Aortic Valve Disease: Evaluation of stenosis

Aortic Valve Disease: Evaluation of Stenosis
Mark A. Taylor, MD, FASE
Pittsburgh, PA
A careful and systematic transesophageal echocardiographic evaluation can lead to new
diagnoses, altered surgical management and improved patient care. In patients
undergoing aortic valve surgery for aortic stenosis, intraoperative TEE has been shown to
alter the surgical plan in 13% of the cases (1). A consensus statement from the American
College of Cardiology, American Heart Association and American Society of
Echocardiography gave intraoperative TEE a Class I designation (“evidence and/or
general agreement that a given procedure or treatment is useful and effective”) in patients
undergoing surgical repair of valvular lesions (2). TEE evaluation of the aortic valve
should be performed upon all patients undergoing cardiac surgery.
TEE Modality
2D/3D
PW
CW
CFD
Focus of Aortic valve examination
Aortic valve architecture
Aortic root and LVOT architecture
LV function and filling
Assessment of valvular lesions and
hemodynamics
Assessment of valvular lesions and
hemodynamics
Assessment of valvular lesion
Anatomy and TEE examination
4 recommended views (3)
Midesophageal aortic valve short axis (ME AV SAX)
Midesophageal aortic valve long axis (ME AV LAX)
Transgastric long axis (TG LAX)
Deep transgastric long axis (deep TG LAX)
ME AV SAX
0Probe at mid esophageal position
0Rotate forward to 30-60 degrees
0 2D and 3 D examination of aortic valve cusps and leaflets
0CFD examination of stenotic lesion
02D imaging with planimetry allows estimation of aortic valve opening
(Figures 1 and 2. Images of 2D ME AV SAX with trileaflet aortic valve open and
closed)
The aortic valve apparatus is comprised of the valve cusps, sinuses of Valsalva, proximal
ascending aorta, and left ventricular outflow tract. The ME AV SAX view provides
detailed 2D and 3D anatomy of the leaflets and annular complex. The normal valve
consists of 3 cusps suspended from an associated sinus of Valsalva. 2D and 3D
examination permits evaluation of individual leaflet architecture and range of motion
throughout the systolic (opening) and diastolic (closing) cycle. The degree of opening can
be measured by planimetry using the trackball and the caliper and trace function. This
method is simple and rapid yet poor reliability exists between observers which creates
error. Overestimation of valve area by planimetry may occur in patients with pliable
leaflets if the ultrasound beam intersects the leaflets below the tips. Errors are also
introduced when the aortic valve is calcified and the orifice of the valve cannot be
identified.
(Figures 3 and 4. Images of ME AV SAX with planimetry measurement of aortic valve
area in a patient with aortic stenosis and AVA of 0.6 cm2. Cartoon representation of the
ME AV LAX view and how the ultrasound beam intersects the aortic valve on different
planes. The possibility to overestimate AVA by planimetry exists if the
echocardiographic imaging plane is not at the level of both leaflet tips.)
ME AV LAX
0Probe at mid esophageal position
0Rotate forward to 120-150 degrees
0 2D and 3 D examination of the left ventricular outflow tract, the aortic root (aortic
valve, sinuses of Valsalva, and the sinotubular junction), and the proximal ascending
aorta. Detailed examination of leaflet morphology, mobility, thickening, and
calcification can be performed. Subaortic pathology can be identified including subaortic
membranes or systolic anterior motion (SAM) of the anterior mitral valve leaflet.
02D imaging with caliper measurements allows estimation of aortic valve opening, and
specific aortic root measurements.
0CFD examination of stenotic and/or regurgitant aortic valve lesions.
0CFD examination allows identification of subaortic flow disturbances.
0M-mode examination of leaflet mobility, thickening and tip separation.
(Figures 5 and 6. Images of ME AV LAX with aortic valve closed and open)
TG LAX
0Probe in transgastric position
0Rotate forward to 90-110 degrees
0 2D and 3 D examination may be limited by aortic valve being in far field position
0CFD examination allows identification of valve position and/or associated stenotic or
regurgitant lesions
0CW or PW Doppler examination due to parallel alignment of blood flow and Doppler
beam. Allows for determination of velocities in the outflow tract and aortic valve.
(Figure 7. Image of TG LAX with aortic valve closed on right side of video display)
Deep TG LAX
0Probe started in the transgastric position, then inserted and anteflexed. Once anteflexed
and inserted, the probe is slowly withdrawn
0 2D and 3D examination may be limited by aortic valve being in far field position
0CFD examination allows identification of valve position and/or associated stenotic or
regurgitant lesions
0CW or PW Doppler examination due to parallel alignment of blood flow and Doppler
beam. Allows for determination of velocities in the outflow tract and aortic valve.
0View provides complementary information to the TG LAX but may be utilized when
the TG LAX does not provide alignment of blood flow and Doppler beam.
0Image acquisition improves with experience (4)
(Figure 8. Image of deep TG LAX with aortic valve closed on left side of video display)
Pathphysiology
Aortic Stenosis
Normal aortic valve area in adults is 3-4 cm2. Obstruction of can occur at three distinct
anatomical sites: valvular, subvalvular, or supravalvular. Valvular obstructions account
for the majority of cases of LVOT obstructions (5). The most common cause of aortic
stenosis in the United States is calcific aortic stenosis of the elderly. This is followed by
congenital abnormalities of the aortic valve including bicuspid and rarely unicuspid or
quadricuspid valves. Of the aortic valve replacements performed in the US and Europe,
bicuspid aortic valves account for approximately 50% and progressive calcification of a
tricuspid valve aortic valve account for the remainder (6). The mechanism of aortic
stenosis in the elderly and in congenital cases is distorted flow through a diseased valve,
which leads to degenerative changes and progressive calcification. Rate of calcification
and stenosis varies widely although elderly men with associated coronary artery disease
as well as individuals with a history of smoking, hypercholesterolemia and elevated
serum creatinine levels demonstrate more rapid disease progression (7-9). The
development of aortic stenosis is not part of routine aging but is an active process
involving chronic inflammation fueled by atherosclerotic risk factors (10).
Etiology
Calcific aortic
stenosis
Factors
Age > 65 years old
Congenital Bicuspid
Age 35-55 years
Rheumatic
Commissural fusion
Features
Common in US and
Europe.
4% of the elderly
have aortic stenosis
(11)
1-2% of US
population have
bicuspid valve (12)
Rare in US,
common worldwide
Other issues
Progressive
degeneration
Coarctation of aorta,
dilation of aortic
root, aortic
dissection
May occurs
irrespective of
hemodynamics and
age suggesting
developmental or
genetic disorder
(13)
Patients undergoing
AVR should have
root replacement if
greater than 4.0 or
4.5 cm (14, 24)
Usually associated
with mitral
involvement
(Figure 9. Zoom image of a trileaflet aortic valve with heavy calcification and a stenotic
orifice)
(Figure 10. Zoom image of a bicuspid aortic valve with a decreased opening consistent
with aortic stenosis)
ECHOCARDIOGRAPHIC ASSESSMENT
Modality
2D/3D
View
ME AV SAX
ME AV LAX
M-mode
ME AV LAX
CFD
ME AV SAX
ME AV LAX
PWD
TG LAX
Deep TG LAX
TG LAX
Deep TG LAX
CWD
Echocardiographic feature
Leaflet restriction,
calcification,
commissural fusion
Planimetry # (15)
Annular measurement
for continuity equation *
(15)
sinus of Valslva,
Sinotubular and
ascending aorta diameter
measure
Septal separation (16)
08 mm critical stenosis
0> 12 mm noncritical stenosis
Identify site of stenosis
Identify associated
regurgitation
Measure LVOT velocity
at a specific site (15)
Measure highest
gradient along LVOT
into ascending aorta (15)
o AS jet velocity *
o Mean transaortic
gradient*
o Valve area by
continuity
equation using
VTI*
o Valve are by
simplified
continuity
equation using
peak velocities #
o Velocity ratio or
dimensionless
index #
* Level I measurement recommendation for all patients with aortic stenosis (15).
# Level II methods for additional information in select patients (15).
The primary echocardiographic technique used to quantify aortic stenosis severity is
Doppler echocardiography and is used to calculate pressure gradients and aortic valve
area. Continuous wave Doppler (CWD) techniques are utilized to measure transvalvular
blood velocity. The peak pressure gradient is then estimated from the peak velocity
measurement using the simplified Bernoulli equation:
Peak Aortic Valve Pressure Gradient (PGAV) = 4 (Aortic Valve velocity)2
∆P= 4 (Aortic Valve velocity)2
The mean gradient is a derived measurement obtained by the ultrasound system by
averaging the instantaneous gradients over the ejection period. Mean aortic valve
pressure gradient can be estimated from the following formula:
Mean Aortic Valve Pressure Gradient (MGAV) = 2.4 (Aortic Valve Velocity)2
When LVOT velocity is greater than 1.5 m/s, the modified Bernoulli equation should be
utilized to prevent overestimation of the pressure gradient and the severity of the aortic
stenosis.
The modified Bernoulli equation:
∆P= 4 (Aortic Valve Velocity2 - LVOT Velocity 2)
Severity of Aortic Stenosis
Indicator
Peak jet velocity (m/s) *
Mean gradient (mm Hg) *
Valve area (cm2) *
Dimensionless index #
Indexed AVA (cm2/m2)
Mild
< 3.0
< 20
1.5
> 0.50
0.85
Moderate
3.0-4.0
20-40
1.0-1.5
0.25-0.50
0.60-0.85
Severe
> 4.0
> 40
< 1.0
< 0.25
< 0.6
* Level I measurement recommendation for all patients with aortic stenosis.
# Level II methods for additional information in select patients (15).
Gradients derived in the operating room can be significantly different from those
obtained during preoperative echocardiographic studies or in the cardiac catheterization
laboratory. Stenotic orifice gradients are flow dependent, and an increase in cardiac
output across the aortic valve will increase the gradient. Conditions that increase forward
blood flow across the aortic valve such as hyperdynamic left ventricular function, sepsis,
severe aortic insufficiency and hyperthyroidism will all increase the pressure gradient.
Conversely, severe LV dysfunction, severe mitral regurgitation and a left to right shunt
will all decrease the transvalvular pressure gradient. Changes in intraoperative loading
conditions, heart rate and contractility may all cause significant disparities between
intraoperative and preoperatively derived transvalvular gradients.
Differences in gradients between the intraoperative echocardiography examination and
catherization data can also occur. Peak left ventricular pressure occurs earlier in systole
than the peak aortic pressure, which occurs later in systole. The measurement obtained
during cardiac catheterization pull back technique is a peak-to-peak measurement. This
measurement is obtained at two different times during systole. Peak left ventricular
pressure to peak aortic pressure (peak to peak) is a smaller difference and occur at two
different time points during systole. The echocardiographic Doppler derived pressure
gradient is a reflection of the same time peak instaneous pressure difference. The
Doppler peak instantaneous pressure difference will be larger than the peak to peak
difference because still rising aortic pressure, which has not attained the peak position.
(Figure 11. Graphic representations of simultaneous pressure recordings from the left
ventricle (red) versus the aorta (purple) over time are shown. The peak pressure in the
left ventricle occurs slightly before the peak pressure measured in the aorta. As such a
peak to peak measurement obtained in the catheterization lab will be less than the peak
instantaneous pressure difference measured by Doppler echocardiography. At the time
when the peak instantaneous pressure is being measured, the left ventricular pressure is at
the peak but aortic pressure is still rising and is less than the peak aorta pressure that
occurs slightly later.)
Pressure gradients can also occur in the LVOT from subvalvular and supravalvular
pathology, therefore it is important to localize the site of the pressure gradient within the
flow stream. 2D imaging can localize the pathology to the aortic valve or somewhere
else within the flowstreams (subvalvular or supravalvular). The ME AV LAX view
obtained with 2D imaging, and supplemented with Color Flow Doppler is useful for
localization of the obstruction. A color flow disturbance will be noted downstream of the
obstruction and this area can be compared to the position of the aortic valve. The shape
of the spectral Doppler envelope can also yield important diagnostic clues. Valvular
aortic stenosis produces a rounded pattern with a midsystolic peak. Left ventricular
outflow tract obstruction produces a late systolic peak and has a dagger shaped or shark’s
tooth spectral pattern.
(Figure 12. Deep TG LAX image with CW Doppler through stenotic aortic valve. The
spectral Doppler envelope has a rounded appearance with a mid systolic peak. Peak
velocity approximates 4 m/s consistent with severe aortic stenosis)
Given the dynamic nature of pressure gradients in relation to trans aortic blood flow,
aortic valve area is considered a more constant and less dynamic measure of aortic valve
stenosis. The continuity equation is utilized to calculate aortic valve area and is based
upon the concept of conservation of mass and continuity of flow. The flow of blood
through the left ventricular outflow tract must equal flow through the aortic valve into the
ascending aorta.
SVAV = SVLVOT
Stroke Volume = Area x Flow rate
SVAV = CSAAV x VTIAV
SVLVOT = CSALVOT x VTILVOT
Where SV = stoke volume and CSA is cross sectional area.
Thus,
CSAAV x VTIAV
=
CSALVOT x VTILVOT
Aortic valve area (CSAAV) = CSALVOT x VTILVOT
VTIAV
Assuming the LVOT is circular:
CSALVOT = π x (d/2)2
CSALVOT = π /4 x (d)2
CSALVOT = 0.785 x (d)2
To obtain the three measurements required to solve the continuity equation for aortic
valve area, one must utilize three different echocardiographic techniques.
Technique
Aortic valve velocity by CWD
LVOT velocity by PWD or CWD
LVOT diameter by 2D with calipers
Tomographic View
TG LAX or deep TG LAX
TG LAX or deep TG LAX
ME AV LAX
The velocity time integral of the left ventricular outflow tract is obtained with either the
deep TG LAX or the TG LAX view, and requires parallel alignment of the Doppler beam
through the left ventricular outflow tract. Pulse wave Doppler is utilized for sampling
LVOT velocities given the need for range specificity. The sample volume is placed
within the LVOT and records sample velocities at a specific location in the LVOT. The
sample volume is slowly moved closer to the aortic valve and records corresponding
sample velocities. As the sample velocities increase and begin to alias because of flow
acceleration, the sample volume is withdrawn slightly back into the LVOT and the
spectral velocity is recorded and saved at this portion of the LVOT. The aliasing should
be eliminated and the spectral profile should demonstrate laminar flow and have a hollow
spectral envelope. Normal peak velocities in the LVOT will range from 0.8 m/s to 1/5
m/s. To have an accurate measure of stroke volume, the LVOT diameter should be
measured at the same point in the LVOT where the LVOT spectral display was recorded.
The ME AV LAX often affords the best image for measuring the LVOT diameter. A
midsystolic frame should be selected and the LVOT diameter measured proximal to the
aortic annulus corresponding to the same anatomic location as the pulsed wave Doppler
recording of the LVOT velocity.
Once 2D imaging and Color Flow Doppler has verified the aortic valve as the source of
the stenosis, continuous wave Doppler (CWD) is applied to either the TG LAX or the
deep TG LAX view. Continuous wave Doppler must be utilized for sampling the stenotic
aortic valves because velocities are usually greater than 2 m/s. Proper alignment of the
Doppler stream to flow across the aortic valve is essential. Color flow Doppler and
audible signaling may help the operator align the Doppler beam, especially as the valve
orifice becomes smaller. The spectral envelope with continuous wave Doppler of the
stenotic aortic valve is solid in character (non laminar flow) and demonstrates a high
velocity that peaks in mid systole. Planimetry is then utilized to trace the spectral
envelope and obtain the aortic valve velocity time integral (VTI) and peak velocity.
Although some consensus statements suggest aortic valve area can be calculated utilizing
either the velocity time integrals or the peak velocities in both the LVOT and the aortic
valve (17), recent EAE/ASE statement has express concerns in using the peak velocities
secondary to higher variability when compared to using the VTI (15).
Accurate measurement of the LVOT diameter is essential given that this variable is
squared when solving the continuity equation for aortic valve area. Any underestimation
of LVOT diameter will cause a resultant significant underestimation of the true aortic
valve area and an overestimation of aortic stenosis severity. Another potential source of
error is the inability to align the Doppler beam to be parallel with flow. Ensuring that
axial alignment deviates no more than 20 degrees from parallel will minimize this error.
In up to 6% of patients the inability to obtain adequate tomographic views limits the TEE
evaluation of aortic stenosis(18,19). In these cases, epicardial echocardiography can
overcome this limitation in 100% of patients and demonstrates excellent correlation with
TEE, TTE, and cardiac catheterization-derived measures (20).
Ideally the pulse wave calculation and the continuous wave calculation would occur with
the same heartbeat and therefore the same stroke volume. The variability in patients in
normal sinus rhythm in stroke volume is negliable. Intraoperative patients with sudden
changes in preload, heart rate and contractility can have an affect on the nonsimultaneous measure of flow across the LVOT and the aortic valve. Marked variability
is also seen in patients with irregular heartbeats, especially atrial fibrillation. It is
recommended in patients with atrial fibrillation that six consecutive beats are analyzed
and averaged to obtain the velocity time integral in both the LVOT and the aortic valve.
Velocity Ratio or Dimensionless Index
CWD can be utilized to calculate both the aortic valve and the left ventricular outflow
tract velocity time integrals from the same beat. This eliminates the beat-to-beat
variability and both the higher velocity related to the aortic valve and a lower denser
pattern consistent with the left ventricular outflow tract are present on spectral display
(21).
Comparison of the LVOT velocity time integral to the Aortic valve velocity time integral
is called the dimensionless index as the LVOT area has been eliminated from the
continuity equation. This index can be utilized for quantification of the severity of aortic
stenosis. In normal valves, the continuous wave VTI for the aortic valve will equal the
VTI of the left ventricular outflow tract (DI=1). With disease progression and worsening
severity of stenosis, the aortic valve velocity increases while the left ventricular outflow
tract velocity will remain unchanged. Severe aortic stenosis is present when the
dimensionless index is less than 0.25 (22).
(Figure 13. Deep TG LAX image with CW Doppler through LVOT and aortic valve. A
double envelope spectral pattern is displayed with the denser spectral display flow
through the LVOT represented by the X trace. The fine feathery display is flow through
the stenotic aortic valve and is represented by the + symbol. The TEE machine measures
velocities through the aortic valve (3.6 m/s) as well as the LVOT (0.974 m/s). The
dimensionless index in this case is 0.974/3.6 and equals 0.27 which does not qualify for
severe aortic stenosis as it is greater than 0.25.)
Associated Echocardiographic Findings
Other diagnostic findings will be present in patients with aortic stenosis. As an adaptive
mechanism to chronic pressure overload, the left ventricle will secondarily hypertrophy.
This concentric increase in wall thickness reduces wall stress by distributing the pressure
overload over a greater myocardial mass. Posterior wall thickness greater than 1.0 cm in
women and 1.1 cm in men is considered abnormal. Left ventricular compliance is altered
markedly by the secondary hypertrophy and traditional estimates of left ventricular
volume based upon left ventricular filling pressures with pulmonary artery catheter data
are unreliable. Transesophageal echocardiography examination can yield direct estimates
of left ventricular volume status and ejection fraction. Systolic and diastolic dysfunction
is also likely to be present in patients with aortic stenosis.
Septal hypertrophy can lead to the development of systolic anterior motion (SAM) of the
mitral valve. This leads to a fall in the cardiac output secondary to left ventricular
outflow tract obstruction (LVOTO) by the anterior mitral leaflet during systole. The
anterior mitral valve leaflet is drawn into to LVOT during systole causing an abrupt
decrease in forward flow through the aortic valve. In addition to LVOTO there is
associated mitral regurgitation (MR) because the anterior mitral leaflet is in the LVOT
during systole and the mitral valve is therefore rendered incompetent. SAM and LVOTO
may occur after an AVR. This postoperative complication may occur after an aortic
valve replacement because of the low preload, a low afterload and an increased LV
contractility that is common in post bypass patients. Left ventricular outflow tract
obstruction (LVOTO) secondary to SAM is diagnosed with TEE and effectively treated
with volume administration, elevation of afterload with vasoconstrictors and the
discontinuation of inotropic and chronotropic medications. The diagnosis LVOTO and
SAM should be excluded in all patients postoperatively. Echocardiographic evaluation of
the mitral valve and LVOT can lead to predictions about the likelihood of this occurring
based upon anatomic factors (23).
Many patients with aortic stenosis will have associated aortic insufficiency. Mitral
regurgitation is common in patients with aortic stenosis and is related to either LV
pressure overload or intrinsic mitral disease. In the majority of patients without intrinsic
mitral disease, mitral regurgitation improves after aortic valve replacement. Dilation of
the ascending aorta may be a consequence of aortic stenosis from an adaptive
mechanism, or may be due to intrinsic disease within the aortic wall. Evaluation of the
ascending aorta, including epiaortic scanning, is recommended to determine the need for
surgical repair and to guide cannulation and perfusion strategies.
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