Aortic stenosis is the commonest major valve lesion, with an incidence of 3% in those >75yrs and 4% in those >85yrs
Isolated AS of non-rheumatic origin is more common in males than females
Degenerative calcification of the valve
Most common form of AS (50% of cases)
Typically affects those >70yrs old
Associated with other risk factors for coronary artery disease such as smoking, hypertension>, diabetes and dyslipidaemia
Mechanical stress over time leads to progressive fibrosis and calcification of an otherwise normal valve
There is antecedent, irregular valve thickening known as aortic sclerosis, without any LVOT obstruction
Congenital bicuspid aortic valve
Is the commonest congenital cardiac malformation (2% of population)
Typically affects those aged 30 - 50yrs
Accounts for 50% of AS in under 70yr olds but only 25% of AS in over 70yr olds
There is turbulent flow through the abnormal two-leaflet valve, which causes fibrosis, calcification and orifice narrowing due to trauma
Others
Rheumatic heart disease
Supra- and sub-valvular stenosis
SLE
Fabry's disease
Paget's disease
AS can be classified according to degree of LV impairment (none, mild, moderate or severe), though is more commonly classified by aortic valve area and the mean pressure gradient across the valve:
Class
Aortic valve area (cm2)
Mean pressure gradient (mmHg)
Normal
2.5 - 3.6
<5
Mild
1.5 - 2.0
15 - 25
Moderate
1.0 - 1.5
25 - 40
Severe
<1
40 - 50
Critical
<0.8
>50
A narrowed aortic valve area with a surprisingly low mean pressure gradient is a worrying sign
It implies LV failure to the extent that it is unable to generate a decent pressure gradient
The LV undergoes concentric hypertrophy (described as LV diastolic thickness >1cm)
This allows it to maintain a pressure gradient across the narrowed valve without dilation or reduced CO
As the obstruction increases with progressive stenosis:
The hypertrophied ventricle becomes stiff and poorly compliant
This leads to diastolic dysfunction
There is normally a preserved LV systolic function
Eventually there is a fixed, low cardiac output state which renders the heart unable to compensate for systemic vasodilation
Reliance on preload and sinus rhythm
The poorly compliant ventricle requires higher filling pressures
As such, a normal LVEDP may actually represent hypovolaemia in these patients
This reliance makes the LV sensitive to changes in either preload or cardiac rhythm
Indeed, LV filling becomes more dependent on atrial systole
Atrial systole contributes 40% to LVEDV (vs. 20% in health) and there is associated atrial hypertrophy
Maintenance of sinus rhythm becomes vital for maintenance of CO
Haemodynamic compromise typically manifests once the aortic valve area is <1cm2
Eventually SV and CO fall, as does pressure gradient across the valve
Myocardial oxygen supply-demand imbalance
Left ventricular myocardial O2 demand increases (at rest 3ml/100g/min), because:
There is increased LV muscle mass i.e. hypertrophy
There is increased LVESP and therefore increased LV wall tension i.e. increased afterload
However, myocardial oxygen supply falls
There is reduced aortic (and thus coronary) blood flow
There is reduced diastolic time
Increased LV diastolic pressure compromises left coronary blood flow during diastole
The net effect is angina, even with normal coronary arteries (relative LV ischaemia)
Symptoms
Long asymptomatic phase
Described as a triad of:
Angina
(Pre-)syncope
Dyspnoea inc. exertional dyspnoea, PND, orthopnoea, pulmonary oedema
Appearance of symptoms a poor prognostic factor, with median survival from onset of:
Angina - 5yrs
Syncope - 3yrs
Cardiac failure - 2yrs
Signs
Low volume, slow rising pulse
May be normal in mild disease, AR or in those with poorly compliant vascular beds e.g. elderly
There may be low SBP and narrowed PP
A pre-cordial thrill heard loudest when leaning forwards
Ejection systolic murmur heard loudest over the aortic valve, radiating to the carotids and apex
May be comes less audible in severe disease with LV failure due to reduced flow through the stenotic valve
Investigations
12-lead ECG
Signs of LVH (85% of those with severe AS)
Sokolov-Lyon criteria: depth of S-wave in V1 + height of R wave height in V5 - 6 >35 mm
P-wave enlargement
Signs of worsening hypertrophy: T-wave inversion and ST-depression in lateral leads
Heart (AV nodal) block or interventricular block
The AVN is close to the aortic valve and calcification infiltrating the conduction system can result in heart block
CXR
May be normal
May demonstrate cardiomegaly
Calcified aortic valve on lateral
Post-stenotic dilatation of the aortic root
Echocardiography is used to:
Assess valvular anatomy
Check valve area & pressure gradient
Assess degree of LV (dys)function
Valve anatomy
2-D examination is used to check valve leaflet number, thickening, mobility and degree of calcification
Valve pressure gradient
Continuous Doppler wave recordings of the LVOT are made
Maximum velocity in the LVOT corresponds to flow through the valve at peak systole
Modified Bernoulli equation can be used to calculate pressure across the valve (maximum pressure gradient across the valve (mmHg) = 4 x velocity2)
Mean pressure gradient is also measured
Valve area
AVA is calculated using the continuity equation
AVA = cross sectional area of the LVOT x (velocity time integral of the LVOT / velocity time integral of the aortic valve)
Medical management
Aims at addressing coalescing cardiovascular comorbidities