AoV assessment

Question 1

Causes of AI

Answer 1

o Degeneration → thickening
o Vegetative lesions → leaflet perforation/deformation
o Torn/flail cusps
o Congenital malformation of leaflets → inadequate coaptation
 Bicuspid AoV, rheumatic valve, calcific valve dz
o Aortic disease → annular dilation
 Marfan syndrome, cystic medial necrosis, familial Ao aneurysm, hypertension, systemic inflammatory dx

Question 2

Echo features of AI

Answer 2

o LV volume overload
o Valvular lesions
o Diastolic flutter of MV and AoV
o ↑EPSS

Question 3

2D/M-mode findings AI

Answer 3

valvular lesions
o Absence of lesion ≠ absence of dz
 Echo not sensitive to show lesions/nodules <2mm
o Degenerative lesions: typically small, smooth, rounded
o Vegetative lesions: large hyperechoic masses
 Floppy, prolapse in LVOT

• Diastolic fluttering of MV = most common M-mode finding (in Hu and dogs)
  o 2nd to turbulence associated w regurgitant jet in LVOT during diastole while MV is open
  o Jet do not have to be directed directly on MV but creates turbulent flow
  o Reverse doming of septal leaflet toward LA
• ↑EPSS: AI jet restrict MV motion
  o Not correlate with AI severity
• MV may close earlier because of ↑LV end diastolic pressures
• Jet lesion on septum or MV

Question 4

LV size and fct w/ AI

Answer 4

• Acute AI = no LV dilation
• Chronic moderate to severe AI → volume overload
  o Higher impact on LV fct vs MR (no flow in low pressure LA during systole)
  o Hemodynamically insignificant AI will not cause LV dilation
  o Myocardial failure suggested if no ↑FS and normal systolic dimension
   EF <50-55% → poor px in Hu w AI

Question 5

Color flow eval AI

Answer 5

Jet size
* Extent of regurgitation in LVOT
o Mild AI: just beyond AoV, dissipate quickly
o Moderate AI: extend at tip of MV
o Severe AI: beyond MV leaflets
* Jet height: proximal to AoV → end of jet
* Jet height/LVOT width ratio
o Mild AI <24%
o Moderate AI = 25-46%
o Severe AI > 47%

Vena contracta
* Smallest width of regurgitant jet on LAX parasternal view
o Mild AI <3mm highly specific
o Severe AI: >5mm highly sensitive, >7mm highly specific
* EROA can be calculated from vena contracta
o EROA >0.3cm2 = severe AI

Proximal isovelocity surface area - As discussed above

Question 6

Effective orifice area calc

Answer 6

EROAAI = pi x (vena contracta/2)2

Question 7

Doppler flow profile AI

Answer 7

Onset at AoV closure → rapid ↑ velocity to 3-5m/s → gradual decline during diastole → abrupt deceleration to baseline during IVCT → baseline at AoV opening
* Shape depend on time varying of PG → severity and chronicity
o Chronic severe AI: ↑Ao pulse pressure + low end diastolic AoP
 Rapid ↓ in AoP = steeper diastolic slope
* Severe AI = T 1/2 <200ms
* Mild AI = T ½ >500ms
o Acute regurgitation: LV compliance not adapted → severe ↑ in LV end diastolic P
 Triangular flow shape
 Linear deceleration

Question 8

Pressure 1/2 time AI

Answer 8

• Slope and pressure ½ time depend on how fast pressures btwn Ao and LV equilibrates = steep and short
  o Rapid ↓ in Ao pressure
  o Rapid ↑ LVP
• Small regurgitant orifice = delay equilibration
  o Plateau shape profile
  o Long pressure ½ time
• Hu:
  o Pressure ½ time >500ms → hemodynamically insignificant AI
  o Pressure ½ time <300ms → severe AI
• Slope and ½ time depend on
  o Size of regurgitant aperture
  o LV compliance
  o Ao diastolic pressure

Question 9

Regurgitant volume calc AI

Answer 9

• In normal heart, Ao SV should = PA SV
• Not accurate if stenotic AoV

Regurgitant volume = PA SV – Ao SV

Question 10

Ao diastolic flow reversal

Answer 10

• Flow in descending Ao: determine if significant reversal of flow in diastole
  o Normally trivial
  o Severe AI will cause flow reversal in proximal abdominal Ao
  o Moderate AI will cause flow reversal in descending Ao
• Analogous to PE finding of diastolic murmur in femoral arteries = Duroziez’s sign

Question 11

types of AS

Answer 11

• Supravalvular: rare
  o Reported in cats
• Valvular
  o Rarely single defect
  o Seen in conjunction w subvalvular stenosis: >90% of dogs w AS
• Subvalvular
  o Narrowed LVOT 2nd to nodules/ridge of fibrous tissue
   Ring may pull MV up to OT
   Dynamic LVOTO → band may extend from MV
  o ↓AoV area → fusion of Ao cusps
  o LVCH
  o ↑ blood flow velocity through stenotic area

Question 12

SAS breeds

Answer 12

Most common in large breed dogs
* Golden Retrievers
* Rottweiler
* Boxer
* German Shepherd
* Newfoundland

Question 13

AS: echo assessment

Answer 13

o MV morphology/motion
o AoV cusps anatomy/motion
o Visualized normal LCA
o Post stenotic dilation of ascending Ao
o Narrow OT and Ao

Question 14

Progression of lesions

Answer 14

Progressive lesions as animal grow → 18 months

Question 15

Lesion classes SAS

Answer 15

o Class 1: nodules
 Tend to develop on ventricular side of AoV
o Class 2: fibrous ridge of tissue
 Small and encircle OT w very little protusion into lumen
 Extensive w small orifice for blood flow
o Class 3: tunnel type stenosis
 Stiff MV forming posterior wall
 IVS forms anterior wall
 Common in Boxers and calves

Question 16

Differentiate congenital fixed SAS from dynamic LVOTO in HCM

Answer 16

Absence of SAM in cats w SAS

Question 17

What 2D measure can provide additional info

Answer 17

• Compare LVOT CSA vs Ao root CSA on R parasternal SAX→ provide additional info
  o Help when flow velocity affected by other factors
  o Normal LVOT:Ao ratio
   Mild >0.5
   Moderate 0.3-0.5
   Severe >0.5

Question 18

Assessment for myocardial fibrosis

Answer 18

Focal areas w ↑ echogenicity
o Common on papillary muscles at base of IVS

Question 19

EOA AS

Answer 19

• Effective orifice area: calculated in Hu
  o Useful if stenosis is valvular
  o Not possible to measure if subvalvular (cannot record OT and Ao velocity separately)
   RVOT not always match LVOT volume calculation
   EOA: cannot differentiate mild stenosis and normal LVOT

Question 20

Continuity equation AoV

Answer 20

o Used to calculate stenotic valve area
o All other measures derived from echo
o Can be normalized to body size (/BSA)

VTIRVOT x PA = normal SV
CSALVOT = ((〖CSA〗_PV x 〖VTI〗_PV))/〖VTI〗_LVOT

SVLVOT = SVAo
SV = CSA x VTI
CSALVOT x VTILVOT = CSAAo x VTIAo

Question 21

M-Mode evaluation AS and changes

Answer 21

• Chronic pressure overload → concentric hypertrophy
  o Tend to normalize LV wall stress
  o Relative wall thickness = wall thickness/radius → measure LVH
  o LV mass: calculated from tracing endo/epicardial borders at end diastole
• Degree of hypertrophy
  o Boxers: correlates w severity of stenosis/pressure gradient
  o Not documented u=in other breeds
  o Cannot be used as indicator of severity
• Normal ratio IVS:LVIDd = 0.22 to 0.34

Question 22

MR w/ SAS

Answer 22

• MR present in many dogs
  o Some from SAM → invariable MR
   Degree/duration of SAM → indicative of PG severity
   Longer apposition to IVS = ↑ severity of obstruction

Question 23

Assessment of ventricular function in SAS

Answer 23

• Systolic function: ↑FS%, Vcf, normal LVET
  o Preserved until later in dz
• Diastolic function: from compensatory LVH
  o Pseudonormal transmitral flow
  o Cause of c/s in Hu: exercise intolerance, lethargy, dyspnea

Question 24

Color flow Doppler eval AS

Answer 24

o MR
 Common w AS from calcification
 Can cause underestimation of stenosis (low volume flow → ↓ transAo PG)
o AI: 50-75% of dogs
 Diastolic flutter of septal MV leaflet
 Endocarditis: 5% of dogs w SAS (1 study)
o CHF may develop 2nd to MR or AI

Question 25

Spectral Doppler eval AS

Answer 25

o Use PW Doppler to determine level of obstruction/ site of ↑ velocity  DDX for LVOTO: fixed subvalvular obstruction, dynamic LVOTO, supravalvular stenosis  Presence of closing click = sample volume is immediately adjacent to valve o High velocity flow through LVOT/Ao → obstruction to outflow  Correlates with PG from KT * Not correlate to peak to peak in KT: peak Ao and peak LV NOT occur simultaneously * Correlate to KT max and mean  Velocity must ↑ as flow moves through narrowed area * L apical views: may underestimate by 26%  Velocity ratio LVOT:Ao * Little obstruction → ratio near 1 * Valve area ½ normal → ratio = 0.5 * Valve area ¼ normal → ratio = 0.35

Question 26

Optimal window to eval Ao flow

Answer 26

subcostal → parasternal windows not provide optimal alignment

Question 27

Underestimation of Ao flow factors

Answer 27

↓ forward flow from: myocardial failure, MR, sedation/anesthesia

Question 28

Ao obst flow profile

Answer 28

* Fixed obstructions: symmetric, with peak in m id systole o Smooth velocity curve, well defined peak velocity, spectral darkening along outer edge o Highest velocity signal = most // angle (5% error with < 15 degree angle) * Dynamic obstruction: dagger shaped during acceleration o Late peak velocity: progressive ↓ in OT as IVS contract or SAM

Question 29

Differentiation of Ao flow from other flows

Answer 29

 MR: start early in systole, flow start at onset of QRS, last longer to end of T wave * LVOT/Ao flow: later in systole, end of QRS * MR pressure gradient can be used to confirm stenosis PG  TR, VSD, PA stenosis, peripheral vascular stenosis (ie subclavian artery)

Question 30

Severity of SAS

Answer 30

pressure gradient  Mild <50mmHg, moderate 50-80mmHg, severe >80mmHg  Will be influenced by: * Low output → myocardial failure * ↑SV → AI, PDA, stress * ↓SV → sedation/anesthesia, MR

Question 31

Normal Ao velocity range

Answer 31

o Normal Ao velocity range: 0.65-2.65m/s depending on study  > 2.5m/s → SAS

Question 32

Causes of discrepancies in measurements of AS severity

Answer 32

* Severe AS by velocity/PG but not valve area o Overestimation of LVOT o LVOT velocity recorded too close to valve o ↑SV: AI, high output state, large body size * Severe AS by valve area but not velocity/PG o Underestimation of LVOT o LVOT velocity recorded too far from valve o Small body size o ↓SV: ↓EF%, small ventricular chamber, MR, mitral stenosis

Question 33

Contrast continuity with Bernoulli in assessment of severity of valvular AS.

Answer 33

Bernoulli equation: * Mean gradient: from velocity curve throughout systole * Accuracy is flow dependent Continuity equation * Volume proximal and w/I stenotic orifice is equal o Product of flow velocity x CSA maintained constant across a stenotic zone  Acceleration of flow: generated by hypertrophied ventricle = ↑ ventricular systolic pressure → ↑ kinetic energy of RBCs  Distal to obstruction: * Peak flow velocity α PG across stenosis → Bernoulli * Marked flow disturbance: loss of kinetic E from heat and friction * Measures effective orifice area * Flow independent o Not affected by the presence of AI (which ↑SV) o Not affected by LV systolic dysfct (which ↓SV) * Requires LVOT diameter + flow velocity → prone w error