Aortic stenosis

John B. Chambers*
Cardiothoracic Centre, Guys & St Thomas Hospitals, Westminster Bridge Road, London SE1 7EH, UK
Received 11 August 2008; accepted 25 August 2008
Aortic stenosis is a common nding at echocardiography. This review describes the assessment of the
aortic valve, the left ventricle, and the rest of the heart. It discusses grading the stenosis including
cases in which there are discrepancies between the different echocardiographic measurements. It
discusses the indications for and interpretation of stress echocardiography and the role of pressure
recovery and wave reectance. It describes, in outline, the medical management of aortic stenosis
and indications for surgery. The minimum dataset is:
Peak instantaneous velocity, mean gradient, effective orice area
LV dimensions and systolic function
Aortic diameter
Mitral valve appearance and function
RV size and function and PA pressure
KEYWORDS
Aortic stenosis;
Doppler echocardiography
Introduction
In Western populations, 25% of people aged over 65 have
aortic valve thickening and 3% aged over 75 have severe
stenosis.
1,2
The most common cause in Europe is calcic
degenerative disease and 2% of the population have
congenitally bicuspid aortic valves. Rheumatic disease is
now rare in the West, but still the most common cause of
aortic stenosis (AS) world-wide.
Natural history
The early lesions of calcic degenerative disease resemble
coronary artery atheroma
3
and many of the risk factors for
AS are common to other atherosclerotic processes.
2
Later
in the disease process, mechanical stresses cause the devel-
opment of cartilage and bone.
4
Stenosis is differentiated
from thickening (sclerosis) by restriction of cusp move-
ment and a raised transaortic peak instantaneous velocity
(V
max
2.5 m/s) on echocardiography. Around 16% of
patients with sclerosis progress to stenosis within 7 years.
5
The rate of progression varies, but the average reduction
in orice area is 0.1 cm
2
each year.
6
Severe AS remains asymptomatic for many years and the
risk of death is then ,1% per year. Once spontaneous symp-
toms develop, mortality rises sharply and the median survi-
val is 4.5 years with exertional chest pain, 2.6 years with
exertional dizziness, and 1 year with overt heart failure.
7
Survival is particularly poor, 20% at 3 years, in the presence
of NYHA III or IV symptoms and an impaired left ventricle
(LV).
8
The mortality is not linear and is 10% in the rst 6
months after the start of symptoms.
9
Exercise testing is
therefore increasingly used to reveal occult symptoms in
younger patients at low surgical risk. They may claim to
be asymptomatic either because they unconsciously reduce
their exertion to avoid symptoms or are poor historians.
Assessment
The main features of the clinical assessment are the symp-
toms, the grade of stenosis, and LV geometry and function.
Other factors affecting the timing and type of surgery are
the state of the mitral valve, right ventricular function,
and PA pressure and the size of the ascending aorta.
A combination of a long ejection systolic murmur with a
silent second sound and slow carotid upstroke suggests
severe stenosis, but the clinical examination is not a reliable
guide particularly when the physician is inexperienced.
10
A
common error is that the presence of systemic hypertension
precludes severe AS. However, hypertension occurs in about
one-half of all patients with AS and only 7% of patients
referred for surgery have a narrowed pulse pressure of
,35 mmHg.
10
Echocardiography is the mainstay of assess-
ment
11
and should be considered in all patients other than
those with no exertional symptoms and clinically benign
signs (short murmur with a well-heard second sound).
12
*
Corresponding author. Tel: 44 20 7188 1047; fax: 44 20 7188 0726.
E-mail address: jboydchambers@aol.com
For permissions please email: journals.permissions@oxfordjournals.org.
European Journal of Echocardiography (2009) 10, i11i19
doi:10.1093/ejechocard/jen240
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2009.

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

Echocardiography
Appearance of the valve
If parasternal or apical images are suboptimal, it may be
possible to obtain a good short-axis view subcostally. The
minimum dataset comprises the number of cusps, the
pattern of thickening, and cusp mobility.
Number of cusps
A bicuspid valve may look tricuspid in the short-axis view in
diastole if the median raphe is mistaken for the edge of a
cusp. The true diagnosis may only be obvious in systole
when the orice is seen as an oval rather than an equilateral
triangle. The most common pattern of bicuspid valve is to
have the raphe directed between the coronary ostia so
that both coronary arteries arise from the anterior cusp.
Pattern of thickening
In calcic degenerative disease, thickening starts at the
base of the cusps and progresses towards the orice
(Figure 1). All three cusps are usually affected but one or
more may be dominant. In bicuspid valves, early thickening
starts at the median raphe. In rheumatic disease, the
thickening is maximal at the commissures. Heavy calcica-
tion is associated with a relatively rapid progression.
13
Mobility
Systolic bowing in the parasternal long-axis view suggests
either a bicuspid or rheumatic valve. If the closure line is
eccentric, the valve is bicuspid and if central, it is likely
to be rheumatic. The grade of stenosis must be judged
from the Doppler assessment, but the stenosis is unlikely
to be severe if the tips open well or if one cusp opens
well, despite the other two being immobile. Conversely,
a heavily thickened and immobile valve suggests
severe stenosis and an apparently moderate continuous
Figure 1 Echocardiographic appearance in aortic stenosis. Parasternal short-axis views in (A) calcic degenerative disease, (B) bicuspid
aortic valve, and (C) rheumatic disease.
Figure 2 Diagram of left ventricular (LV) hypertrophy and geo-
metric remodelling. Concentric remodelling is dened by normal
LV mass, but a relative wall thickness above 0.45. Relative wall
thickness is calculated as: (2 posterior wall thickness/LV diastolic
diameter). Concentric hypertophy is dened by LV hypertrophy with
a relative wall thickness above 0.45. Eccentric hypertrophy as
occurs in aortic regurgitation is dened by LV hypertrophy, but
with normal relative wall thickness. Redrawn from Seiler and
Jenni.
14
J. Chambers i12

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

wave signal should be rechecked. Planimetry of the orice
on transoesophageal echocardiography is described, but
does not closely agree with the effective haemodynamic
area.
The left ventricle
The minimum dataset comprises standard LV dimensions,
an estimate of ejection fraction, and the subaortic
velocity integral
Pressure overload causes LV remodelling,
14
then hypertro-
phy,
15
(Figure 2) and ultimately cavity dilatation develops.
Left ventricular mass is only moderately related to the
aortic gradient and also affected by gender and genetic
factors.
15
Left ventricular dilatation is more common in
men and may be related partly to the presence of coronary
disease.
16
There is a wide variation in LV geometry and func-
tion in relation to wall stress (Figure 3). At one extreme,
seen predominantly in women, the LV has a small cavity
and thick walls with normal or even supra-normal fractional
shortening in association with low wall stress.
17,18
At the
other extreme, more common in men, the LV is dilated
with relatively thin walls and a reduced fractional shorten-
ing in association with high wall stress.
15
This is an important
relationship. It means that a low LV ejection fraction (EF)
need not imply a poor LV. The LV with a low EF is using
its energy to overcome the resistance of the aortic valve
rather than to eject a normal volume of blood at normal
ow rates. The EF is expected to return towards normal
after aortic valve replacement. In practice, surgery is indi-
cated even in asymptomatic AS if there is reduced LV systolic
function,
19,20
usually taken as an LV EF below 50%. If the LV is
hypokinetic, but the V
max
is .3.5 m/s, the implication is
that LV has near-normal contractility and stress echocardio-
graphy is not necessary. The patient can have surgery with a
good expectation of success. However, if the mean gradient
is ,30 mmHg, this is low ow AS. Stress echocardiography
is necessary (see Stress echo for low ow aortic stenosis)
to determine whether there is genuinely severe AS and
whether there is contractile reserve implying a reasonable
expectation of recovery after surgery. In those with a preo-
perative LV EF below 45%, about one-third do not rise above
50% after surgery.
21
This is either because there is another
cause of LV dysfunction such as myocardial infarction or
alcohol, or because there has been irreversible brosis as
a result of the signicant LV hypertrophy.
Left ventricular long-axis function, assessed by Doppler
tissue or longitudinal M-mode falls earlier than conventional
measures of transverse function like EF.
22
However, they are
not used clinically except to conrm the impression of a fall
in EF if image quality is suboptimal. Diastolic function is not
used clinically either, but there is good evidence
23
that
outcome is better related to diastolic function than LV
mass with a step-up in mortality as the transmitral pattern
changes from slow-lling to pseudonormal. This argues
Figure 4 The effect of different windows on continuous wave
recording. In this patient with a heavily thickened aortic valve,
the peak instantaneous velocity (V
max
) was 3.0 from the apex (A)
but 4.3 from the right intercostal space (B).
Figure 3 Plot of fractional shortening against meridional end-
systolic wall stress. The grey zone denotes the normal range for
the stress-shortening relationship. The female pattern left ventricu-
lar response to aortic stenosis gives a thick wall and small cavity and
consequently relatively low stress associated with high fractional
shortening. The male pattern is a dilated left ventricle with conse-
quently high stress associated with low fractional shortening.
Redrawn from Carroll et al.
18
Table 1 Common equations used in aortic stenosis
Equation 1. Long form of the modied Bernoulli equation
Peak DP (mmHg) 4 (v
2
2
2v
1
2
)
Equation 2. Systolic ow
Flow (ml/s) CSA VTI
1
EJT/100
Equation 3. Continuity equation
EOA (cm
2
) CSA VTI
1
/VTI
2
CSA is the left ventricular outow cross-sectional area (cm
2
)
calculated as p(d/2)
2
, VTI
1
the subaortic velocity integral (cm)
and VTI
2
the aortic velocity integral (cm), v
2
the transaortic
peak velocity (m/s) and v
1
the subaortic peak velocity (m/s),
EJT the ejection time (ms) (measured between the opening and
closing artefacts on continuous wave).
Aortic stenosis i13

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

that this change could be a criterion for surgery but this is
not yet generally accepted. However it can be used clini-
cally to support other conventional indications for surgery.
Doppler measurements
Unless the aortic valve disease is obviously mild shown by
good cusp mobility and V
max
,3.0 m/s with a normal LV,
record the continuous waveform using the stand-alone
probe from the apex and at least one other approach
(usually suprasternal or right intercostal, occasionally
suprasternal) in addition to steerable continuous wave
(Figures 4 and 6C). The minimum dataset is V
max
, mean gra-
dient, and effective orice area (EOA) using the continuity
equation.
V
max
The approach with the clearest signals and the highest peak
should be chosen. Trace round the densest part of the signal
avoiding the artifactual hair. Choose a representative
cycle and avoid a post-ectopic beat. In atrial brillation,
average 5 beats. If the continuous wave V
max
is ,3.5 m/s
and you wish to estimate peak pressure difference (peak
DP), use the long form of the Bernoulli equation [Eq. (1),
Table 1].
The ASE/EAE guidelines suggest that the waveform shape
may be helpful. In severe AS, it is arched whereas in mild or
moderate AS, it is triangular (Figure 5). This is intended only
as a qualitative guide, but one study
24
suggests a way of
quantifying this from the peak to mean gradient ratio
taken from the continuous wave signal. If the ratio is
,1.5, the AS is always severe, .1.7 usually mild, and
1.51.7 intermediate.
Mean gradient
This is calculated from multiple mean instantaneous calcu-
lations around the whole waveform. It cannot be calculated
from the mean velocity. It is therefore more representative
of the AS than the V
max
which describes only one point on
the waveform.
Effective orice area
Systolic ow [Eq. (2), Table 1] is a measure of how quickly
the stroke volume is driven across the valve and the gradient
depends on ow not EF. Flow may vary widely even if LV
Figure 5 Waveform shape. (A) Waveform shape diagrammatically in moderate and severe aortic stenosis. (B) A signal recorded from the
apex in a patient with moderate aortic stenosis and regurgitation with a preserved left ventricle; (C) recorded in a patient with severe
aortic stenosis but a low ejection fraction and signicantly reduced ow. In both (B) and (C), the V
max
is 3.0 m/s, but in (B), the signal
is triangular and in (C), it is arched.
Table 2 Grading aortic stenosis
Mild Moderate Severe
AoV
max
(m/s) 2.53.0 3.04.0 .4.0
Peak gradient (mmHg) ,40 4065 .65
Mean gradient (mmHg) ,20 2040 (50)
a
.40 (50)
a
EOA (cont eq) (cm
2
) .1.5 1.01.5 ,1.0
EOAi (cm
2
/m
2
) .0.85 0.600.85 ,0.60
Velocity ratio .0.50 0.250.50 ,0.25
a
EAE guidelines only,
20
otherwise both EAE and ASE.
19,20
J. Chambers i14

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

function appears normal by eye. It is therefore important to
calculate EOA in every case since this is relatively indepen-
dent of ow [Eq. (3), Table 2]. The diameter is taken from
inner to inner edge just below the base of the cusps with
the outow tract maximally opened out (Figure 6A). The
current ASE/EAE guidelines
11
suggest averaging three
measurements. The pulsed waveform is recorded by
placing the sample in the middle of the LV outow tract in
the ve-chamber view at the level of ow acceleration
shown on colour (Figure 6B). The sample is then moved a
little up and down using the depth control until a clean
signal is obtained.
A simplication using the ratio of peak velocities rather
than velocity integrals is only valid if the subaortic and con-
tinuous wave shapes are the same. The dimensionless ratio
of the velocities or of the velocity integrals can be used
for serial studies to avoid estimating the relatively inaccur-
ate subaortic cross-sectional area.
Grading severity
All measures are used (Table 2). The straightforward case is
when V
max
, mean gradient, and EOA are concordant and also
agree with the visual impression of the valve. If there is
discordance, the shape of the waveform and appearance
of the valve may help decide whether V
max
or EOA is the
more representative, but sometimes further measurements
are necessary.
The straightforward case
Table 2 is based on an ASE/EAE consensus.
11
Previous differ-
ences in EOA have been eliminated, but there is still uncer-
tainty over mean gradient with US sources taking 40 and
European taking 50 mmHg as the cut-point for severe. This
means in practice that we have a wide range of values
making it far easier to establish agreement with EOA than
with a single cut-point. Sometimes, there are still problems
in classication (see The problem of V
max
,4.0 and EOA ,
1.0 and The problem of V
max
.4.0 and EOA . 1.0).
The problem of V
max
<4.0 and EOA < 1.0
Check the valve appearance. This situation is common mainly
because the cut-offs between the grades for V
max
, mean
gradient, and EOA are necessarily arbitrary. The most
common situation is an EOA of 0.9 cm
2
with V
max
3.5
3.9 m/s in the presence of apparently normal LV systolic
function. If the waveform is triangular and the valve opens
well, this is moderate AS. If the valve does not open well,
check the VTI
1
carefully and if low (,15 cm), this is
effectively low ow AS (see Stress echo for low ow aortic
Figure 6 Calculation of the continuity equation. The left ventricular (LV) outow tract diameter is measured from inner to inner edge in
mid-systole (A). The pulsed waveform is recorded in the LV outow tract at the level of ow acceleration (B) and the signal is traced to
obtain the subaortic velocity integral. The best continuous wave signal from at least two windows is recorded and the dense part of the wave-
form traced to obtain the aortic velocity integral. See Table 1, Eq. (3).
Aortic stenosis i15

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

stenosis). Even with apparently normal LV systolic function
assessed by eye, ow may be relatively low.
The situation is compounded by the fact that EOA should
be indexed to body habitus, usually to BSA (Table 2). An
EOA of 1.30 cm
2
(apparently moderate) in a small person
(BSA 1.5) gives an EOAi 0.87 cm
2
(mild AS) whereas in a
big person (BSA 2.5), the EOAi is 0.52 cm
2
(severe AS).
If the LV EF is reduced, low ow AS is present if the EOA ,
1.0 cm
2
and mean gradient ,30 mmHg.
25
In this situation,
there is either severe AS causing LV systolic dysfunction or
moderate AS with another cause of LV dysfunction (e.g. myo-
cardial infarction or alcohol). This situation requires
low-dose dobutamine stress echocardiography.
The problem of V
max
>4.0 and EOA > 1.0
This can be caused by erroneous placement of the subaortic
pulsed sample too far into the valve so that the VTI
1
com-
ponent of the continuity equation is too high. It can also
occur if the measurement of the LV outow diameter is erro-
neously large. It also occurs if there is high ow, for
example, with moderate aortic regurgitation or anaemia.
A triangular-shaped continuous wave signal (Figure 5A)
together with good mobility of one or more cusps suggests
that the EOA is the more representative measure.
The problem of symptoms despite only moderate AS
Sometimes, the patient has symptoms despite the AS being
moderate even taking into account the secondary factors
of waveform shape, valve appearance, and indexed EOA.
There may often be other possible causes for the exertional
breathlessness including coronary disease, obesity, lung
disease, and anaemia.
A theoretical consideration is the existence of pressure
recovery (see Effects of events downstream), although this
is not usually clinically important in adults. Aortic physiology
(see Effects of events downstream) is also important and it is
likely that systemic hypertension exacerbates the effect of
AS on the LV and symptoms.
26
Sometimes observing the
patient during a modied Bruce protocol exercise test with
measurement of PEFR may help.
27
A high blood BNP level
suggests that the AS is clinically signicant.
28
The most helpful test is stress echocardiography to reveal
LV wall motion abnormalities and to test the compliance of
the aortic valve. Compliance means the ability of the
valve to open as ow increases during exercise.
29
Most mod-
erately stenotic valves open relatively well, but some do not
and become effectively severely stenotic during stress.
Stressors used are recumbent bicycle, treadmill, and dobu-
tamine up to 20 mg/kg/min. The difference between peak
and baseline mean gradient divided by the difference in
ow gives the pressure drop-ow slope. A slope .0.2 is
severe, but an easier guide is an increase in the mean gradi-
ent by .15 mmHg during stress.
30
The rest of the heart
Aortic regurgitation
This is graded according to established ASE/EAE
guidelines.
31
The right heart
Severe AS is associated with pulmonary hypertension and
ultimately right ventricular failure. The risk of surgery is
then substantially raised, to 30%.
32
The mitral valve
Functional mitral regurgitation may develop in severe AS as
the LV starts to dilate. Mitral surgery is likely to be necessary
if the mitral valve is anatomically abnormal (e.g. prolapsing)
or the regurgitation is more than moderate.
33
The aorta
Aortic root dilatation (Figure 6C) and coarctation are associ-
ated with a bicuspid aortic valve. Surgery may be indicated
for aortic dilatation even if the AS remains symptom-free.
19
Stress echo for low ow AS
Low-dose dobutamine is infused starting at 5 then 10 mg/kg/
min dobutamine (occasionally 15 then 20 mg/kg/min,
especially if there is prior beta-blockade). This requires
medical supervision because of the risk of cardiac arrhyth-
mia, although the risk is not great at low infusion rates.
The infusion can be stopped if the subaortic velocity integral
(VTI
1
) rises .20% or the heart rate increases.
Judge the severity of AS and whether there is LV contrac-
tile reserve (Table 3).
3436
Mortality at surgery is substan-
tially higher in the absence of contractile reserve.
Contractile reserve was also thought to identify those in
whom the LV EF would recover after surgery, although long-
term recovery now appears to be similar with or without
contractile reserve.
36
Effects of events downstream
Pressure recovery
As ow decelerates downstream from a stenosis, it loses
momentum. Since, by the Bernoulli theorem, the sum of
kinetic and potential energy will be constant, a fall in
kinetic energy will lead to a rise in static pressure.
37
It
would be possible for the pressure downstream from the
orice to rise to the same level as within the LV. However,
turbulence causes loss of energy as heat and this limits the
gain in pressure. Doppler estimates the maximum pressure
difference (gradient) at the vena contracta which is
immediately downstream from the orice. The pressure
difference between the LV and the fully recovered pressure,
which is usually 10 orice diameters downstream, will be
lower than this. How much lower will depend on the initial
pressure drop and on the diameter of the aorta.
In severe AS, pressure recovery is absolutely greater than
in mild AS, but a smaller proportion of the gradient. It is only
Table 3 Stress echocardiography in low ow aortic stenosis
Is there severe aortic stenosis?
Mean gradient .40 mmHg and EOA , 1.2 cm
2
at any time during
the infusion
Is there LV contractile reserve?
Subaortic velocity integral (VTI
1
) (or ejection fraction) rises by
.20%
J. Chambers i16

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

of importance when the aorta is small, ,3 cm in diameter
38
and this does not occur often. In practice, correction for
pressure recovery is not made. However, in AS on the bor-
derline between moderate and severe, the signicance of
the stenosis is expected to be greater if the aorta is
narrow. The main signicance of pressure recovery is as
one cause of the discrepancy between Doppler and
catheter-derived gradients. This problem can be avoided
by not crossing the aortic valve with a catheter.
Aortic physiology
39,40
As the pressure wave generated by the left ventricle travels
down the arterial tree, it is reected wherever there is a
change in calibre, at a branch-point, or a change in the
elastic properties of the arterial wall. It then returns to
modify the incident pressure wave. In a normal subject, the
reected wave returns to the root of the aorta in diastole
and this augments coronary artery lling. The forward
speed of the wave, the pulse wave velocity, is measured
between two points, usually the carotid and femoral arteries,
and is faster if the artery is less compliant. Wave reectance
is measured directly with a transducer-tipped catheter or by
geometrical transformation of a digital pulse. There is little
work in AS, but it appears that the pulse wave velocity is
increased and wave reectance occurs early leading to aug-
mentation of the systolic rather than diastolic pressure.
This tends to increase afterload and reduce coronary ow.
41
Wave reectance, in addition to pressure recovery,
affects haemodynamic events in the proximal aorta and
may lead to physiological effects not predicted by the trans-
aortic pressure difference measured by Doppler. This is
of practical importance in patients with symptoms in the
presence of apparently moderate AS.
Other methods of assessment
Cardiac catheterization
Coronary angiography is needed before aortic valve surgery,
but the valve should almost never be crossed. The risk of
death, stroke, or pulmonary oedema is 7% crossing the
valve and 3% for coronary angiography alone.
42
Catheter
and Doppler-derived gradients are related but different
and not directly comparable. They may differ because:
(i) Doppler estimates pressure at the vena contracta just
beyond the aortic orice whereas the catheter esti-
mates the difference between the LV and a point in
the aorta downstream from the valve where pressure
is usually completely recovered (see Effects of events
downstream). This effect is most important in mild AS;
(ii) Doppler estimates peak instantaneous pressure
whereas cardiac catheterization estimates peak-to-
peak gradient;
(iii) unless the AS is severe, the short form of the modied
Bernoulli equation underestimates gradient by
neglecting subaortic peak velocity;
(iv) errors may occur. If the aortic signal is not optimized,
the AS will be underestimated. However, coronary
angiography introduces major systematic errors
based on the limitations of uid-lled systems.
Multislice CT and cardiac magnetic resonance
CT can image the anatomic orice but produces no infor-
mation comparable with EOA and gradient on echocardio-
graphy.
43
It is better than echocardiography for quantifying
the calcium within the valve and aorta. Cardiac magnetic
resonance (CMR)
44
provides anatomic orice area and can
produce haemodynamic information from ow mapping.
Both CT and CMR provide better anatomical information
than echocardiography about the aorta. CT of the aorta is
used in some centres in planning transcatheter implantation
of aortic valves. Both CT and CMR produce better esti-
mations of LV mass for research studies than using 2D echo-
cardiography, although they are only better than 3D
echocardiography if echocardiographic windows are subopti-
mal. Neither technique is used in routine clinical practice.
Medical management
Specialist valve clinic
45
Patients with no symptoms require monitoring annually for
moderate stenosis and every 6 months for severe stenosis.
I believe that ideally this should be done in a specialist
valve clinic, although there are no guidelines to say so
yet. Our clinic has a cardiologist, specialist sonographer,
and nurse. Others have a sonographer supported by a cardi-
ologist. A valve clinic allows guidelines to be applied more
reproducibly than in a general clinic and to have more
rapid reaction times. This is important in AS where the mor-
tality is 34% in the rst 3 months after the onset of
symptoms.
Medication
Hypertension may increase the rate of progression and
should be treated with an angiotensin-converting enzyme
inhibitor.
15
Although previously contraindicated, there is
good evidence that these drugs improve the LV response to
pressure-overload. They may also improve symptoms and
exercise time in patients unable to have surgery.
46
Lipid low-
ering is not effective at slowing the rate of progression of
AS, although it reduces the incidence of cardiovascular
events.
47
Nitrates should be used with caution in patients
with AS and angina to prevent the occurrence of orthostatic
hypotension and syncope. Beta-blockers are avoided
because the patient may be critically sensitive to a small
fall in contractility in the presence of tight AS. Antibiotic
prophylaxis before dental work is no longer routinely
recommended.
48
Table 4 Indications for surgery in aortic stenosis
Symptoms
Severe AS and symptoms (Class I)
Prophylactic
Severe AS and EF ,50% (Class I)
Moderate or severe AS undergoing other cardiac surgery (Class I)
Dilated aortic root (Class I)
Severe AS (Vmax .5.0) and surgical risk ,1% (Class IIb)
Rapid rate of progression (Class IIb)
Surgery might be delayed at symptom-onset (Class IIb)
LVH . 15 mm (Class IIb)
a
a
EAE only;
20
otherwise both EAE and ASE.
19,20
Aortic stenosis i17

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

Surgery
The indications for surgery are given in Table 4. Surgery is
only usually indicated in the elderly (aged .75) for signi-
cant spontaneous exertional breathlessness, chest pain, or
dizziness.
19,20
For younger patients, surgery may be per-
formed for symptoms induced by treadmill exercise and
prophylactically for severe stenosis (V
max
.5.0 m/s) or
rapidly progressive AS (V
max
increasing by .0.3 m/s over a
year in the presence of heavy aortic valve calcication).
13
The risk in an unselected population is 15% for AVR alone
whereas in octogenarians, most modern series report an
operative mortality of 310%.
49
For patients who have
severe AS and signicant symptoms, but also comorbidities
that preclude conventional surgery, transcatheter valve
implantation is developing rapidly.
50
This can be performed
via the femoral artery or, if the arteries are too narrow,
through the apex of the LV. The technique is far more
expensive than conventional surgery and still has a signi-
cant morbidity and mortality, but results are very encoura-
ging with haemodynamic results as good as those obtained
by conventional surgery.
Conclusion
Aortic stenosis is a common nding at echocardiography. The
grading of the stenosis and the decision for surgery may
often be inuenced by the rest of the heart, particularly
the LV and aorta. Moderate AS can be particularly difcult
to separate from severe AS. Echocardiography remains the
mainstay of assessment. The minimum dataset is:
(i) peak instantaneous velocity, mean gradient, and
EOA;
(ii) LV dimensions and systolic function;
(iii) aortic diameter;
(iv) mitral valve appearance and function;
(v) right ventricular size and function and PA pressure.
Conict of interest: none declared.
References
1. Lindroos M, Kupari M, Heikkala J, Tilvis R. Prevalence of aortic valve
abnormalities in the elderly: an echocardiographic study of a random
population sample. J Am Coll Cardiol 1993;21:12205.
2. Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, Smith VE
et al. Clinical factors associated with calcic aortic valve disease:
Cardiovascular Health Study. J Am Coll Cardiol 1997;29:6304.
3. Otto CM, Kuusisto J, Reichenbach DD, Gown AM, OBrien KD.
Characterization of the early lesion of degenerative valvular aortic
stenosis: histologic and immunohistochemical studies. Circulation 1994;
90:84453.
4. Rajamannan NM, Gersh B, Bonow RO. Calcic aortic stenosis: from bench
to the bedsideemerging clinical and cellular concepts. Heart 2003;89:
8015.
5. Cosmi JE, Tunick PA, Rosenzweig BP, Freedberg RS, Katz ES. The risk of
development of aortic stenosis in patients with benign aortic valve
thickening. Arch Intern Med 2002;162:23457.
6. Otto CM, Burwash IG, Legget ME, Munt BI, Fujioka M, Healy NL et al.
Prospective study of asymptomatic valvular aortic stenosis. Clinical,
echocardiographic, and exercise predictors of outcome. Circulation
1997;95:226270.
7. Horstkotte D, Loogen F. The natural history of aortic valve stenosis. Eur
Heart J 1988;9:5764.
8. Bouma BJ, van den Brink RBA, van der Meulen JHP et al. To operate or not
elderly patients with aortic stenosis: the decision and its consequences.
Heart 1999;82:1438.
9. Chambers J, Das P. Exercise testing in aortic stenosis. Heart 2001;86:
3612.
10. Das P, Pocock C, Chambers J. The patient with a systolic murmur: severe
aortic stenosis may be missed during cardiovascular examination. Q J
Med 2000;93:6858.
11. Baumgartner H, Hung J, Bermejo J, Chambers J, Evangelista A, Grifn BP
et al. Echocardiographic assessment of valve stenosis: EAE/ASE rec-
ommendations for clinical practice. In press.
12. Chetlin MD, Alpert JS, Armstrong WF et al. ACC/AHA/ASE Guideline
update for the clinical application of echocardiography: summary
article. Circulation 2003;108:114662.
13. Rosenhek R, Binder T, Porenta G et al. Predictors of outcome in severe
asymptomatic aortic valve stenosis. N Engl J Med 2000;343:6117.
14. Seiler C, Jenni R. Severe aortic stenosis without left ventricular hypertro-
phy: prevalence, predictors, and short-term follow-up after aortic valve
replacement. Heart 1996;76:2505.
15. Chambers J. The left ventricle in aortic stenosis. Evidence for the use of
angiotensin-converting enzyme inhibitors. Heart 2006;92:4203.
16. Vekshtein VI, Alexander RW, Yeung AC, Plappert T, Sutton MG St J, Ganz P
et al. Coronary atherosclerosis is associated with left ventricular dysfunc-
tion and dilatation in aortic stenosis. Circulation 1990;82:206874.
17. Rohde LEP, Zhi G, Aranki SF, Beckel NE, Lee RT, Reimold SC. Gender-
associated differences in left ventricular geometry in patients with
aortic valve disease and effect of distinct overload subsets. Am J
Cardiol 1997;80:47580.
18. Carroll JD, Carroll EP, Feldman T, Ward DM, McGaughey D, Karp RB. Sex-
associated differences in left ventricular function in aortic stenosis of the
elderly. Circulation 1992;86:1099107.
19. Bonow RO, Carabello BA, Chatterjee K et al. ACC/AHA 2006 guidelines for
the management of patients with valvular heart disease. J Am Coll
Cardiol 2006;48:e1148.
20. Vahanian A, Baumgartner H, Bax J et al. Guidelines on the management
of valvular heart disease. Eur Heart J 2007;28:23068.
21. Rediker DE, Boucher CA, Block PC, Akins CW, Buckley MJ, Fifer MA.
Degree of reversibility of left ventricular systolic dysfunction after
aortic valve replacement for isolated aortic valve stenosis. Am J
Cardiol 1987;60:1128.
22. Takeda S, Rimington H, Smeeton N, Chambers J. Long axis excursion in
aortic stenosis. Heart 2001;86:526.
23. Gjertsson P, Caidahl K, Farasati M, Oden A, Bech-Hanssen O. Preoperative
moderate to severe diastolic dysfunction: a novel Doppler echocardio-
graphic long-term prognostic factor in patients with severe aortic
stenosis. J Thorac Cardiovasc Surg 2005;129:8906.
24. Chambers J, Rajani R, Hankins M, Cook R. The peak to mean pressure
drop ratio: a new method of assessing aortic stenosis. J Am Soc Echocar-
diogr 2005;18:6748.
25. Chambers J. Low gradient, low ow aortic stenosis. Heart 2006;92:
5548.
26. Bermejo J. The effects of hypertension on aortic valve stenosis. Heart
2005;91:2802.
27. Das P, Rimington H, Chambers J. Exercise testing to stratify risk in aortic
stenosis. Eur Heart J 2005;26:130913.
28. Gerber IL, Stewart RA, Legget ME, West TM, French RL, Sutton TM et al.
Increased plasma natriuretic peptide levels reect symptom onset in
aortic stenosis. Circulation 2003;107:188490.
29. Das P, Rimington H, Smeeton N, Chambers J. Determinants of symptoms
and exercise capacity in aortic stenosis: a comparison of resting haemo-
dynamics and valve compliance during dobutamine stress. Eur Heart J
2003;24:125463.
30. Lancellotti P, Lebois F, Simon M, Tombeux C, Chauvel C, Pierard L.
Prognostic importance of quantitative exercise Doppler echocardiography
in asymptomatic valvular aortic stenosis. Circulation 2005;112:137782.
31. Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD,
Levine RA et al. Recommendations for evaluation of the severity of
native valvular regurgitation with two-dimensional and Doppler echo-
cardiography. J Am Soc Echocardiogr 2003;16:777802.
32. Pai RG, Varadarajan P, Kapoor N, Bansal RC. Aortic valve replacement
improves survival in severe aortic stenosis associated with severe pul-
monary hypertension. Ann Thorac Surg 2007;84:856.
33. Ruel M, Kapila V, Price J, Kulik A, Burwash IG, Mesana TG. Natural history
and predictors of outcome in patients with concomitant functional mitral
regurgitation at the time of aortic valve replacement. Circulation 2006;
114:I-5416.
J. Chambers i18

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m

34. Monin J-L, Quere J-P, Moncho M, Petit H, Baleynaud S, Chauvel C et al.
Low-gradient aortic stenosis. Operative risk stratication and predictors
for long-term outcome: a multicenter study using dobutamine stress
hemodynamics. Circulation 2003;108:31924.
35. Nishimura RA, Grantham JA, Connolly HM, Schaff HV, Higano ST, Holmes D.
Low-output, low-gradient aortic stenosis in patients with depressed
left ventricular systolic function: the clinical utility of the dobutamine
challenge in the catheterization laboratory. Circulation 2002;106:80913.
36. Quere J-P, Monin J-L, Levy F et al. Inuence of preoperative left
ventricular contractile reserve on postoperative ejection fraction in
low-gradient aortic stenosis. Circulation 2006;113:173844.
37. Baumgartner H, Stefenelli T, Niederberger J, Schima H, Maurer G. Over-
estimation of catheter gradients by Doppler ultrasound in patients with
aortic stenosis: a predictable manifestation of pressure recovery. J Am
Coll Cardiol 1999;33:165561.
38. Laskey WK, Kussmaul WG. Pressure recovery in aortic valve stenosis.
Circulation 1994;89:11621.
39. Westerhof N, Sipkema P, van den Bos GC, Elzinga G. Forward and back-
ward waves in the arterial system. Cardiovasc Res 1972;6:64856.
40. Nichols W, ORourke M. McDonalds Blood Flow in Arteries. Arnold; 1998.
41. Ronak R. Vascular Alterations in Aortic Stenosis. Unpublished MD thesis.
London University, 2008.
42. Chambers J, Bach D, Dumesnil J, Otto C, Shah P, Thomas J. Crossing the
aortic valve in severe aortic stenosis: no longer acceptable? J Heart Valve
Dis 2004;13:3446.
43. Baumgartner H. Is there a role for multislice computed tomography in
aortic stenosis? Eur Heart J 2006;27:29234.
44. John AS, Dill T, Brandt RR, Rau M, Ricken W, Bachmann G et al. Magnetic
resonance to assess the aortic valve area in aortic stenosis. J Am Coll
Cardiol 2003;42:51926.
45. Taggu W, Topham A, Hart L, Patel N, Lloyd G. Technician-led follow-up
clinics both improve the quality and reduce the cost of care in a broad
cross-section of heart valve disease patients. (Abstract). Heart 2005;
92(Suppl. I):i41.
46. Chockalingam A, Venkatesan S, Subramaniam T, Jagannathan V,
Elangovan S, Alagesan R et al. Safety and efcacy of angiotensin-
converting enzyme inhibitors in symptomatic severe aortic stenosis:
Symptomatic Cardiac Obstruction-Pilot Study of Enalapril in Aortic
Stenosis (SCOPE-AS). Am Heart J 2004;147:L18.
47. Rossebo AB, Pedersen TR, Brudi P, Boman K, Chambers JB, Egstrup K et al.
Intensive lipid lowering therapy with simvastatin and ezetimibe in mild
to moderate valvular aortic stenosisa randomized trial. N Engl J Med
2008 doi:10.1056/NEJMoa0804602 [Epub ahead of print].
48. Prophylaxis against infective endocarditis. NICE Clinical Guidelines 64.
March 2008, ISBN 1846296218.
49. Iung B. Management of the elderly patient with aortic stenosis. Heart
2008;94:51924.
50. Descoutures F, Himbert D, Lepage L, Iung B, Detaint D, Tchetche D et al.
Contemporary surgical or percutaneous management of severe aortic
stenosis in the elderly. Eur Heart J 2008;29:14107.
Aortic stenosis i19

b
y

g
u
e
s
t

o
n

D
e
c
e
m
b
e
r

2
2
,

2
0
1
1
h
t
t
p
:
/
/
e
j
e
c
h
o
c
a
r
d
.
o
x
f
o
r
d
j
o
u
r
n
a
l
s
.
o
r
g
/
D
o
w
n
l
o
a
d
e
d

f
r
o
m