thus it is possible that this is data you may be asked to interpret in your exam.

Echocardiographic criteria are discussed below. Alongside these, often valve morphology will be included in a report in case the stenosis occurs in the context of a bicuspid aortic valve.

Alongside echocardiography, early investigations should include a 12-lead ECG, chest Xray, blood tests including full blood count, urea and electrolytes and NT pro-BNP. 

A 12-lead ECG may show signs of left ventricular hypertrophy with increased voltages and left axis deviation. Chest xray may show little aside from pulmonary congestion if present, while blood tests may show a significantly elevated NT pro BNP, while often other routine bloods can be normal.

For patients with asymptomatic severe disease, CT of the aortic can be used to assess valve calcium, and a treadmill test can be used to unmask symptoms that aren’t present at rest. 

If being considered for intervention then typically patients will undergo coronary artery assessment, either via invasive coronary angiography, or via CT coronary angiography. This is in order to assess whether there is significant coronary artery disease that will need concomitant bypass grafting, which, if present, would push the patient towards a surgical intervention as opposed to transcatheter.

Grading Severity 

Severity of AS is classified as mild, moderate or severe according to standard imaging parameters. Severity on echo is assessed by calculating the pressure gradient across the valve using the Bernoulli equation which can then be used to extrapolate an aortic valve area. An explanation of this is beyond the scope of this chapter but a table outlining relevant values for assessment of severity is included below.

Occasionally patients have values that do not fit nicely into the above table, where the velocity is not in the severe category but the aortic valve area or dimensionless index calculations would be classified as severe. In the first instance these values often need remeasurement as measuring error is a common cause for discordant grading. 

For patients with non-severe velocities but severe valve area calculations in the context of heart failure and reduced ejection fraction, a dobutamine stress echo can be performed to assess for an increase in velocity across the stenotic valve after the addition of an inotropic agent. If velocities then reach the severe range, then this confirms a diagnosis of severe, low-flow, low-gradient AS which is treated the same way as other forms of severe AS.

Criteria for interventional treatment 

Interventional management is typically not recommended until the valve lesion is considered to be severe and symptomatic. In this case, the patient can be referred for consideration of intervention which will be discussed below. 

If non-severe then the disease is typically followed up with routine outpatient echocardiography.

If stenosis is severe but the patient remains asymptomatic, currently a watch and wait strategy is recommended, unless the below criteria are met, in which case interventional treatment should be considered:

• LVEF <55% of no other cause
• Typical symptoms of AS on exercise testing
• Sustained fall in blood pressure (>20mmHg) on exercise testing
• Very severe stenosis (Vmax >5m/s, mean gradient >60mmHg)
• Severe valve calcification (males >2000 Agatston units, females >1200 Agatston units) 
• Aortic Vmax progression by ≥0.3m/s/year
• NT Pro BNP levels ≥3 x the upper limit of normal
• Undergoing cardiac surgery for an alternative reason such as coronary artery bypass grafting

If the patient’s lifespan is expected to be <1 year or there is another significant life-limiting comorbidity then it is likely that conservative management would be pursued instead, irrespective of disease severity.

Treatment options for severe AS

If heart failure is a consequence of AS then diuretics can be used for symptomatic management but there are no evidence-based pharmacological therapies for the definitive management of AS.

For a patient with limited quality of life and a poor prognosis irrespective of their valve disease then interventional management may not be suitable. In addition, it may be the patient’s wishes not to undergo any form of intervention which must be respected, along as they are making their decision with capacity in full understanding of the consequences. 

Aside from the above, the vast majority of patients fulfilling the above criteria will be offered interventional management for their valve disease. The two options here are surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR).

SAVR

SAVR typically involves an open sternotomy with subsequent removal and replacement of the AV. The new valve can either be bioprosthetic (typically porcine or bovine pericardium is used), or mechanical. Within mechanical valves there are a number of different mechanical valve subtypes but this is beyond the scope of this chapter. 

Bioprosthetic valves typically have a lifespan of somewhere between 10-15 years though obviously there are exceptions to the rule. Towards the end of their lifespan they will begin to restenose, as turbulent flow through the valve causes degeneration and calcification.

In the absence of complications, mechanical valves will last for an entire lifespan, but necessitate lifelong anticoagulation with a vitamin K antagonist. The International normalised ratio (INR) target will vary dependent upon both valve characteristics and patient specific-factors and will typically be documented in the surgical notes. 

In the absence of an alternative indication for antiplatelet or anticoagulant therapy, current post-procedural antithrombotic/anticoagulant strategies in bioprosthetic valve replacements lack good quality evidence. Current guidelines recommend the use of either low dose aspirin (75-100mg OD) or anticoagulation with a vitamin K antagonist (VKA) for the first 3 months.

TAVR

TAVR typically involves accessing the femoral artery with large catheters, then feeding a new AV valve up the descending aorta and through the old diseased valve. Once in place the TAVR valve is then opened up inside the old valve. Once in place the TAVR acts similarly to the bioprosthetic AV valve. Subclavian and trans-apical TAVRs are also feasible but markedly less commonly performed. 

Subsequent to TAVR, it is recommended that patients remain on lifelong single antiplatelet therapy if there is no alternative indication for anticoagulation such as atrial fibrillation, in which case either a VKA or more likely direct oral anticoagulant (DOAC) would be continued post procedure.

Deciding between interventional therapies

Choice of therapies is typically made during a multidisciplinary team meeting. For those <75 years and low risk for surgery, or whose anatomy is unsuitable for TAVR, SAVR is typically recommended. For those >75 years or those who are high risk for surgery a TAVR is typically recommended. 

If being considered for TAVR then the patient will have a dedicated TAVR CT to assess femoral access and aortic root dimensions to assess for suitability. If either the access options or the morphology of the aortic root is not suitable for TAVR then this will be rejected. 

As part of the workup for valve intervention, most patients will be screened for concomitant coronary disease, either with a CT coronary angiogram or with invasive coronary angiography. For those patients with significant coronary disease (typically significant stenosis of the proximal left anterior descending or left main stem arteries) then they will be more likely to be offered a SAVR with concomitant coronary artery bypass grafting. Patients will also typically receive a dental check up to assess for ongoing dental disease which would need to be fixed prior to valve intervention, as well as pulmonary function testing, and carotid artery doppler assessment to assess for carotid artery pathology requiring intervention prior to valve intervention.

Balloon valvotomy

Balloon valvotomy involves placing a balloon through the diseased aortic valve and expanding it to increase the effective orifice area. As definitive management this is now effectively an outdated practice. Nowadays balloon valvotomy can be used as a palliative measure in certain patients, or as a temporising measure for an acutely unwell patient while awaiting definitive management.