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MOHAMMAD TARIQ ALI
Epidemiology -
 1-2 % age 65 yr or older & 12 % age 75 yr or older
 Aortic valve sclerosis without stenosis –irregular
thickening or calcification - 9 % at mean age 54 yr to
42% at mean age 81 yr
 Rate of progression from sclerosis to stenosis – 1.8%/yr
Aortic stenosis: Classification based on location
Valvular-
most common type.
Subvalvular.
Supravalvular.
Valvular Aortic Stenosis: Etiology
Calcific Aortic Stenosis of trileaflet valve
Bicuspid Aortic Valve
Bicuspid Aortic Valve
Rheumatic aortic stenosis
Subvalvular aortic stenosis
Supravalvular aortic stenosis
Congenital aortic valve disease -
 M/C Abnormality –failure of cusp formation
 bicuspid ,Uncuspid , quadricuspid , dome shaped
diaphragm
Quantitation of aortic stenosis severity
 Standard evaluation of stenosis severity includes-
(EAE/ASE Recommendations for Clinical Practice 2009).
1. Maximum aortic jet velocity ( Vmax)
2. Mean transaortic pressure gradient
3. Continuity equation valve area ( EOA)
Classification of ASseverity
(based on 2014 AHA/ACC Valvular heart diseaseguideline)
Peak transvalvular velocity measurement
Peak transvalvular velocity
Peak transvalvular velocity
Mean transvalvular gradient
Mean transvalvular gradient
Sources of error for pressure
gradient calculations
Sources of error for pressure gradient
calculations
Aortic valve area Continuity equation
Aortic valve area Continuity
equation
Advantage of the Continuity Equation over
Peak velocity Pressure gradient
Pitfalls of the Continuity Equation
Pitfalls of the Continuity Equation
Other indicies of severity of AS
 Simplified continuity equation
AVA = LVOT area X LVOT velocity / AS velocity
 Dimentionless index = LVOT VTI / AS VTI
< 25 % of the normal i.e o.75 – 1.0 cm2 - severe AS ( NORMAL 3-4 sq cm )
 Planimetry of Aortic anatomicvalve area – difficult in
severe calcified valve – 3D > 2D , TEE>TTE
 Projected Ao Valve area at normal flow-
AVAPROJ = AVAREST - VC (250 - Qbasal ) @ DSE
 Valvoarterial impedence (Zva) =mmHg/ml/sq m
Zva = Pmean + SBP / SV index
Used in special condition -
 LV STROKE WORK LOSS
 RECOVERED PRESSURE GRADIENT
 ENERGY LOSS INDEX
 AORTIC VALVE RESISTANCE
3 variants of severe AS-
1. NORMALFLOW–HIGH GRADIENT SEVERE AS WITH NORMAL EF (
stage c & d1)
2. CLASSIC– LOWFLOW–LOWGRADIENT SEVERE AS WITH REDUCED
EF ( <50%) ( stage d2)
(A) TRUE
(B) PSEUDO
3. PARADOXICALLOWFLOW–LOWGRADIENT SEVERE AS WITH
NORMAL EF(stage d3)
Classic LG-LF severe AS with low EF
(STAGE D2 ) -
 EOA < 1.0 cm2
 iEOA < 0.6 cm2 /m2
 Low mean trans valvular gradient < 40 mmHg
 Low EF < 40 %
 Low flow – Cardiac index < 3 L/min/m2
stroke volume index < 35ml /m2
2 types – TRUE & PSEUDO (20-30%)
 TRUE severe AS – LG/LF- 1’ Culprit valve ds
LV dysfunction -2’ or concomitant
benefits from AVR
 PSEUDO severe AS – LG/LF – 1’ Myocardial ds
AS severity is overestimated d/t incomplete
opening of Ao valve in relation to LF state
may NOT benefit from AVR
LV Flow reserve –
 Percentage increase in stroke volume > 20% during
DSE or catheterization k/a flow reserve & carries
better prognosis & lesser operative mortality than No
flow reserve ( <20%) which has higher prevalence of
multivessel CAD
 Imp predictor of operative risk & survival after AVR
DOBUTAMINE STRESS ECHO -
 To differentiate b/w true & pseudo ( ACC/AHA-
ESC/EACTS Class II a (LOE-B )
 To assess LV flow reserve
 pseudo AS- peak stress mean gradient <30 or 40
mmHg , peak stress EOA >1.0 or 1.2 cm2 &/or absolute
incr EOA >0.3 cm2, Vmax < 4 m/sec
 Results – EOA <1 cm2 , Vmax >4 m/sec , any flow-true
EOA <1 cm2 , Vmax < 4 m/sec –persistant
area – gradient mismatch
NEWER parameter
 PROJECTED EOA – ambiguous response of DSE d/t
unpredictability of flow augmentation
TOPAS study ( true or pseudosevere AS )
At standard flow rate of 250ml/sec ESP severe AS with
no contractile reserve
 Mutislice CT
>1650 Agatston
Unit
NEWER CLASS-
Paradoxical LF-LG Severe AS ( stage D3) -
 Normal EF ( >50%)
 Pronounced LV concentric remodelling
 Small LV cavity size
 Restricted physiology leading to impaired LV filling
 Altered myocardial function
 Low flow with normal EF –Under estimation of AS
 Worse prognosis
 Parameters :- EOA < 1.0 cm2 , i EOA <0.6 cm2/m2 ,
restrictive physiology resulting into low CO ( <3
l/min/m2 or indexed SV < 35 ml/m2 ) & lower than
expected tranvalvular gradients (<40mm Hg) despite
the presence of preserved LVEF (>50%) -
LG/LF-AS-pEF - PARADOXICAL AS
Pathophysiology & clinical presentation of paradoxical
LG-LF AS -
 Many similarities with HFpEF = older age , female
gender , concomitant syst HTN , restrictive physiology
therefore LV pump function & stroke vol markedly
reduced despite preserved LVEF
 Distinctive feature – (1) more pronounced LV conc
remodelling & myocardial fibrosis- dec LV size ,
compliance & filling
(2)marked reduction of intrinsic LV function NOT
evident by LVEF but by more sensitive parameters like
GLS d/t advanced fibrosis in sub endocardial layers
So paradoxical AS represent advanced stage of both
valvular & ventricular ds despite normal LVEF
 Pseudo normalization of BP – d/t LF inspite of redu
systemic arterial compliance &/or incr vascular
resistance
 High Valvulo-Arterial impedence ( Zva )- global LV
hemodynamic load
 Severe ,normal flow , high gradient ,AS with normal
EF vs Paradoxical LG/LF severe AS with normal EF –
AVR ( Best Vs worst outcome ) , medical Vs surgical
 Class II a ( LOE –C) recently inspite of High Operative
mortality & increased chances of pt prosthesis
mismatch d/t small Lv cavity
TAKE HOME MASSAGE.....
 LF-LG AS with normal or reduced LVEF – most challenging
situation in valvular heart disease
 DSE greatly aid in risk stratification & clinical decision
 Valve calcium score- MD CT & plasma BNP helpful esp in
NO flow reserve pt with non dx DSE
 GLS has definite role in sub clinical systolic dysfunction &
early treatment in AS
 Paradoxical LG-LF Severe AS with Normal EF – recently
described entity with advanced ds & worse prognosis
 Role of TAVR – in LG/LG AS to be determined in future
Assessment of as

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Assessment of as

  • 2. Epidemiology -  1-2 % age 65 yr or older & 12 % age 75 yr or older  Aortic valve sclerosis without stenosis –irregular thickening or calcification - 9 % at mean age 54 yr to 42% at mean age 81 yr  Rate of progression from sclerosis to stenosis – 1.8%/yr
  • 3. Aortic stenosis: Classification based on location Valvular- most common type. Subvalvular. Supravalvular.
  • 5.
  • 6. Calcific Aortic Stenosis of trileaflet valve
  • 9.
  • 10.
  • 13.
  • 15. Congenital aortic valve disease -  M/C Abnormality –failure of cusp formation  bicuspid ,Uncuspid , quadricuspid , dome shaped diaphragm
  • 16.
  • 17.
  • 18. Quantitation of aortic stenosis severity  Standard evaluation of stenosis severity includes- (EAE/ASE Recommendations for Clinical Practice 2009). 1. Maximum aortic jet velocity ( Vmax) 2. Mean transaortic pressure gradient 3. Continuity equation valve area ( EOA)
  • 19. Classification of ASseverity (based on 2014 AHA/ACC Valvular heart diseaseguideline)
  • 20.
  • 24.
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  • 28. Sources of error for pressure gradient calculations
  • 29. Sources of error for pressure gradient calculations
  • 30. Aortic valve area Continuity equation
  • 31.
  • 32. Aortic valve area Continuity equation
  • 33.
  • 34. Advantage of the Continuity Equation over Peak velocity Pressure gradient
  • 35. Pitfalls of the Continuity Equation
  • 36. Pitfalls of the Continuity Equation
  • 37. Other indicies of severity of AS  Simplified continuity equation AVA = LVOT area X LVOT velocity / AS velocity  Dimentionless index = LVOT VTI / AS VTI < 25 % of the normal i.e o.75 – 1.0 cm2 - severe AS ( NORMAL 3-4 sq cm )  Planimetry of Aortic anatomicvalve area – difficult in severe calcified valve – 3D > 2D , TEE>TTE  Projected Ao Valve area at normal flow- AVAPROJ = AVAREST - VC (250 - Qbasal ) @ DSE  Valvoarterial impedence (Zva) =mmHg/ml/sq m Zva = Pmean + SBP / SV index
  • 38. Used in special condition -  LV STROKE WORK LOSS  RECOVERED PRESSURE GRADIENT  ENERGY LOSS INDEX  AORTIC VALVE RESISTANCE
  • 39. 3 variants of severe AS- 1. NORMALFLOW–HIGH GRADIENT SEVERE AS WITH NORMAL EF ( stage c & d1) 2. CLASSIC– LOWFLOW–LOWGRADIENT SEVERE AS WITH REDUCED EF ( <50%) ( stage d2) (A) TRUE (B) PSEUDO 3. PARADOXICALLOWFLOW–LOWGRADIENT SEVERE AS WITH NORMAL EF(stage d3)
  • 40.
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  • 42.
  • 43.
  • 44. Classic LG-LF severe AS with low EF (STAGE D2 ) -  EOA < 1.0 cm2  iEOA < 0.6 cm2 /m2  Low mean trans valvular gradient < 40 mmHg  Low EF < 40 %  Low flow – Cardiac index < 3 L/min/m2 stroke volume index < 35ml /m2 2 types – TRUE & PSEUDO (20-30%)
  • 45.  TRUE severe AS – LG/LF- 1’ Culprit valve ds LV dysfunction -2’ or concomitant benefits from AVR  PSEUDO severe AS – LG/LF – 1’ Myocardial ds AS severity is overestimated d/t incomplete opening of Ao valve in relation to LF state may NOT benefit from AVR
  • 46. LV Flow reserve –  Percentage increase in stroke volume > 20% during DSE or catheterization k/a flow reserve & carries better prognosis & lesser operative mortality than No flow reserve ( <20%) which has higher prevalence of multivessel CAD  Imp predictor of operative risk & survival after AVR
  • 47. DOBUTAMINE STRESS ECHO -  To differentiate b/w true & pseudo ( ACC/AHA- ESC/EACTS Class II a (LOE-B )  To assess LV flow reserve  pseudo AS- peak stress mean gradient <30 or 40 mmHg , peak stress EOA >1.0 or 1.2 cm2 &/or absolute incr EOA >0.3 cm2, Vmax < 4 m/sec  Results – EOA <1 cm2 , Vmax >4 m/sec , any flow-true EOA <1 cm2 , Vmax < 4 m/sec –persistant area – gradient mismatch
  • 48.
  • 49. NEWER parameter  PROJECTED EOA – ambiguous response of DSE d/t unpredictability of flow augmentation TOPAS study ( true or pseudosevere AS ) At standard flow rate of 250ml/sec ESP severe AS with no contractile reserve  Mutislice CT >1650 Agatston Unit
  • 50.
  • 51.
  • 52. NEWER CLASS- Paradoxical LF-LG Severe AS ( stage D3) -  Normal EF ( >50%)  Pronounced LV concentric remodelling  Small LV cavity size  Restricted physiology leading to impaired LV filling  Altered myocardial function  Low flow with normal EF –Under estimation of AS  Worse prognosis
  • 53.  Parameters :- EOA < 1.0 cm2 , i EOA <0.6 cm2/m2 , restrictive physiology resulting into low CO ( <3 l/min/m2 or indexed SV < 35 ml/m2 ) & lower than expected tranvalvular gradients (<40mm Hg) despite the presence of preserved LVEF (>50%) - LG/LF-AS-pEF - PARADOXICAL AS
  • 54. Pathophysiology & clinical presentation of paradoxical LG-LF AS -  Many similarities with HFpEF = older age , female gender , concomitant syst HTN , restrictive physiology therefore LV pump function & stroke vol markedly reduced despite preserved LVEF  Distinctive feature – (1) more pronounced LV conc remodelling & myocardial fibrosis- dec LV size , compliance & filling (2)marked reduction of intrinsic LV function NOT evident by LVEF but by more sensitive parameters like GLS d/t advanced fibrosis in sub endocardial layers So paradoxical AS represent advanced stage of both valvular & ventricular ds despite normal LVEF
  • 55.
  • 56.  Pseudo normalization of BP – d/t LF inspite of redu systemic arterial compliance &/or incr vascular resistance  High Valvulo-Arterial impedence ( Zva )- global LV hemodynamic load  Severe ,normal flow , high gradient ,AS with normal EF vs Paradoxical LG/LF severe AS with normal EF – AVR ( Best Vs worst outcome ) , medical Vs surgical  Class II a ( LOE –C) recently inspite of High Operative mortality & increased chances of pt prosthesis mismatch d/t small Lv cavity
  • 57.
  • 58. TAKE HOME MASSAGE.....  LF-LG AS with normal or reduced LVEF – most challenging situation in valvular heart disease  DSE greatly aid in risk stratification & clinical decision  Valve calcium score- MD CT & plasma BNP helpful esp in NO flow reserve pt with non dx DSE  GLS has definite role in sub clinical systolic dysfunction & early treatment in AS  Paradoxical LG-LF Severe AS with Normal EF – recently described entity with advanced ds & worse prognosis  Role of TAVR – in LG/LG AS to be determined in future