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ASSESSMENT OF AS
SEVERITY AND WHEN
TO INTERVENE ?
Presenter - Dr.R.SPANDANA, 2nd year postgraduate
EPIDEMIOLOGY
1-2 % aged 65 or older
12 % aged 75 or older
3.4% aged older than 75 had severe AS.
Rate of progression from aortic sclerosis to stenosis –
1.8% to 1.9% per year.
Braunwald 12th edition pg 1399
Valvular AS – 3 principal causes:
A congenital bicuspid valve with superimposed
calcification,
calcification of a normal trileaflet valve,
and rheumatic disease.
AS – severe atherosclerosis of the aorta and aortic valve
(rare – homozygous type II hyperlipoproteinemia, severe
hypercholesterolemia)
Fixed obstruction to left ventricular (LV)
outflow
Above the valve (supravalvular stenosis)
Below the valve (discrete subvalvular stenosis)
Dynamic subaortic obstruction - caused by
hypertrophic cardiomyopathy
Unicuspid, bicuspid, tricuspid, & quadricuspid.
Unicuspid valves usually are severely narrowed at birth and
produce symptoms in infancy.
Normal aortic valve
Congenital bicuspid
aortic stenosis. A false raphe is present at
6 o’clock.
Rheumatic aortic stenosis. The
commissures are fused with a fixed
central orifice.
Calcific aortic stenosis
Generally, repeat imaging is performed every 6 to 12
months for severe AS, every 1 to 2 years for moderate AS,
and every 3 to 5 years for mild AS,
ESC 2021 GUIDELINES ON VALVULAR HEART DISEASE
Severity depends upon measurement of mean pressure
gradient (the most robust parameter), peak transvalvular
velocity (Vmax), and valve area.
Discordant cases should take account of additional parameters:
functional status, stroke volume, Doppler velocity index,156
degree of valve calcification, LV function, the presence or
absence of LV hypertrophy, flow conditions, and the adequacy
of BP control.
Natriuretic peptides –predict
free survival and outcome in
normal and low-flow severe
aortic stenosis
Exercise testing may
unmask symptoms and is
recommended for
risk stratification of
asymptomatic patients with
severe aortic stenosis.
Exercise echocardiography
provides additional
prognostic
information by assessing the
increase in mean pressure
gradient and change in LV
function.
Diagnostic workup
CCT is the preferred imaging tool to assess:
(i) aortic valve anatomy,
(ii) annular size and shape,
(iii) extent and distribution
of valve and vascular calcification,
(iv) risk of coronary ostial obstruction,
(v) aortic root dimensions, (vi) optimal fluoroscopic projections
for valve deployment, and (vii) feasibility of vascular access (femoral,
subclavian, axillary, carotid, transcaval or transapical).
Myocardial fibrosis is a major driver of LV decompensation in
aortic stenosis (regardless of the presence or absence of CAD),
which can be detected and quantified using CMR.
Amyloidosis is also frequently associated with aortic stenosis in elderly patients
(incidence 9 - 15%).
When cardiac amyloidosis is clinically suspected, based on symptoms
(neuropathy and hematologic data), diphosphonate scintigraphy and/or CMR
should be considered
Clinical, anatomical and procedural factors that
influence the choice of treatment modality for an individual
The prognosis of patients with normal-flow, low-gradient
aortic
stenosis and preserved ejection fraction is similar to that of
moderate aortic stenosis—regular clinical and
echocardiographic surveillance is recommended
Special patient populations
CAD and aortic stenosis frequently coexist.
Both simultaneous SAVR and CABG, and SAVR late after CABG, carry a
higher procedural risk than isolated SAVR.
Patients aged <70 years with mean gradient progression >5 mmHg/year
benefit from SAVR at the time of CABG once baseline peak gradient
exceeds 30 mmHg. ESC 2021 VALVULAR HEART DISEASE GUIDELINES
PCI and TAVI - Combined or staged
SURTAVI trial, there was no significant difference in the
primary endpoint (all-cause mortality or stroke at 2-year
follow-up) in intermediate-risk patients with severe aortic
stenosis and noncomplex CAD (SYNTAX score <22)
undergoing either TAVI and
PCI or SAVR and CABG [16.0% (95% CI, 11.122.9) vs.
14% (95% CI, 9.221.1); P= 0.62].
ESC LVEF <55% (IIA)
DECISION MAKING?
CASE #1 : ASYMPTOMATIC PATIENT WITH SEVERE AS
(STAGE C 1)
75 YEAR old women with calcific AS
Asymptomatic (confirmed by ETT)
BNP :190pg/ml
LVEF:60%
Grading of AS severity on ECHO:
Severely calcified valve
Peak jet velocity :5.1m/s (1 year ago:4.8m/s)
Peak/mean gradient : 104/64 mmHg
AVA:0.65 cm² Indexed AVA:0.35cm²/m²
Clinical dilemma in true asymptomatic severe AS
( C1 stage)
Early << Prophylactic >> AVR?
Or
Watchful waiting?
CASE 2#
82 year woman,
HTN – ACEI
No CAD
NYHA III, HF hospitalization
LVEF – 65%
Global longitudinal strain : 13%
Grade 2 diastolic dysfunction
Echo: AVA :0.64 cm2, iAVA:0.36cm2/m2
Doppler velocity index :0.19
Peak/mean gradient : 44/26mmHg
SVI: 29 ml/m2
Paradoxical low flow, low gradient
Class I indication of AVR (2021 – ACC-AHA)
CASE 3:
AC01.0005011140
74 YEAR OLD,
DM
ANEMIA
EF-60%
Asymptomatic
Exercise testing: normal
Next year came with symptoms
Echo:
AVA : 0.9cm2,
Peak/mean gradient : 107/67mmHg
CASE 4
AC01.0003681487
Name: ABC
Age: 84 years, female
Asymptomatic severely calcified AS
ACS-NSTEMI
NSVT, Paroxysmal AF
HFpEF
NTproBNP: 9620 pg/ml
ECHO: E/e: 22.5
PG: 123 mmHG, MG : 73 mmHG
AVA : 0.5 cm2

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AORTIC STENOSIS ECHO CARDIOLOGY/MEDICINE.PPTX

  • 1. ASSESSMENT OF AS SEVERITY AND WHEN TO INTERVENE ? Presenter - Dr.R.SPANDANA, 2nd year postgraduate
  • 2. EPIDEMIOLOGY 1-2 % aged 65 or older 12 % aged 75 or older 3.4% aged older than 75 had severe AS. Rate of progression from aortic sclerosis to stenosis – 1.8% to 1.9% per year. Braunwald 12th edition pg 1399
  • 3. Valvular AS – 3 principal causes: A congenital bicuspid valve with superimposed calcification, calcification of a normal trileaflet valve, and rheumatic disease. AS – severe atherosclerosis of the aorta and aortic valve (rare – homozygous type II hyperlipoproteinemia, severe hypercholesterolemia)
  • 4. Fixed obstruction to left ventricular (LV) outflow Above the valve (supravalvular stenosis) Below the valve (discrete subvalvular stenosis) Dynamic subaortic obstruction - caused by hypertrophic cardiomyopathy
  • 5. Unicuspid, bicuspid, tricuspid, & quadricuspid. Unicuspid valves usually are severely narrowed at birth and produce symptoms in infancy.
  • 6. Normal aortic valve Congenital bicuspid aortic stenosis. A false raphe is present at 6 o’clock.
  • 7. Rheumatic aortic stenosis. The commissures are fused with a fixed central orifice. Calcific aortic stenosis
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  • 9. Generally, repeat imaging is performed every 6 to 12 months for severe AS, every 1 to 2 years for moderate AS, and every 3 to 5 years for mild AS, ESC 2021 GUIDELINES ON VALVULAR HEART DISEASE
  • 10. Severity depends upon measurement of mean pressure gradient (the most robust parameter), peak transvalvular velocity (Vmax), and valve area. Discordant cases should take account of additional parameters: functional status, stroke volume, Doppler velocity index,156 degree of valve calcification, LV function, the presence or absence of LV hypertrophy, flow conditions, and the adequacy of BP control.
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  • 17. Natriuretic peptides –predict free survival and outcome in normal and low-flow severe aortic stenosis Exercise testing may unmask symptoms and is recommended for risk stratification of asymptomatic patients with severe aortic stenosis. Exercise echocardiography provides additional prognostic information by assessing the increase in mean pressure gradient and change in LV function.
  • 18. Diagnostic workup CCT is the preferred imaging tool to assess: (i) aortic valve anatomy, (ii) annular size and shape, (iii) extent and distribution of valve and vascular calcification, (iv) risk of coronary ostial obstruction, (v) aortic root dimensions, (vi) optimal fluoroscopic projections for valve deployment, and (vii) feasibility of vascular access (femoral, subclavian, axillary, carotid, transcaval or transapical).
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  • 20. Myocardial fibrosis is a major driver of LV decompensation in aortic stenosis (regardless of the presence or absence of CAD), which can be detected and quantified using CMR. Amyloidosis is also frequently associated with aortic stenosis in elderly patients (incidence 9 - 15%). When cardiac amyloidosis is clinically suspected, based on symptoms (neuropathy and hematologic data), diphosphonate scintigraphy and/or CMR should be considered
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  • 23. Clinical, anatomical and procedural factors that influence the choice of treatment modality for an individual
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  • 26. The prognosis of patients with normal-flow, low-gradient aortic stenosis and preserved ejection fraction is similar to that of moderate aortic stenosis—regular clinical and echocardiographic surveillance is recommended
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  • 33. Special patient populations CAD and aortic stenosis frequently coexist. Both simultaneous SAVR and CABG, and SAVR late after CABG, carry a higher procedural risk than isolated SAVR. Patients aged <70 years with mean gradient progression >5 mmHg/year benefit from SAVR at the time of CABG once baseline peak gradient exceeds 30 mmHg. ESC 2021 VALVULAR HEART DISEASE GUIDELINES
  • 34. PCI and TAVI - Combined or staged SURTAVI trial, there was no significant difference in the primary endpoint (all-cause mortality or stroke at 2-year follow-up) in intermediate-risk patients with severe aortic stenosis and noncomplex CAD (SYNTAX score <22) undergoing either TAVI and PCI or SAVR and CABG [16.0% (95% CI, 11.122.9) vs. 14% (95% CI, 9.221.1); P= 0.62].
  • 35. ESC LVEF <55% (IIA)
  • 37. CASE #1 : ASYMPTOMATIC PATIENT WITH SEVERE AS (STAGE C 1) 75 YEAR old women with calcific AS Asymptomatic (confirmed by ETT) BNP :190pg/ml LVEF:60% Grading of AS severity on ECHO: Severely calcified valve Peak jet velocity :5.1m/s (1 year ago:4.8m/s) Peak/mean gradient : 104/64 mmHg AVA:0.65 cm² Indexed AVA:0.35cm²/m²
  • 38. Clinical dilemma in true asymptomatic severe AS ( C1 stage) Early << Prophylactic >> AVR? Or Watchful waiting?
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  • 40. CASE 2# 82 year woman, HTN – ACEI No CAD NYHA III, HF hospitalization LVEF – 65% Global longitudinal strain : 13% Grade 2 diastolic dysfunction Echo: AVA :0.64 cm2, iAVA:0.36cm2/m2 Doppler velocity index :0.19 Peak/mean gradient : 44/26mmHg SVI: 29 ml/m2
  • 41. Paradoxical low flow, low gradient Class I indication of AVR (2021 – ACC-AHA)
  • 42. CASE 3: AC01.0005011140 74 YEAR OLD, DM ANEMIA EF-60% Asymptomatic Exercise testing: normal Next year came with symptoms Echo: AVA : 0.9cm2, Peak/mean gradient : 107/67mmHg
  • 43. CASE 4 AC01.0003681487 Name: ABC Age: 84 years, female Asymptomatic severely calcified AS ACS-NSTEMI NSVT, Paroxysmal AF HFpEF NTproBNP: 9620 pg/ml ECHO: E/e: 22.5 PG: 123 mmHG, MG : 73 mmHG AVA : 0.5 cm2