Basics
Aortic
stenosis may be detected incidentally (keen houseofficer noticing the
classical ejection systolic murmur radiating to the carotids) or may
present with its classical triad of symptoms that can be remembered as 'DAD':
• exertional dyspnoea
• etertional angina
• exertional dizziness
It is a common condition, affecting 2-7% of the population over 65 years of age.
Signs of aortic stenosis include:
• ejection systolic murmur radiating to carotids
• slow rising pulse
• narrow pulse pressure
• heaving apex beat
Things which suggest severe aortic stenosis include:
• LVF
• soft S2 – if the second heart sound disappears this is specific but not sensitive to severe AS
• paradoxically split A2
• S4
Investigations
The key diagnostic tool for diagnosing aortic stenosis is echocardiography.
Normal aortic valve area is between 3cm and 4cm in adults.
The formal divisions of severity are as follows:
Stress
echocardiography (using low-dose dobutamine) can be helpful to
distinguish true severe AS from pseudosevere AS; in pseudosevere AS a
stress echo will show marked increase in valve area but only small
changes in gradient, whilst in true severe AS a stress echo will show
only a small increase in valve area but a large change in gradient.
ETT is contraindicated in patients with symptomatic severe AS but can be useful for stratisfying risk in asymptomatic patients who have severe AS on echo.
ECG changes which may be associated with aortic stenosis include:
• p mitrale
• LVH
• LAD
• poor R wave progression
• complete heart block if calcification involves the conduction tissue.
Aetiology
The main causes of aortic stenosis are:
- calcification of the valve
- bicuspid aortic valve
- (rheumatic fever)
Risk factors for calcification of the aortic valve include:
• male gender
• hypertension
• high LDL
• smoking
Higher incidence of aortic stenosis are found in patients with chronic kidney disease and who have had previous radiotherapy.
Management
There is some evidence to suggest that statins slow the progression of aortic stenosis (Rovusatation affecting aortic valve endothelium study) but other studies have not shown statins to be effective.
Atherosclerotic risk factors should be addressed.
Atherosclerotic risk factors should be addressed.
Patients with moderate to severe AS should be followed up 6 monthly. Those with mild AS should be reviewed yearly.
Treatment is surgical
once a patient is symptomatic. Aortic valve replacement carries an
operative mortality of around 20-25% if there is LVF, 3-5% if not and
the patient is under 70 or 5-15% in the over 70s. After successful
surgery survival is comparable to that of individuals in a control
population.
TAVI (transcatheter aoritc valve insertion) is an option in those not fit enough for surgery; it has a 90% initial success rate and 1 yr survival of 60-80%.
Balloon valvuloplasty is not overly useful in adults as it has a high complication rate (>10%) and overall outcome is essentially the same as if there had been no intervention. It may however be used as a ‘bridge’ whilst awaiting surgery or palliatively to temporarily improve symptoms.
Without treatment, once symptoms appear the prognosis is poor with only 15-50% surviving to 5 yrs.
AVR should also be considered in those with a LVEF of <50%.
TAVI (transcatheter aoritc valve insertion) is an option in those not fit enough for surgery; it has a 90% initial success rate and 1 yr survival of 60-80%.
Balloon valvuloplasty is not overly useful in adults as it has a high complication rate (>10%) and overall outcome is essentially the same as if there had been no intervention. It may however be used as a ‘bridge’ whilst awaiting surgery or palliatively to temporarily improve symptoms.
Without treatment, once symptoms appear the prognosis is poor with only 15-50% surviving to 5 yrs.
AVR should also be considered in those with a LVEF of <50%.
Small print gem:
Heyde Syndrome, first described by Edward Heyde in 1958, links aortic
stenosis to gastrointestinal bleeding. The believed mechanism behind
this is the high shear stress exerted by AS exposes a bond in the Von
Willebrand molecule making it vunerable to being broken down, resulting
in a defiency in Von Willebrand’s factor and thus impairing cloting
which causes previously clinically silent angiodyplasia to bleed.
(last updated: March 2013)
(last updated: March 2013)
References
