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232
C. O’Brien and C. F. Barnett
a
b
Fig. 17.3 Bicuspid AoV anatomy. (a) True bileaet aor-
tic valve. Left panel, the aortic annulus develops as an
ellipse rather than circular shape. The solid, bidirectional arrow highlights the plane between the leaets.
The dotted, bidirectional arrow identies the peak excursion along the mid-line of the valve. Right panel, shows
systolic doming. (b) Left panel, shows leaet fusion of
the LCC and RCC.Right panel, image taken in peak systole illustrating restricted leaet mobility. As seen here,
turbulent ow can lead to sclerosis of the free edges of
involved leaets. LCC left coronary cusp, RCC right
coronary cusp
ab c
Fig. 17.4 Sclerotic AoV disease. (a) Sclerotic AoV in
PLAX showing echo bright calcication involving the
leaet tips and annulus. (b) Sclerosis can be seen here
tethering leaets to both the annulus as well as each other
restricting leaet excursion. (c) Doppler image demonstrating ow acceleration through stenotic AoV orice
17 Aortic Stenosis
233
carditis can lead to mechanical restriction of leaflet motion, and post-infectious inammation can
lead to leaet fusion as well.
Identifying andAssessing Severity
ofAortic Stenosis
Anatomic Evaluation
Bicuspid valves can be identied by recognizing distinctive echocardiographic features [5].
True bicuspid leaets attach to the aortic annulus forming a semi-circular leaet base. The
semi- circular base creates tension along the free
edge of the valve preventing full excursion giving a classic domed appearance in systole in
PLAX (Fig. 17.3a). In PSAX, true bicuspid
valves should have a single commissure and two
equally sized leaets. Leaets may or may not
be calcied depending on patient age and presence of other mediators of valvular sclerosis.
Leaet fusion is best described in PSAX
(Fig. 17.3b). The fused leaets will move
together generally creating ow acceleration
away from the leaets. The fusion between leaflets commonly appears thickened and hyperechoic due to calcication, sclerosis, or
redundant leaet tissue.
Prosthetic valves may also become stenotic;
however, identication of prosthetic valve stenosis is more complex. All prosthetic valves have
transvalvular pressure gradients greater than
native valves. Normative values are specic to
the type and size of the prosthetic valve.
Additionally, valve size and patient body surface
area must be considered as patient prosthesis
mismatch (typically caused by a prosthetic valve
too small for the patient) can cause ow acceleration that mimics stenosis but unrelated to leaet
dysfunction.
Supravalvular and subvalvular aortic stenosis
are congenital conditions commonly identied at
birth or during childhood. Supravalvular stenosis
is caused by a narrowing around the level of the
sinotubular junction and should be expected when
ow acceleration is seen above the level of the
valve. Subvalvular stenosis is more common and
is caused by a subaortic membrane that grows in
the LVOT.There are multiple subtypes of subvalvular stenosis including discrete thin membranes,
thick bromuscular ridge, and brous ingrowth
creating a tunnel within the LVOT [6].
Lastly, care must always be taken to distinguish AS from ow obstruction either due to
cavitary obstruction or systolic anterior motion
of the mitral valve. Outow obstruction is associated with an abrupt loss of doppler signal during
systole giving a classic “dagger shape” to continuous wave (CW) doppler while AS usually
gives a classic dome with a mid-systolic peak
(Fig.17.5). The doppler pattern is critically evaluated as to not misconstrue out ow obstruction
for AS.
Fig. 17.5 Continuous wave doppler through the AoV.Left pane, showing a doppler pattern for AS.Right pain, showing
the dagger pattern created by left ventricular outow tract obstruction
234
()
cd
C. O’Brien and C. F. Barnett
Hemodynamic Evaluation
There are multiple complimentary approaches to
assessing AS severity. The most commonly utilized measurements are the estimated aortic valve
area combined with the peak blood ow velocity
and mean transvalvular pressure gradient.
1. Estimated Aortic Valve Area (AVA): AVA has
been shown to be a highly sensitive and specic estimate of AS, which has also been
shown to predictive of outcome [7–9] . AVA
can be estimated using the continuity equation (Fig. 17.6a). The continuity equation
utilizes the conservation of mass principle,
which assumes ow through the LVOT must
be equal to ow through the AoV. To estimate SV in the LVOT, the diameter of the
a
LVOT (LVOTd) must be measured in the
PLAX in peak systole within 5mm of aortic
cusp insertion (Fig.17.6b). Measuring inner
edge to inner edge in mid-systole is recommended. Using the LVOTd, the cross-sectional area (CSA) of the LVOT can be
estimated.
CSA
LVOT
=
π
D /2
2
Using pulse wave (PW) doppler in either
the 5-chamber (Fig. 17.6c) or 3-chamber
view, a LVOT velocity time integral (VTI)
must be measured. The PW signal must be
measured above the level of the cusps, which
can be determined by an absence of high-density doppler signal at the end of systole and
diastole. In the same view, a CW doppler of
b
Fig. 17.6 Calculating AVA and gradients. (a) Diagram of
the continuity equation showing points of measurement to
execute the continuity equation solving for AVA. (b) AoV
in PLAX during peak systole. Red dotted line demonstrates
proper sampling for measuring LVOTd using edge- to- edge
technique. (c) Apical four-chamber view, dotted circle
shows proper PW doppler sampling position for measuring
LVOT VTI. (d) Apical four-chamber view showing proper
doppler sampling of the AoV using CW doppler. Peak and
mean AoV gradients are estimated using CW doppler
×=×
ms
()
17 Aortic Stenosis
235
the LVOT, AoV, and aortic root is taken and an
aortic VTI measured (Fig.17.6c). Values are
then entered into the continuity equation to
solve for AVA
VTICSA VTI AVA
LVOT LVOT AoV
A common pitfall of the AVA estimate is
the over- or underestimation of the LVOTd.
Given this contributes to continuity equation
through a squared value even a small error of
1–2 mm can lead to a signicant change in
estimated AVA.
2. Peak Velocity and Pressure Gradients: By sampling CW doppler over the AoV, a VTI
AoV
can
be measured and traced to estimate peak velocity, peak gradient, and mean gradient over the
Aov. Measurements should be acquired in multiple views to ensure maximal gradients are
obtained and that signal from concomitant
mitral regurgitation (MR) is not bleeding into
the doppler signal. Using a PEDOF probe from
the suprasternal notch can help ensure exclusion of MR. Peak and mean gradients measured by echocardiography have been shown to
correlate with invasive gradients [7, 9–11].
Peak pressure gradient can be estimated applying the peak velocity in the Bernoulli
equation:
Pressure gradient Velocity
=×
4
2
/
While peak gradients measured by echocardiography and catheterization correlate,
vascular compliance has been shown to signicantly inuence pressure transmission
between the LV and aorta, which makes peak
pressures prone to overestimating aortic stenosis [12, 13]. In Fig. 17.7a, the pressure
transmission delay between the ventricle and
aorta is demonstrated by the green dotted line.
This highlights an important limitation in
echocardiography. As AS becomes more
severe, the delay in pressure transmission
between the left ventricle and aorta becomes
pronounced. In early systole LV pressure and
AoV ow peak while aortic pressure remains
low, illustrated in Fig.17.7 by the red dotted
line. This describes why the peak gradient
measured by echo is greater than the peak-topeak gradient reported in catheterization.
Pressure recovery is another important
concept that carries particular relevance in
the estimation of aortic stenosis in the setting
of critical illness. During systole, there is a
loss of kinetic energy as blood moves over
the leaet tips of the AoV leading to a drop
in pressure immediately above the valve. The
pressure rapidly recovers in the ascending
aorta. Given spectral doppler only measures
the greatest ow over the sampled vector,
there is no opportunity to factor in pressure
Fig. 17.7 Comparison of AoV gradients sampled by
catheterization compared to echocardiography. Both
samples recorded from the same patient. Left, simultaneous pressure sampling from the ascending aorta and left
ventricle. Green line shows peak-to-peak estimate of
peak gradient while red line shows the timing of where
peak gradient is estimated by echo emphasizing how
peak LV pressure is achieved before peak aortic pressure
leading to an overestimation of the peak gradient shown
on the right
236
C. O’Brien and C. F. Barnett
recovery, leading to an overestimation of the
gradient between the LV and true aortic pressure, which is captured on invasive measurements. Pressure recovery is affected by
vascular size and tone [14], but is likely only
signicant when ascending aorta diameter is
<30mm [15].
Mean gradient demonstrates better correlation with invasive gradients across a diversity
of hemodynamic states [16]. Mean gradient is
calculated by averaging instantaneous gradients throughout the ejection period, which can
be performed automatically by most clinical
echocardiography software.
a
Given peak velocity and peak gradient
track well and mean gradient is less prone to
overestimation of gradient across hemodynamic states, peak velocity and mean gradient
are most commonly reported in hemodynamic
assessments. AS is considered severe when
mean gradients measure ≥40mmHg and peak
velocity is ≥4m/s.
3. Planimetry: Two-dimensional and threedimensional planimetry are useful and commonly underutilized tools for assessing
AS. Planimetry is the process of measuring
the minimum orice of the AoV (Fig.17.8a).
Transesophageal echocardiography (TEE) is
b
Fig. 17.8 Manual measurement of AVA. (a) AoV
visualized in peak systole in the mid-esophageal view
by TEE.Green dotted line shows proper technique for
using planimetry to directly measure AVA. (b)
M-mode sampling of the AoV in peak systole. Left
panel shows sampling of a normal, trileaflet
AoV.Right panel shows sampling of a sclerotic AoV
with significant stenosis. Green arrows show peak
valve opening. Red arrows show valvular closure in
early diastole
17 Aortic Stenosis
237
the gold standard technique given optimal
AoV resolution. In the mid-esophageal window, an enface view of the AoV can be
obtained at ~45o [17]. The TEE probe can
then be withdrawn or advanced to the level of
the smallest orice of the AoV during peak
systole. Using TTE, measurements can be
made using the PSAX at the level of the aorta,
but poor resolution in this view often limits
accuracy.
Depending on the etiology of stenosis,
sclerosis and calcication can make tracing
the orice of the AoV challenging. Color
ow, 3D echocardiography, and X-plane are
useful methods for identifying the leaet tips
and orice.
4. M-mode: M-mode can be useful for estimating valve orice. In the PLAX, the view of
the AoV leaet tips is optimized. Color ow
can help identify the point of peak ow. An
M-mode sample is taken with the sample
vector set at 90o to the leaet tips during
peak systole. The maximal aortic cusp separation (MACS) can then be measured.
Figure17.8b shows an example of M-mode
sampling from a normal trileaet
AoV.Figure17.8c shows an example of calcic AS with reduced MACS.
M-mode can support an assessment of
AoV composition. As is shown in Fig.17.8b,
calcied leaets will appear echo bright, and
leaet tips will not contact the aorta in peak
systole. MACS can be used as a screening
study for AS, but is inadequate in isolate for
making the diagnosis. MACS <8 mm has
been shown a strong correlation with presence
of severe AS [18] (Table17.1).
Caveats andPitfalls
Low-ow low-gradient aortic stenosis is a commonly underappreciated hemodynamic state.
Evidence is growing showing these patients are
prone to poor outcomes and can benet from
structural intervention [19]. Low-ow lowgradient AS is dened as AVA <1 cm2, peak jet
<4.0m/s, and mean gradient <40mmHg. These
hemodynamic parameters are seen commonly
when a patient’s SV fall below 35mL/m2 [20].
Recognizing that this physiology is dictated by
SV is an important lesson as this can be seen in
common lesions such as heart failure with preserved (HFpEF), heart failure with reduced ejection fraction (HFrEF), and severe mitral
regurgitation.
When interrogating the AoV in a low ow
state, understanding the limitations of each calculation is essential. Estimating AVA in a low ow
state can be inuenced by incomplete valve opening due to a low-pressure differential across to
AoV rather than intrinsic valve restriction. This
can be induced by either severe cardiomyopathy
or malignant hypertension. Optimization of afterload and initiation of dobutamine can increase
SV. SV and AVA can be serially measured at
increasing levels of inotropic support (Fig.17.9).
In pseudo-severe AS, AVA will increase and gradients will either remain unchanged or marginally increase while in true AS AVA will be
unchanged and gradients will increase. The validity of dobutamine stress is best dened in
HFrEF. Myocardium in HFpEF is commonly
poorly responsive to dobutamine, making an
absence of gradient augmentation difcult to
interpret. Previously, an absence of response
Table 17.1 Grading of aortic stenosis
AVA
(cm
Normal 3.0–4.0 <5 <2.5 N/A N/A
Mild AS >1.5cm <20 2.6–2.9 >0.5 N/A
Moderate AS1.0–
Severe AS
≤1.5
≤1.0 ≥40
Mean gradient
2
)
(mmHg)
20–40 3.0–4.0 0.5–0.25 N/A
Peak jet velocity
(m/s)
>4 <0.25 <8mm
Dimensionless
index
Maximal aortic cusp
separation
238
ac
bd
C. O’Brien and C. F. Barnett
Fig. 17.9 Low-ow low-gradient aortic stenosis. (a, b) PW
and CW Doppler, respectively, showing low SV leading to
estimation of moderate AS based on mean AoV gradient. (c,
(increase in SV of ≥20%) was felt to carry a poor
prognosis, but this opinion has been reconsidered
[21]. Evidence now shows that valve intervention
in low-ow low-gradient AS is associated with
better prognosis [22].
In contrast, when AVA is found to be <1cm
the setting of a peak velocity<4.0m/s, mean gradient is <40mmHg, and SV is >35mL/m2 outcomes appear to be more similar moderate AS
[23, 24]. Given this is a rare hemodynamic scenario, measurement accuracy, especially LVOTd,
should be conrmed.
Dimensionless index (DI) has emerged as a
valuable tool for identifying severe AS in low
ow states. Dimensionless index is a simple
ratio of the peak velocity in the LVOT measured by PW doppler to the peak velocity
across the AoV measured by CW doppler
(V
: V
LVOT
). A DI< 0.25 has been shown to
AoV
predict severe AS and is associated with
increased mortality [25].
d) PW and CW Doppler sampled after administration of
dobutamine leading to a signicant increase in SV estimated
by LVOT VTI as well as mean gradient diagnosing severe AS
DI is also valuable for determining patient
prosthesis mismatch and stenosis within prosthetic valves in both low and normal ow states.
A DI < 0.25 is a good indicator that further
screening is necessary.
2
in
Valvular calcium assessed by CT scan can be
helpful in predicting the likelihood of severe
AS.In men and women, a calcium score >3000
and >1600 arbitrary units (AU), respectively,
make severe AS very likely while <1600AU and
<800AU, respectively, make severe AS unlikely
[26, 27].
A proposed diagnostic workow better dening AS in the context of an AVA <1cm2 is outlined in Fig.17.10.
Atrial brillation can also pose signicant
challenges in estimating gradients. Irregular
rhythm leads to variable left ventricular lling
and SV.Experts recommend averaging ve separate measurements and using the average value
for calculations [4].
17 Aortic Stenosis
239
Fig. 17.10 Diagnostic approach to low-ow, low-gradient AS
240
C. O’Brien and C. F. Barnett
Aortic regurgitation (AR) increases ventricular loading, but does not affect mean gradient or
velocity assessment of AS. It should be noted,
however, that moderate or greater AR associated
with moderate or greater AS carry high event
rates and are commonly treated like isolated
severe valve disease [28].
Similarly, high ow states lead to hemodynamics achieving peak velocity> 4 m/s, mean
gradient >40mmHg, and AVA <1cm2. States like
septic shock, shunts, anemia, and hyperthyroidism should be ruled out. These states should still
be considered a state of pressure overload for the
left ventricle. As high output state is reversed,
aortic gradients should be re-evaluated.
Summary Points
• AS is caused by congenital or acquired leaet
restriction leading to a pressure overload state
in the left ventricle.
• Severe AS is dened by an AVA <1cm2 com-
bined with a mean AoV gradient >40mmHg
and evidence of ow acceleration over the
AoV evidenced by a peak velocity >4m/s.
• Low-ow, low-gradient AS requires a SV of
<35mL/m2 and assessment must be tailored to
patient physiology.
• DI can be a valuable tool for assessing the
presence of severe AS across all hemody-
namic states.
Acknowledgments The authors would like to thank Drs.
Kirsten Tolstrup and Atif Qasim for contributing images
for this chapter.
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