This is my presentation on updated guidelines on echo assessment of aortic stenosis (EACVI/ASE) to echo department of my institute.

1. How to echo series…..
AORTIC STENOSIS
Practical considerations..
Stepwise approach…
Integrative algorithm….
Dr.VinayakVadgaonkar

2. OUTLINE
Morphology
Basic assessment of severity – Level 1 recommendation
Alternate measures – Level 2 recommendation
Experimental descriptors of severity – Level 3 recommendation
Echocardiographic discordance ; Special subgroups
New Classification (Flow/Gradient/AVA/EF)
LV assessment
Ascending aorta
Essential hypertension
Integrated Algorithm
Suggested stepwise approach
Case studies

3. MORPHOLOGY
 The most common causes of valvular AS are
calcific stenosis of a tricuspid valve, a bicuspid
aortic valve with superimposed calcific
changes, and rheumatic valve disease.
 Zoomed view of PLAX/SAX is usually
sufficient.
 Start the anatomic evaluation by counting the
number of cusps and commissures/and or
raphe if present.(In systole).
 Comment on cusp mobility, thickness and
calcification.
 TEE better than TTE for assessment of
phenotype

4. Aortic valve calcification
 Defined as calcium deposition on aortic valve leaflets, as tiny spots or up
to extensive calcification greatly affecting the mobility of the valve
leaflets. On echocardiographic images, it presents as high echogenic
(white) spots found on the valve leaflets.
 El-Yousry 2012 developed a 5 score AVC system.
 A still frame of the aortic valve in the parasternal short axis view at the
end-diastolic phase with fully closed aortic valve leaflets was used to
score AVC by assigning a single score to the whole valve.
 Semi-quantitative AVC assessment of real-time cine loops from both TEE
and TTE correlated well with intra-operative evaluation of AVC. Applying
a predefined scoring system for AVC evaluation assures a high
interobserver correlation.

5. 1 Normal leaflets with no evidence of
thickening or calcification
2 Evidence of thickening (sclerosis), but
no evidence of calcification
3 Calcification (small calcium spot(s) not
exceeding one-third of the leaflet area)
4 Moderate calcification (calcification
not exceeding two-thirds of the leaflet
area)
5 Heavily calcified (calcification covering
more than two-thirds of the leaflet area
AVC GRADE DESCRIPTION

6. Basic assessment of severity Alternate measures of severity
Level 1 Recommendations
 Peak velocity
 Mean transaortic pressure
gradient
 Effective orifice area by CE
Level 2 Recommendations
Simplified CE
Velocity/VTI ratio
AVA planimetry

7. PEAKVELOCITY
 Multiple acoustic windows to acquire the highest velocities
and to use and report the same window in sequential studies.
 Aortic jet occurs in 3 dimensions and is unpredictable;
Therefore careful patient positioning with adjustment of
transducer position and angulation. No angle correction.
 A dedicated small dual-crystal CWDtransducer (pencil or
PEDOFpulse echo Doppler flow velocity meter probe) is
strongly recommended.
 High wall pass filters; Lower gains; sweep speed of 50-
100mm/s.
 Averaging of 3 beats in NSR/5 beats in AF.
 The shape of the CWD velocity curve is helpful in
distinguishing the level and severity of obstruction..
 The shape of the CWD velocity curve also can be helpful in
determining whether the obstruction is fixed or dynamic.

8. Mean transaortic pressure gradient (Sources of errors)
 Misalignment of the ultrasound beam with the AS jet results in significant
underestimation of jet velocity…importance of multiple acoustic window
 Neglect of elevated proximal velocity.
The peak gradient calculated from the maximum Doppler velocity represents the
maximum instantaneous pressure difference across the valve, not the difference between
the peak left ventricular (LV) and peak aortic pressure that is commonly measured from
the pressure tracings.
When the ascending aorta is < 30 mm, one should be aware that the initial pressure drop
from LV to theVC by echo, may be significantly higher than the actual net pressure drop
between the LV and the ascending aorta, which represents the pathophysiologically
relevant measurement.MG can be overestimated if PR is significant.
Inadvertent recording of MR signal.(Both are systolic/high velocity/directed away fromTx)

9. AS jet vs MR jet
AS jet
Shape – Early systolic peak “v”
shaped;exception critical AS
Duration – AS<MR;No flow
during isovolumic signals
Diastolic signals – Mitral inflow
not continuous with AS
Velocity – MR>AS
MR jet
Shape – Mid to late systolic peak
“parabolic” except in acute severe
MR
Duaration – MR>AS ;Includes
IVRT/IVCT
Diastolic signals – Mitral inflow
continuous with MR
Velocity – MR>AS;Possible to
calculate AS MG from MR jet

10. Aortic valve area by CE
SVAV = SVLVOT
AVA X VTIAV =CSALVOT X VTILVOT
AVA = CSALVOT X VTILVOT
VTIAV

11. AVA by CE “Sources of error”
 LVOT is not circular but elliptical.....Underestimation of LVOT CSA- SV-AVA( by
0.2sqcm)
 It is difficult to ensure that LVOTd and velocity are measured at same level due to
flow acceleration.
 In some patients calcium may extend from the aortic annulus to the base of the
AML and protruding into the LVOT might yield an incorrectly small LVOT
diameter.
 LVOT dimeter in sigmoid septum.
 Sometimes image quality is suboptimal and LVOT imaged more clearly at end-
diastole.

12. AVA by CE “Sources of error”
Interobserver measurement variability for LVOT diameter ranges from 5 to 8%.
With dynamic subaortic obstruction or a subaortic membrane, SV calculations at
this site are not accurate.
Combined AS/AR high subaortic flow rates may result in a skewed flow profile
across the outflow tract that may limit the accuracy.
When LVOT velocity must be measured with some distance to annulus owing to
flow convergence, the velocity profile may no longer be flat but rather skewed
with highest velocities present at the septum.
With a dilated LVOT, centrally measured velocities may also be significantly higher
than the average velocity across the LVOT, which may result in SV and AVA
overestimation

13. Alternate measures of severity
Simplified CE AVA = CSALVOT* VLVOT/VAV:
• The ratio of LVOTVTI to aortic jetVTI is nearly identical to the ratio of the LVOT maximum velocity to
aortic jet maximum velocity.
• SV assessment has become standard and is of utmost importance in low gradient AS, requiringVTI
measurements.
Velocity ratio/VTI ratio VR=VLVOT/VAV ;VTI ratio =VTILVOT/VTIAV
• This dimensionless velocity orVTI ratio expresses the size of the valve effective area as a proportion of the
CSA of the LVOT.
• In the absence of valve stenosis, the velocity ratio approaches 1,with smaller numbers indicating more
severe stenosis
AVA planimetry
• TEE should be used. Calcification causes acoustic shadows/reverbations.
• Ensure that the minimal orifice area is identified rather than the larger area proximal to the cusp tips.
• EOA is significantly smaller than the anatomic AVA because of flow contraction.

14. Experimental descriptors of severity
(Actually very useful….)
Valvuloarterial impedence
Global systolic load imposed lo the LV, where the numerator represents an accurate
estimation of total LV pressure.
• MG+SBP/SVi ; >5-5.5mmhg/ml/m2
Projected Aortic valve area
Estimation ofAVA at normal flow rate by plottingAVA vs. flow and calculating the slope of
regression (DSE).Accounts for the variable changes in flow during DSE in low flow, low
gradientAS, provides improved interpretation of AVA changes.
• AVAPROJ = AVAREST +VC*(250-QREST)
Aortic valve resistance –
Resistance to flow caused by AS, assuming the hydrodynamics of a tubular (non flat)
stenosis Initially suggested to be less flow-dependent in low-flowAS.
• (MG/Q)*1333 ; Q = SV/ET

15. Experimental descriptors of severity
(Actually very useful….)
 LV Stroke work loss %
• Work of the LV wasted each systole for flow to cross the aortic valve, expressed as
% of total systolic work.Very easy to measure. Related to outcome in one
longitudinal study.
• (MG/MG+SBP) ; >25% is significant
Recovered pressure gradient
Energy loss index

16. RECOMMENDATIONS FOR GRADING AS SEVERITY
Aortic Sclerosis Mild Moderate Severe
Peak velocity (m/s) <= 2.5 m/s 2.6–2.9 3.0–4.0 >= 4
Mean gradient (mmHg) - <20 20-40 >=40
AVA (cm2 ) - > 1.5 1.0 - 1.5 < 1.0
Indexed AVA (cm2/m2) - >0.85 0.60 - 0.85 < 0.6
Velocity ratio - > 0.50 0.25 - 0.50 < 0.25
CONCORDANCE

17. ASSESSMENT OF FLOW IN AORTIC STENOSIS
Transaortic flow =Transaortic Stroke volume = 0.785D2*LVOTvti/BSA.
 Normal flow (35-58)ml/m2 ; Low flow state <35ml/m2.
In clinical practice, the diagnosis of low flow AS is most secure if multiple approaches
to calculation of SVi yield similar results.
Although 2D and 3D echocardiographic measurement of LV EDV and ESV to calculate
SV is not affected by LVOT geometry, this approach also can underestimate SV.
Reasonable explanation of low flow state like concentric remodeling with small
volumes and hypertrophied ventricles; Severe LV systolic dysfunction.
Technical reasons for low flow state include elliptical LVOT shape; small body size and
severe hypertension during study.
With increasing severity of AS, the ejection time may prolong and even patients with a
normal SV may indeed have reduced transvalvular flow.
In that case ,Calculate transaortic flow rate –SV/ET; Normal (220-240)ml/s

18. DISCORDANT CRITERIA
GRADIENT PEAKVELOCITY AVA VELOCITY RATIO
Clinical scenarios
MG>40mmhg ; PV>4m/s ; AVA>1sqcm MG<40mmhg ; PV<4Am/s ; AVA<1sqcm
When this happens get systematic
First step is to review your old images and Doppler for measurement errors
Inconsistencies in cut off values for AVA and velocity/gradient

19. Resolution of the discrepencies
MG>40mmhg ; PV>4m/s ; AVA>1sqcm
• Recheck LVOT diameter with
previous studies comparison.
• LVOT velocity signal for flow
acceleration.
• Indexed AVA if BSA<1.5sqcm/
BMI<22.
• AR severity
• High flow states/high CO like
Anemia,AV shunts,large body size.
MG<40mmhg ; PV<4Am/s ; AVA<1sqcm
• Recheck LVOT diameter with
previous studies comparison.
• LVOT velocity signal for distance
from the valve.
• Indexed AVA if BSA<1.5sqcm/
BMI<22.
• MR severity
• Associated Mitral stenosis

20. THE DISCORDANT SUBGROUPS
Low Flow Low Gradient AS with Reduced EF
Effective AVA <1.0 cm2.
Mean aortic transvalvular pressure gradient <40 mmHg.
LVEF <50%.
SVi < 35 mL/m2.
Low Flow Low gradientAS with Preserved EF
Everything same as above except LVEF > 50%
Normal Flow Low gradientAS with Preserved EF
Effective AVA < 1sqcm
Mean aortic transvalvular pressure gradient <40 mmHg
LVEF >50%
Svi (35-58)ml/m2

22. DECISION MAKING IN LF/LG SEVERE ASWITH LOW LVEF

23. DECISION MAKING IN LF/LG SEVERE AS WITH PRESERVED EF

24. AV EOA <1sqcm
FLOW GRADIENT EJECTION FRACTION
Normal
Flow( 35-
58)ml/m2
Low
Flow<35ml/
m2
HIGH LOW < 50% > 50 %
PV <=4 m/s
MG< 40mmhg
PV >=4 m/s
M> 40mmhg
NEW CLASSIFICATION BASED ON GUIDELINES

25. LV ASSESSMENT
LV geometry parameters – RWT and LV mass by linear methods.
Concentric LVH~NF/HGAS nEF; Eccentric LVH~LF/LGAS lEF; Concentric remodelling PLF/LG AS
nEF; Normal geometry – NF/LGAS nEF
LVEF Biplane Simpson's / 3D / Flow estimation (<35ml/m2).
MAPSE – Related to LV subendocardial fibrosis.Value of <9mm had an excellent accuracy to
differentiate between moderate and severe aortic stenosis.
TDI S` velocity low values with stress; No absolute cut off values.
GLPSS from STE
< 13% Basal segments - Cardiac events
< 15.9% Average GLPSS – Cardiac events
<18% Predicted abnormal exercise response (Sen;68%/Spec 77%)
Impaired circumferential strain – Advanced stage of the disease
 LV diastolic function parameters
E/ septal E`>13 ~ PCWP 15mmhg ; Indexed LA area >12cm2/m2
Increased LV torsion and delayed LV diastolic untwisting.

26. LV FIBROSIS ASSESSMENT
Development of diffuse fibrosis has emerged as a key mechanism for the
progression of heart failure in AS and a potential treatment target.
LGE CMR is the gold standard.
Integrated calibrated ultrasonic backscatter; Not in clinical practice.
There are 3 reproducible indirect estimates :
a. BNP
b. MAPSE Indirect evidence/surrogate marker ?Longitudinal function
c. STE Strain Peak systolic LS <-11.6% predicted myocardial fibrosis (>10% LGE
CMR) with Sen/Spe of 65%/75%.

27. Av GLPSS-15.9%

28. Ascending aorta in AS
DILATATION OF ASCENDINGAORTA
 In addition to evaluation of AS aetiology and haemodynamic
severity, the echocardiographic evaluation of adults with
aortic valve disease should always include careful evaluation
of the aorta with measurement of diameters at the sinuses
of Valsalva, the sinotubular junction and the ascending
aorta.
 Dilation of the aortic root and/or the tubular ascending aorta
is associated with bicuspid aortic valve disease and aortic
size may impact the timing and type of intervention.
 Normal value for AA
Males 3.0+_0.4cm / Indexed 1.5+_0.2cm/m2
Females 2.7+_0.4cm / Indexed 1.6+_0.3cm/m2

29. Small Ascending aorta <3Omm
 In patients with small AAs (STJ/AA) and doppler EOA between 0.8-
1.2sqcm, measurement of EOA by Doppler echocardiography may
lead to over-estimation of severity.
 As blood flow velocity decelerates between the valve and the
ascending aorta, part of the kinetic energy is reconverted back to
static energy due to a phenomenon called pressure recovery, and
hence the net gradient recorded at catheterization is always less than
the maximum pressure gradient measured by Doppler.
 Pressure recovery can be accounted by following formulae :
Recovered pressure gradient = 4v2*2(AVA/AAA)*(1-AVA/AAA)
Energy loss coefficient (ELCO) = (AAA*AVA)/(AAA-AVA)/BSA
( <0.5-0.6sqcm/m2) significant
 Short cut http://www.parameterz.com/tools/aortic-valve-area-and-
pressure-recovery.
 The stroke work loss, which is the ratio of the mean transvalvular
gradient to the estimated LV systolic pressure, is another index that
indirectly accounts for the pressure recovery

30. Hypertension in Aortic stenosis
 Concomitant arterial hypertension is found to be present in a large proportion (35% to
51%) of patients with AS.
Symptoms of AS develop at a lower degree of stenosis severity in hypertensive patients,
most likely because of the additional hemodynamic load due to hypertension.
It should be emphasized that a normal blood pressure does not exclude an increase in
vascular load since these pressures may be pseudo-normalized in up to 30% of patients
with decreased systemic arterial compliance due to LV dysfunction and a concomitant
decrease in cardiac output.
 Given that hypertension may interfere with the assessment ofAS severity and that there
is no easy means of correcting for this distortion, the increase in global hemodynamic load
can be ascertained by 2 variables :
Total Systemic arterial compliance – (indexed SV/PP) ; Abnormal-<0.6ml/m2/mmhg
Systemic vascular resistance – 80*(MAP)/CO ; Abnormal - >2000 dynes/s/cm5

31. Normal flow low gradient AS (almost always moderate )

32. Integrated Algorithm

33. Suggested stepwise algorithm for our echo lab
Look at the valve
If there is calcification, grade it
Assess loading conditions (BP/HR/Associated conditions)
Spend time on LVOT diameter/SV assessment
Estimate flow/transaortic flow rate in all patients
Report the same window for peak velocities/MG in sequential studies
Grade AS by new classification
If Ascending aorta < 3cm,account for PR
If BP >140/90mmhg,account for vascular load
EF by Biplane Simpsons/GLPSS in all patients

34. CASE 1
53 years/Bah/Male
CRHD
Status post Mitral valve replacement 1988;Jordan;Bileaflet mechanical
valve
Chronic paroxysmal Atrial fibrillation
Followed up in our clinic with Aortic stenosis and aortic regurgitation
Labelled as asymptomatic severe Aortic stenosis
Good functional capacity 10 METS
Referred for Stress echo

39. Echo Report RelevantTo Aortic Stenosis
Peak velocity 6.01m/s
Peak / Mean transaortic gradient 144/71mmhg (Right parasternal)
Flow 42.5ml/m2
Effective orifice area 0.5sqcm
Moderate Aortic regurgitation
Biplane Simpson,s LVEF 60%
Subendocardial longitudinal function GLPSS -14.9%
Stress response
• Hypotension 212/100mmhg – 123/71mmhg;NSVT
Final diagnosis: Normal flow high gradient critical rheumatic
Aortic stenosis with abnormal stress response

40. CASE 2
43 years/Bah/Male
Type 2 DM/Essential HTN/Dyslipidemia
Chronic heavy smoker
CAD History-PCI to LCX (2014);PCI to PDA (2015)
Echo in June 2015
Type A BAV with superimposed calcification. AA 3cm
MG 28mmhg;PV 3.1m/s;EOA-0.99sqcm;VR- 0.28;LVEF 60%
Ambiguous/Equivocal symptoms
Referred for Stress echo for ischemia assessment

44. Echo Report RelevantTo Aortic Stenosis
TypeA BAV with Grade 5 calcification (El-yousry classification)
Peak velocity –
Peak/mean transaortic gradient -80/47mmhg
Flow
Effective orifice area- 0.8sqcm
VTI Ratio 0.25
Biplane Simpson’s LVEF-50% ;Subendocardial LV function GLPSS -15.8%
Final diagnosis :Normal flow high gradient severe calcific Aortic
stenosis
Stress echo deferred; referred back to team.

45. CASE 3
75 years/Bah/Male
Type 2 DM/Essential HTN/Dyslipidemia
Type AWPW syndrome
Non-critical double vessel disease 2009
Prior echo
• Normal LV sizeWMAs in LCX/RCA territory. LVEF 55%
• AV tricuspid and calcified; PV-3.4m/s; MG 27mmhg;EOA 0.8sqcm;VR 0.26
• AA is 2.7cm
• Preserved LV function 60%
Referred for Stress echo

50. Key in this patient is AA of 2.7cm
Baseline hemodynamics
Peak velocity 3.8m/s ; Peak/mean gradient 51/30mmhg
Stroke volume 78.5ml ; Flow 47ml/m2; Transvalvular flow rate 244ml/s
AVA CE 0.9sqcm ;VR 0.31
Since AA < 3cm
• Energy loss index 0.74cm2/m2
• Adjusted AVA 1.19sqcm
• Recovered Pressure gradient 16mmhg;Net recovery 41mmhg
• Preserved GLPSS of -24.7%
Final diagnosis : Normal flow Low gradient Moderate Aortic stenosis

51. THANK YOU
For patient listening……