8. MORPHOLOGY AND ETIOLOGY
Most common
Bicuspid aortic
Senile or
Degenerative
calcific AS
• Rheumatic AS
Less common
• Congenital
• Type 2
Hyperlipoprote
inemia
• Onchronosis
9. Anatomic evaluation
Combination of short and long axis images to identify
Number of leaflets
Leaflet mobility
Thickness
Calcification
Combination of imaging and doppler -determination
of the level of Obstruction
Subvalvular
Valvular
Supravalvular
Transesophageal echocardiography may be helpful
when image quality is suboptimal.
10. CALCIFIC AORTIC STENOSIS
Nodular calcific masses
on aortic side of cusps
No commissural fusion
Free edges of cusps are
not involved
Stellate-shaped systolic
orifice
11. CALCIFIC AORTIC STENOSIS
PLAX showing echogenic and
immobile aortic valve
PSAX showing calcified aortic
valve leaflets.
Immobility of the cusps results
only a slit like orifice in systole
13. GRADING CALCIFICATION
Semi-quantitative
Degree of valve calcification -
predictor of clinical outcome
Heart failure
Need for AVR
Death
Mild
Few areas of dense echogenicity with little acoustic shadowing
Moderate
Multiple larger areas of dense echogenicity
Severe
Extensive thickening and increased echogenicity with a prominent
acoustic shadow
14. Aortic sclerosis
Thickened calcified cusps with preserved
mobility
Typically associated with peak doppler
velocity of less than 2.5 m/sec
15. RHEUMATIC AS
Commissural fusion
Triangular systolic orifice
Thickening and
calcification mostly
along the edges of the
cusps.
Concomitant
involvement of mitral
valve seen
17. Bicuspid aortic valve
Fusion of the right and left
coronary cusps (80%)
Fusion of the right and
non-coronary cusps(20%)
Rarely
Fusion of the left and non-
coronary cusps
Valves with two equally
sized cusps (“true”bicuspid
valve)
18. Bicuspid Aortic valve PSAX
Two cusps are seen in systole with only two
commissures framing an elliptical systolic
orifice(the fish mouth appearance).
Diastolic images may mimic a tricuspid valve
when a raphe is present.
19. Bicuspid Aortic valve PLAX
An asymmetric
closure line
Systolic doming
Diastolic prolapse of
the cusps
Less specific than a
short-axis systolic
image
20. Bicuspid Aortic valve
In children, valve may be stenotic Without
extensive calcification.
Or may be functionally normal except for
systolic dooming – but needs follow up
Rarely unicuspid or quadracuspid
In adults, stenosis is due to calcific changes
Often obscures the number of cusps, -
bicuspid vs tricuspid is determination difficult
Loot for aortic root dilataton & AR
21. SUPRAVALVULAR AS
Type I(Hourglass type) –Thick
fibrous ring above the aortic valve
with less mobility
Type II - Thin, discrete fibrous
membrane above the aortic valve
membrane usually mobile and may
demonstrate doming during systole
Type III- Diffuse narrowing
22. SUBVALVULAR AS
Distinguished from valvular stenosis based on the site of the
increase in velocity seen with colour or pulsed Doppler
(1)Thin discrete membrane
consisting of endo cardial fold
and fibrous tissue
(2) A fibro muscular ridge
(3) Diffuse tunnel-like narrowing
of the LVOT
(4) accessory or anomalous
mitral valve tissue.
23. AS STAGING
Stage A
At Risk of as
Stage B
Mild to moderate AS
Stage C
Assymptomatic Severe AS
C1: Without LV
Dysfunction EF>50
C2:With LV
Dysfunction EF <50
Aortic Vmax <2 m/s Mild AS:
Vmax 2.0–2.9 m/s
Mean PG<20 mm Hg
Moderate AS:
Vmax 3.0–3.9 m/s
Mean PG 20–39 mm
Hg
Vmax >4 m/s
Mean PG ≥40 mm Hg
AVA ≤1.0 cm2 (or AVAi <0.6cm2/m2)
Very severe as is an aortic
Vmax ≥ 5 m/s
Mean pg≥60 mm Hg
BAV
Aortic sclerosis
Pseudo severe AS
24. AS STAGING
Stage D
Symptomatic Severe AS
AVA ≤1.0 cm2 (or AVAi <0.6cm2/m2)
D1 D2 D3
Vmax >4 m/s
Mean PG ≥40 mm Hg
Mean PG <40 mm Hg
LVEF< 50
Dobutamine stress +
Mean PG <40 mm Hg
LVEF> 50
SVI < 35 mL/min
25. SEVERITY ASSESMENT
Echocardiogram is the current standard –
catheterization no longer recommended for
routine evaluation
Integrative approach in grading the severity
Doppler
2D data
Clinical presentation
26. SEVERITY ASSESSEMENT
Level 1 Recommendation= appropriate in all
patients with AS
Echocardiographic Assessment of Valve Stenosis: EAE/ASE Recommendations for
Clinical Practice
AS peak jet velocity.
Mean transvalvular pressure gradient
Aortic valve area by continuity equation
27. PEAK TRANSVALVULAR VELOCITY
Continuous-wave Doppler
ultrasound
Multiple acoustic windows
Apical and suprasternal or
Right parasternal most
frequently yield the highest
velocity
Rarely subcostal or
supraclavicular windows may
be required
28. PEAK TRANSVALVULAR VELOCITY
Dedicated small dual-crystal CW transducer is
recommended
Time scale on the x-axis of 100 mm/s
Wall filters are set at a high level
Gain is decreased to optimize identification
of the velocity curve.
Grey scale is used – Most validated
Contrast?
29. PEAK TRANSVALVULAR VELOCITY
Highest velocity From any window.
Any deviation from a parallel intercept angle
results in velocity underestimation
5% or less if the intercept angle is within 15⁰ of
parallel.
‘Angle correction’ should not be used
30. LOCATION OF HIGHEST VELOCITY
Apical Parasternal Suprasternal Supraclavicular
HIGHEST VELOCITY
Thaden et al. JASE 2015
31. PEAK TRANSVALVULAR VELOCITY
A smooth velocity
curve with a dense
outer edge and clear
maximum velocity
should be recorded
Fine linear signals at
the peak of the curve
not be included
VTI also calculated
32. NO OF MEASUREMENTS
Sinus Rhythm – 3 Measurements
Irregular Rhythm – 5 Measurements
33. SHAPE OF IMAGE
The shape of the CW Doppler velocity curve is helpful in
distinguishing the level and severity of obstruction.
Severe obstruction -
maximum velocity
occurs later in systole
and the curve is more
rounded in shape
Mild obstruction - the
peak is in early systole
with a triangular shape
of the velocity curve
Dynamic sub aortic
obstruction - shows
characteristic late
peaking velocity curve,
34. MEAN TRANSVALVULAR GRADIENT
The difference in pressure between the left ventricle
and aorta in systole
Gradients are calculated from velocity information
Simplified Bernoulli equation
ΔP =4V²
The maximum gradient is calculated from maximum
velocity
ΔP max =4V² max
The instantaneous gradient at any point of time is
calculated similarly from the instantaneous velocity
And averaged to get the mean gradient (mean
gradient not derived from mean velocity)
35. BERNOULLI EQUATION
The simplified Bernoulli equation assumes
that the proximal velocity can be ignored
When the proximal velocity is over 1.5 m/s or
the aortic velocity is <3.0 m/s, the proximal
velocity should be included in the Bernoulli
equation
ΔP max =4 (v² max- v² proximal)
36. MEAN TRANSVALVULAR GRADIENT
Peak gradient no additional information
Mean Gradient - mean of different
instantaneous velocities recorded
37. SOURCES OF ERROR FOR PRESSURE
GRADIENT CALCULATIONS
Misalignment of jet and ultrasound beam.
Recording of MR jet
Any underestimation of aortic velocity results
in an even greater underestimation in
gradients, due to the squared relationship
between velocity and pressure difference
Neglect of an elevated proximal velocity.
38. MR V/S AR
MR Jet
Wider
More symmetrical
Not recorded in Suprasternal window
Superimposed LVOT gradient suggest AS Jet
For a given patient MR faster than AS
39. CORRELATION WITH CATH
Doppler Echo - Max instantaneous pressure
difference across the valve,
Pressure tracings - difference between the peak
left ventricular (LV) and peak aortic pressure
40. PRESSURE RECOVERY
Potential energy converted to kinetic
energy across a narrowed valve results in a
high velocity and a drop in pressure.
Distal to the orifice , flow decelerates.
Some amount of Kinetic energy dissipates
as heat (depends on turbulence)
Remaining will be reconverted into
potential energy with a corresponding
increase in pressure, the so-called PR
Pressure recovery is greatest in stenosis
with gradual distal widening
Aortic stenosis with its abrupt widening
from the small orifice to the larger aorta -
unfavorable geometry for PR
41. PRESSURE RECOVERY
PR= 4v²× 2EOA/AoA (1-EOA/AoA)
The ratio between effective aortic orifice and Ascending
Aortic area determines the magnitude of PR
The net Pressure gradient ( measured gradient–
pressure recovery) determines the hemodynamic
significance
Most adults magnitude small to be ignored unless
Aortic width < 3 cm
Smaller aortas echo evaluation overestimates pressure
gradient
42. PG CATH vs DOPPLER
Currie PJ et al. Circulation 1985;71:1162-1169
44. LVOT MEASUREMENT
Zoomed PLAX in mid-systole
(inner-to-inner) of the septal
endocardium to the anterior
mitral leaflet,
Parallel to the aortic valve
plane.
At the annulus or within 0.3–
1.0 cm of the valve orifice
Average of 3 in sinus & 5 in
irregular rhythms
CSALVOT = 𝝅(𝒅/𝟐) 𝟐
45. LVOT MEASUREMENT- DIFIFICULTIES
Calcium extension from annulus to
the base of anterior mitral leaflet.
‘Sigmoid septum’ - the LVOT
diameter often appear smaller than
the flow area at the annulus
Outflow tract not imaged clearly at
mid systole end-diastole
A practical approach - measure LVOT
in the frame that yields the largest
diameter.
LVOT not perfectly cylindrical
If TTE not adequate TEE can be used
to determine LVOT
46. VELOCITY MEASUREMENT
Apical 5 chamber view or
3chamber view
PW sample volume is
positioned just proximal to the
aortic valve ideally at the level
of measurement of LVOT dm
Velocity of valve –CWD
47. VELOCITY MEASUREMENT
Optimally positioned - smooth velocity curve with a well-
defined peak is obtained.
Only closing click seen
Severe calcific AS – may have to move sample volume more
towards apex , measure LVOT dm at same level
48. LIMITATIONS - CONTINUITY EQUATION
Intra- and inter observer variability (3 variables)
AS jet and LVOT velocity 3 to4%.
LVOT diameter 5% to 8%.
LVOT assumed circular
MDCT , 3D echo - better
When sub aortic flow velocities are abnormal SV
calculation at this site are not accurate
Sample volume placement near to septum or anterior
mitral leaflet
Observed changes in valve area with changes in flow
rate
Normal LV function - Effects of flow rate minimal
Significant in presence concurrent LV dysfunction.
49. SUMMARY
Measurement Severity
Criteria
Advantages Limitations
AS peak
velocity.
> 4 m/s • Strong Predictor of
clinical outcome
• Parallel alignment important
• Overestimates LV energy loss -
small aortas
• Under or over estimates in
presence of SHTN
• Under estimates Low flow cases
• Easy
• Low Inter / Intra observer
variability
• High Specificity
• Strong predictor of
clinical outcome
Mean
pressure
gradient
> 40 mm
Hg
• Comparable to invasive
values
Valve area -
continuity
equation
< 1
cm2(EOA)
<0.6
cm2/m2
BSA (EOAi)
• Relatively flow
independent
• EOA Reflects clinical
severity
• Can be used in almost all
patients
• Same limitations applicable as
above
• Susceptible to measurement
errors
• EOA – over estimated in thin
individuals
• EOAi – under estimated in
obese individuals
50. ALTERNATIVE MEASUREMENTS
Level 2 Recommendations = reasonable when
additional information needed in selected patients
Echocardiographic Assessment of Valve Stenosis: EAE/ASE Recommendations for
Clinical Practice
Simplified continuity equation
Velocity ratio and VTI ratio (dimensionless
index
AVA Planimetry
51. SIMPLIFIED CONTINUITY EQUATION
Native aortic valve stenosis the shape of
the velocity curve Similar in AV & LVOT
So ratio of peak velocity mean velocity
and VTI similar.
𝑨𝑽𝑨 = 𝑪𝑺𝑨 𝑳𝑽𝑶𝑻 X
𝑽
𝑳𝑽𝑶𝑻
𝑽
𝑨𝑽
This method is less well accepted
because results are more variable than
using VTIs in the equation.
Also VTI required for calculating stroke
volume
52. VELOCITY RATIO
To reduce error related to LVOT diameter measurements by
removing CSA from the continuity equation.
This dimensionless velocity ratio expresses the size of the
valvular effective area as a proportion of the CSA of the LVOT.
𝑽𝒆𝒍𝒐𝒄𝒊𝒕𝒚 𝑹𝒂𝒕𝒊𝒐 =
𝑽
𝑳𝑽𝑶𝑻
𝑽
𝑨𝑽
𝑽𝑻𝑰 𝑹𝒂𝒕𝒊𝒐 =
𝑽𝑻𝑰
𝑳𝑽𝑶𝑻
𝑽𝑻𝑰
𝑨𝑽
The velocity ratio approaches 1 in the absence of valve stenosis
Smaller numbers indicating more severe stenosis.
Severe stenosis is suggested VR < 0.25 or less, corresponding to
a valve area 25% of normal
53. AVA PLANIMETRY
Calculates anatomic orifice area (AOA)
AOA>EOA
Acceptable alternative when Doppler
estimation of flow velocities is unreliable
Inaccurate if valve calcification causes
shadows or reverberations (limits
identification of the orifice)
TEE has shown better correlation with
Invasive data / continuity equation /MDCT
and is prefered
57. DIFFICULTIES & SPECIAL
SITUATIONS
Ideally there should be concordance between
different measurements
All measurements should be made when
patient has a normal BP
Integrate with other imaging & clinical data
before final judgemnt
58. DIFFICULTIES & SPECIAL
SITUATIONS
Valve area >1.0 cm2 peak velocity<4 m/s and mean
gradient<40 mmHg but strong clinical suspicion
Index to BSA
Consider Low Flow states
Valve area > 1 cm2 but Velocity & Gradient high
Concomitant AR or shunt lesions
Reversible causes of increased flow (fever, anaemia,
hyperthyroidism, AV shunts for dialysis, etc.) must be
excluded
Valve area <1.0 cm2 peak velocity<4 m/s and mean
gradient<40 mmHg
Exclude measurement errors
Small Stature
Low Flow Low gradient
59. DIFFICULTIES & SPECIAL
SITUATIONS
Low flow, low gradient AS with reduced
ejection fraction ( Classical LFLG AS)
Effective orifice area < 1.0 Cm2
Mean pressure gradient < 30–40 mmHg
SVi <35 mL/m2
LV ejection fraction <50%.
True Severe AS or Moderate AS with
low(Pseudosevere AS) EF??
60. DOBUTAMINE STRESS ECHO
CLASS IIa (B) recommendation ACC /AHA / ESC guidelines
Measures
Contractile response - change in ejection
fraction and increase in SV (flow reserve)
Changes in aortic velocity, mean gradient, and
valve area as flow rate increases
Helps in identifying severe v/s pseudo-severe
AS
Severe AS causing LV systolic dysfunction
Moderate AS with another cause of LV
dysfunction
62. DOBUTAMINE STRESS ECHO
LVOT – Baseline measurement
Aortic and LVOT velocity recorded at each
stage
EF should be measured at least twice at
baseline and peak effect
A patient with a low ejection fraction but
High gradient and velocity does not have
impaired LV systolic function -Stress echo not
indicated
63. DOBUTAMINE STRESS ECHO
TRUE SEVERE AS
EOA – Little or no Change
Mean Gradient >40 mm hg
PSEUDO SEVERE AS
EOA becomes >1 cm2
Mean Gradient < 40 mm hg
64. TRUE SEVERE AS
No Significant change in EOA
Mean gradient Increased from 32 to 56
65. PSEUDO SEVERE AS
Significant change in EOA from 0.7 to 1.1
Mean gradient remains fairly constant
66. LOW FLOW RESERVE
Increase in SVI < 20%
30-40% LFLG with low EF patients
DSE fails to demonstrare response
Alternative options
Projected AVA
MDCT – Calcium scoring (> 1650 Agatston units
has 90 % sensitivity and specificity )
67. PROJECETED AVA
AVA increase during each stage of DSE
projected to a flow of 250 ml/min (average
flow rate achieved in patients with Severe AS
and normal LV function)
Minimum of 15 % increase in SV needed to
calculate AVAproj (not seen in 10-20 % cases)
69. LOW FLOW, LOW GRADIENT AS WITH
PRESERVED EJECTION FRACTION
(PARADOXICAL LFLG AS)
5-15% of patients with AS
Hypertrophied, small ventricles with low EDV
Elderly patients , Long standing SHTN
Reduced transvalvular flow (SVi < 35
mL/m2)despite normal EF.
Always rule out technical errors before
diagnosing LFLG AS with preserved EF
Severe AS highly unlikely when peak velocity is
<3.0 m/s and mean PG <20 mmHg.
70. DIAGNOSING LFLG AS WITH PRESERVED EF
Very Difficult , DSE not helpful as there is not
much further increase in flow rate
First
R/O SHTN during examination
R/O technical errors
Clinically confirm whether AS is moderate only
Only definitive indicator for severe AS – high
calcium score in MDCT
74. M MODE- AORTIC STENOSIS
Maximal aortic cusp separation (MACS)
Vertical distance between right CC and non
CC during systole
Aortic valve area MACS Measurement Predictive value
Normal AVA >2Cm2 Normal MACS >15mm 100%
AVA>1.0 > 12mm 96%
AVA< 0.75 < 8mm 97%
Gray area 8-12 mm …..
DeMaria A N et al. Circulation.Suppl II. 58:232,1978
75. ASSOCIATED SHTN
Associated in 35-40%
Aortic stenosis can conceal hypertension
especially when there is low flow states.
&
Hypertension can mask aortic stenosis severity
(Primarily affect flow and gradients but less AVA
measurement).
Control of blood pressure is recommended
before echocardiographic evaluation
Global LV load depends on both AS severity and
vascular after load which is not assessed in usual
measurements of severity
76. VALVULO ARTERIAL IMPEDENCE
Amount of energy in mmHg needed to pump 1
ml of blood by the left ventricle against the load
imposed by both the Valve and PVR
Global systolic load to LV and thus assess the
hemodynamic consequences
Superior in predicting symptoms and events
ZVA =
𝑺𝑩𝑷+ 𝜟𝑷𝒏𝒆𝒕
𝑺𝑽𝑰
Zva > 4.5 mmHg/ml/m2 indicates severe disease
77. VALVULO ARTERIAL IMPEDENCE
In asymptomatic moderate or severe AS
Zva>4.5–5.0 mmHg/ml/m2 predicts reduced
event-free survival and a 2.8-fold increased risk
of death
Drawback
Does not identify the relative contributions of
the valve and PVR that is necessary to guide
management (i.e. AVR versus BP control)
78. ASSOCIATED AR
80% of adults with AS have concomitant AR
Usually mild or moderate - does not affect
severity assessment
Flow rate, maximum velocity, and mean
gradient will be higher than expected for a
given valve area
Quantitative severity of both lesions to be
reported
79. MITRAL VALVE DISEASE
Miral valve diseases should be looked for esp
in Rheumatic AS
Severe MR, transaortic flow rate may be low
resulting in a low gradient even when severe
AS is present;
AVA calculations remain accurate (if flow is
calculated in the LVOT and not by volumetry)
High-velocity MR jet mistaken for the AS jet
Mitral stenosis (low cardiac output) May
result in low flow, low gradient AS.
80. ASCENDING AORTA
Should also be assessed as a part of AS
evaluation
Diameters at the sinuses of Valsalva, the
sinotubular junction and the ascending aorta
measured .
Dilation of the aortic root associated with
bicuspid aortic valve disease and aortic size
may impact the timing and type of
intervention.
81. PROGNOSTIC INDICATORS
IN ASYMPTOMATIC SEVERE AS
Peak aortic jet velocity
Severity of valve calcification
LV ejection fraction
Rate of hemodynamic progression
Increase in gradient with exercise
Excessive LV hypertrophy
Abnormal longitudinal LV function (in particular
GLS)
Pulmonary hypertension
82. PROGNOSTIC INDICATORS
IN ASYMPTOMATIC SEVERE AS
Peak aortic jet velocity >5.5 m/s;
Combination of severe valve calcification with
a rapid increase in peak transvalvular velocity
of>_0.3 m/s/year;
Increase of mean pressure gradient with
exercise by> 20mmHg.
83. STRESS ECHOCARDIOGRAPHY
In True asymptomatic patients
AVR
MG increase > 20 mm Hg
Reduction in LVEF
Follow up
MG increase < 20 mm Hg
No reduction in LVEF
Every 6-12 months in severe AS
Every 12-24 months in Moderate AS
84. AORTIC VALVE RESISTANCE
Resistance offered by the valve to flow of blood through it
Relatively flow-independent measure of stenosis severity
Depends on the ratio of mean pressure gradient and mean
flow rate
Resistance =
𝜟𝑷𝒎𝒆𝒂𝒏
𝜟𝑸𝒎𝒆𝒂𝒏
× 1333 dynes/cm2
There is a close relationship between aortic valve resistance
and valve area
The advantage over continuity equation not established
85. LV STROKE WORK LOSS %
Work of LV wasted in ejecting blood through
the aorta and to keep valves open
SWL(%) =
𝜟𝑷𝒎𝒆𝒂𝒏
𝜟𝑷𝒎𝒆𝒂𝒏+𝑺𝑩𝑷
𝒙 100
A cutoff value more than 25% effectively
discriminates between patients experiencing
a good and poor outcome.
Kristian Wachtell. Euro Heart J.Suppl. (2008) 10 ( E), E16–E22
87. TO SUMMARISE
The 3 primary haemodynamic parameters recommended for evaluation
of AS severity are
(i) AS peak jet velocity
(ii) mean aortic transvalvular pressure gradient
(iii) valve area by continuity equation.
Make measurements when BP normal and r/o hyperdynamic circulatory
states
AS peak jet velocity:
A peak gradient >_4 m/s is consistent with severe aortic stenosis.
AS peak jet velocity should be obtained in multiple views.
Mean aortic transvalvular pressure gradient:
A mean gradient of>_ 40mmHg is consistent with severe aortic stenosis.
The mean gradient is calculated by averaging the instantaneous gradients
over the ejection period.
Cannot be calculated from the mean velocity.
A common source of error for gradient measurement is misalignment of
the beam - importance of using multiple acoustic windows
88. TO SUMMARISE
AVA
An AVA of< 1.0 is consistent with severe aortic stenosis.
AVA by continuity-equation calculation - well validated predictor of clinical
outcome
LVOT diameter is measured in a PLAX view - inner edge to inner edge of the septal
endocardium, and the anterior mitral leaflet in mid-systole
LVOT velocity is recorded with PWD from an apical 5 chamber or 3 chamber view.
The pulsed Doppler sample volume is positioned just proximal to the aortic valve
at the aortic annulus to get a smooth velocity curve can be obtained
Flow acceleration at the annulus level may make it necessary to move the sample
volume apically by 0.5–1.0 cm.
Major limitation of the continuity equation LVOT not circular - LVOT area and
consequently flow and AVA will be underestimated
Follow up measurements –
Aortic jet velocity same window (Always give report with window of max
velocity )
If AVA changes, look for changes in Individual components. LVOT size rarely
changes over time in adults
89. TO SUMMARISE
Low flow, low gradient AS with reduced EF is defined as
(i) AVA <1.0 cm2, (ii) mean aortic transvalvular
PG<40mmHg, (iii) LVEF<50%, and (iv) SVi <35mL/m2.
Low-dose DSE can help distinguish between pseudo severe
AS from true severe AS.
Low flow, low gradient AS with preserved EF is defined
as (i) AVA <1 cm2, (ii) peak velocity <4 m/s, (iii) mean
PG <40mmHg, and (iv) normal LVEF (>_50%)
R/o measurement errors (esp. LVOT area and thus flow).
Clinically moderate AS (despite an AVA < 1.0 cm2) in a
patient esp. with small body size.
Calcium scoring
Notas do Editor
Calcification of a tricuspid aortic valve is most prominent in the
central and basal parts of each cusp while commissural fusion is absent,
resulting in a stellate-shaped systolic orifice. Calcification of a bicuspid
valve is often more asymmetric
Echocardiography has become the standard means for evaluation of
aortic stenosis (AS) severity. Cardiac catheterization is no longer
recommended1–3 except in rare cases when echocardiography is
non-diagnostic or discrepant with clinical data.
The acoustic window that provides the highest aortic jet velocity
is noted in the report and usually remains constant on sequential
A grayscale signal intensity look-up table is used because
this scale maps signal strength using a decibel scale that allows visual
separation of noise and transit time effect from the velocity signal. In
addition, all of the validation and inter-observer variability studies
have been performed using this mode.
In case of poor acoustic quality, the use of echo contrast
media has been suggested31,32 but is not used in many echocardiography
laboratories. In case of its use, proper machine settings
(e.g. adequate adjustment gain lowering) are crucial to avoid artefacts
and overestimation of velocities
Special care must be taken to select representative
sequences of beats and to avoid post-extrasystolic beats.
Gradients are calculated from velocity information,
and therefore the peak gradient obtained from the peak velocity
does not add additional information when compared with peak velocity
Although there is overall good
correlation between peak gradient and mean gradient, this relationship
depends on the shape of the velocity curve, which varies with stenosis
severity and flow rate. Transaortic pressure gradient (DP) is calculated
from velocity (v) using the simplified Bernoulli equation as:
Gradients are calculated from velocity information,
and therefore the peak gradient obtained from the peak velocity
does not add additional information when compared with peak velocity
. The peak LV and peak aortic
pressure do not occur at the same point in time; so, this difference
does not represent a physiological measurement and is less than the
maximum instantaneous pressure difference
Although a circular assumption for LVOT provides a reasonable
approach that has been validated in experimental and human studies,
3D echo and CT have shown that the LVOT area is not truly circular
but more elliptical (see under Limitations of the ‘standard approach’
continuity-equation valve area section for more details).
Ideally, LVOT diameter should be measured in mid-systole, and at the same time of maximum LVOT velocity in a cardiac cycle. But, sometimes image quality is suboptimal in mid-systole, and the outflow tract imaged clearly at end-diastole
Although a circular assumption for LVOT provides a reasonable
approach that has been validated in experimental and human studies,
3D echo and CT have shown that the LVOT area is not truly circular
but more elliptical (see under Limitations of the ‘standard approach’
continuity-equation valve area section for more details).
significant AS when the sample volume is positioned at the annulus, owing to flow convergence resulting in
spectral dispersion at this level. In many cases, the sample volume
must be slowly moved towards the apex until a smooth velocity
curve is obtained.
When a smooth velocity
curve can be obtained at the aortic annulus, this site is preferred
(i.e. particularly in congenital AS with a doming valve). However, flow
acceleration at the annulus level and even more proximally may
occur, particularly in patients with calcific AS, so that it may be necessary
to move the sample volume apically by 0.5–1.0 cm to obtain a
laminar flow curve without spectral dispersion
The advantages of diameter measurement at
the annulus level are (i) higher measurement reproducibility owing to
clear anatomic landmarks, (ii) easier to ensure diameter and Doppler
data are recorded at the same level by showing the aortic closing click
in the Doppler signal, and (iii) better correlation with the annulus
measurement needed for sizing transcatheter valves. However, there
is no general consensus and many laboratories measure the diameter
routinely at the annulus level whereas others measure more apically
in the LVOT, depending on the flow pattern in each patient.
When trans-thoracic images are not adequate for the measurement of LVOT diameter then TEE used.
more attention advent of transcatheter aortic
valve implantation, particularly for selection of valve type and size
prior to implantation. MSCT studies have now confirmed that the
aortic valve annulus as well as LVOT are elliptical in most patients,
which has led to the use of this approach for valve sizing atmost institutions.
However, echocardiography remains the standard for the
measurement of AS severity because these parameters have been
shown to be strong predictors of clinical outcomes, despite assuming
a circular LVOT shape in the continuity equation.
Accuracy of SV measurements in the outflow tract also assumes
laminar flow with a spatially flat profile of flow (e.g. velocity is the
same in the centre and at the edge of the flow stream). When subaortic
flow velocities are abnormal, for example, with dynamic subaortic
obstruction or a subaortic membrane, SV calculations at this
site are not accurate
To some extent, the velocity ratio is
normalized for body size because it reflects the ratio of the actual
valve area to the expected valve area in each patient, regardless of
body size. However, this measurement ignores the variability in
LVOT size beyond variation in body size.
Caution is also needed to ensure that the minimal orifice area is identified
rather than the larger area proximal to the cusp tips, particularly
in congenital AS with a doming valve. In addition, as stated previously,
effective, rather than anatomic, orifice area is the primary predictor of
outcome. In this context it has to be pointed out again that the EOA is
significantly smaller
continuous spectrum of aortic valve disease from aortic
sclerosis without haemodynamic consequences to very severe flow
obstruction. The measures of disease severity need therefore to be
viewed as a continuum.
Any one of the three criteria: a
valve area<1.0 cm2, a peak velocity>_4.0 m/s, or a mean gradient>_40
mmHg can be considered to suggest severe AS. Ideally, there should be
concordance with all criteria in the severe range. In cases where there is
discordance of criteria, it is important to integrate these criteria with
additional imaging findings and clinical data before a final judgement
Otherwise integrate with other imaging & clinical data before final judgemnt
Otherwise integrate with other imaging & clinical data before final judgemnt
When LV systolic dysfunction with reduced SV co-exists with severe
AS, the AS velocity, and gradient may be low, despite a small valve
area.50,51 A widely used definition of low flow, low gradient AS with
reduced EF includes the following conditions:
A patient with a low ejection fraction but a resting AS velocity>_4.0
m/s or mean gradient >_40mmHg generally does not have impaired
LV systolic function. The ventricle is demonstrating a normal response
to high afterload (severe AS), and ventricular function will improve
after relief of stenosis. This patient does not need a stress
echocardiogram.
Moderate AS (i.e. pseudosevere AS) with another cause of LV dysfunction
(e.g. myocardial infarct or a primary cardiomyopathy): The
EOA is then low because the LV does not generate sufficient energy
to overcome the inertia required to open the aortic valve to
its maximum possible extent. In this situation, aortic valve replacement
may not lead to a significant improvement in LV systolic function.
Valve replacement has not been shown to be of benefit in this
group and medical heart failure treatment is recommended.54
Thus, this diagnostic distinction has important clinical relevance.
Low dose dobutamine ( 20ug/kg/min) increases myocardial contractility by recruiting myocardial reserve
LV FLOW RESERVE PRESENT - Stroke Volume has to increase from baseline by 20 %
A patient with a low ejection fraction but a resting AS velocity>_4.0
m/s or mean gradient >_40mmHg generally does not have impaired
LV systolic function. The ventricle is demonstrating a normal response
to high afterload (severe AS), and ventricular function will improve
after relief of stenosis. This patient does not need a stress
echocardiogram.
(Qmean) was determined by integrating the area under the flow curve and dividing it by the measured systolic ejection time. The mean pressure gradient (Δpmean) was calculated by integrating the difference between ventricular and aortic pressure throughout systole and dividing it by the ejection period.