1
Clinical Features
Examination
Slow-rising, low-volume pulse
Narrow pulse pressure in severe disease
Heaving, usually undisplaced apex beat
Systolic thrill in the aortic area
Harsh ejection systolic murmur, loudest at the right upper sternal edge and radiating to the carotids
Soft or absent second heart sound in severe disease
Signs of pulmonary congestion or heart failure in advanced disease
Markers of severe AS
Late-peaking ejection systolic murmur
Soft or absent A2, sometimes with paradoxical splitting of S2
Palpable systolic thrill in the aortic area
S4 and a sustained, heaving apex beat
2
Differential Diagnosis
Pulmonary stenosis
- Murmur loudest at the left upper sternal edge, with no carotid radiation; may have a pulmonary ejection click and delayed P2.
Hypertrophic obstructive cardiomyopathy
- Murmur loudest at the left lower sternal edge, increases with standing/Valsalva and decreases with squatting—the opposite of AS.
Flow murmur from anaemia/high-output state
- Usually softer, with a normal pulse and S2; no carotid radiation or other signs of fixed outflow obstruction.
3
Investigations
Focused history
Bloods including FBC, U&Es LFTs CRP BNP and troponin only if patient has presented with chest pain.
ECG
- Left ventricular hypertrophy
- Lateral “strain” pattern
- Left atrial enlargement
- Atrial fibrillation or conduction disease
Chest X-ray
Aortic valve calcification
- Dilatation of the ascending aorta
- Cardiomegaly
- Pulmonary congestion in heart failure
Transthoracic echocardiography
- Valve anatomy and calcification
- Peak velocity
- Gradient
- Valve area
- Left ventricular size and systolic function
- Other valve disease and pulmonary pressures
Severe AS:
Peak velocity ≥4.0 m/s
Mean gradient ≥40 mmHg
Aortic valve area ≤1.0 cm²
4
Management
General principles
- Explain the condition and advise the patient to report new breathlessness, chest pain, presyncope or syncope promptly.
- Echo surveillance when intervention not needed.
- Treat RFs and associated coronary disease appropriately.
- Use diuretics cautiously if pulmonary congestion develops.
Definitive treatment
If acutely unwell with pulmonary oedema, syncope, angina, or hypotension, this would require A to E assessment, urgent cardiology review and possibly cardiology highcare.
If stable I would optimise his heart failure control with lifestyle modifications such as salt/fluid intake, modification of cardiovascular risk factors, guideline directed heart failure therapy while monitoring their weight, U&Es and refer him to the cardiology valve MDT.
If he has symptomatic severe aortic stenosis, definitive treatment is aortic valve replacement, either surgical AVR or TAVI, depending on surgical risk, anatomy, frailty, comorbidities and patient preference.
I would avoid aggressive vasodilation (nitrates, hydralazine) or over-diuresis because patients with severe AS are preload dependent.
Indications for intervention
The main indication is symptomatic severe aortic stenosis.
Asymptomatic severe aortic stenosis with LV dysfunction, usually LVEF <50%.
Severe aortic stenosis when the patient is already undergoing cardiac surgery, such as CABG or another valve operation.
Selected high-risk asymptomatic patients, for example those with very severe AS, abnormal exercise test, rapidly rising gradients
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