Aortic stenosis
Station 3: Cardiology examination
Likely vignette: "This person has presented with chest pain / breathlessness / collapse"
Examination features:
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Pulse:
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Slow-rising pulse – weaker and later compared to normal pulse
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Imagine a pulse rolling across your fingers, rather than a discrete pulsation​
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Eyes:
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Anaemia – conjunctival pallor, possible manifestation of angiodysplasia or haemolysis (rare in native heart valves, more common in prosthetic valves)
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Neck:
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Check JVP, if raised suggestive of decompensation
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Precordium:
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Ejection systolic murmur
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Typically crescendo-decrescendo in nature
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Loudest over the aortic area and in held expiration
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Radiates to the carotids, but may be heard elsewhere
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Is S2 well heard? If not, this is a sign of severity
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May be associated with a palpable thrill
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Lung bases:
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Bibasal crepitations suggestive of decompensation of heart failure
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Legs:
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Pitting oedema suggestive of decompensated heart failure
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Differential diagnosis for a systolic murmur
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Aortic sclerosis - softer murmur, typically does not radiate
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Mitral regurgitation - pansystolic, best heard at the apex, radiates to axilla
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Ventricular septal defect - loud pansystolic murmur, best heard at left lower sternal edge
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Hypertrophic cardiomyopathy - ejection systolic murmur, best heard at left lower sternal edge, likely to be a young patient
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Pulmonary stenosis - rare, likely to be a younger patient with congenital aetiology
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Key tip
Consistency is key. If you can tell that the murmur is ejection systolic, then you will be able to present a more concise list of differential diagnoses.
If you are unsure but know that is is a systolic murmur, give differentials for a systolic murmur but justify why it’s unlikely to be something else.
Aetiology of aortic stenosis:
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80% degenerative calcification – aged 70-85yrs
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5-10% Congenital bicuspid valve – 40-60yrs
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Rheumatic fever (rare)
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Investigations:
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Bedside:
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12-lead ECG:
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LV hypertrophy due to AS
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Conduction defects e.g. LBBB or any degree of heart (AVN) block
- ​10% of patients go onto have a pacemaker post-TAVI
- This is due to the proximity of the aortic valve annulus to the AV node during deployment of the valve
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Bloods:
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Routine blood tests – FBC, U&Es, LFTs, coagulation
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These may affect what drugs are given post-operatively and for long-term management
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Not usually critical to diagnosis
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Imaging:
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​Echocardiogram to:
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Qualify diagnosis:
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Calcified cusps
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Restricted opening of valve leaflets
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Bicuspid valve
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Quantify severity:
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Mean gradient >40mmHg (peak gradient >64mmHg but this is less valued by the British Society of Echocardiography in severity assessment)
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Dimensionless index: ratio of blood flow velocity across aortic valve to velocity in LVOT, severe is <0.25
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Valve area is still relevant, <1cm is classed as severe
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LV function assessment
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CXR: any evidence of pulmonary oedema, cardiomegaly or other signs of heart failure
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Special tests:
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Gated CT TAVI – to measure valve annulus size (so they can choose the correctly sized valve), and assess suitability of peripheral vascular access
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Lung function tests – often done pre-operatively if the patient is a current or previous smoker
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Coronary angiogram – it is often possible to perform CABG surgery at the time of valve replacement
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Carotid doppler – no longer routine but may be asked for by cardiothoracic surgeons if high risk for stroke
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Management:
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Dr Dorman's view:
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>75yrs – default management should be TAVI unless not technically favourable
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<75yrs – default should be surgical aortic valve replacement
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There are no evidence-based drug options that prevent or treat aortic stenosis
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Balloon valvuloplasty can be used as a palliative measure for symptom control
Common examiner questions
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What are the pros and cons of TAVI versus surgical AV​
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What are the complications of untreated aortic stenosis?
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Heart failure
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Brady / tachyarrhythmias
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Injury from falls following syncope
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Anaemia due to haemolysis, angiodysplasia or Heyde’s syndrome
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What are the most significant complications of TAVI?
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Pacemaker (10%)
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Vascular access complications (5%)
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Stroke, MI, blockage of coronary artery, annular rupture, apex perforation (2%)
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References
1. Petrou, L. and Shah, B. 2018. Aortic valve disease. Medicine, 46(11), pp.676-681
2. Nickson, C. Life in the Fast Lane. [Internet]. Updated Nov 3, 2020. Available from: https://litfl.com/murmurs-ddx/
3. Ring, L., Shah, B.N., Bhattacharyya, S. et al. Echocardiographic assessment of aortic stenosis: a practical guideline from the British Society of Echocardiography. Echo Res Pract 8, G19–G59 (2021). https://doi.org/10.1530/ERP-20-0035
4. Jabbour Richard J., Latib Azeem, Colombo Antonio et al. 2021. Editorial: Transcatheter Aortic Valve Implantation—Current Challenges and Future Directions. Frontiers in Cardiovascular Medicine. 8; 2021. doi: 10.3389/fcvm.2021.748376
5.