Aortic Valve Disease

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Aortic Valve Disease

• S.Craft

2
Aortic Stenosis-symptoms

• Symptoms often not seen until AS is moderate or
  severe
• Clinical symptoms include CP, DOE, can have
  syncope
• On exam, harsh systolic ejection murmur
  crescendo-decrescendo in shape

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AS-causes

• Common causes include
• Degenerative or senile degenerative
  calcification is most common cause ( 65-70yrs)
• Congenital bicuspid valve subaortic membrane
  supravalvular coarctation
• Rheumatic post-inflammatory response, look for
  MV involvement also

4
Echo features

• Thickened, dense leaflets
• Decreased motion of leaflets
• Concentric LVH
• Post-stenotic dilatation of Ao root possible
• In congenital AS, leaflets may be less thickened,
  BUT 2D will show that tips of leaflets are
  tethered, restricted and doming in early systole

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M-mode of AS
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2D is superior to M-mode for evaluating AS raph
e
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LVH in AS
Concentric LVH confirmed in both
views. Gives evidence of increase in
afterload/harder work of LV. Progression of LVH
can be monitored with serial echo.
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Sclerosis Vs Stenosis

• Cusps are thickening, calcified fibrotic
  without obstruction to flow

• Still thickened etc, but orifice size is reduced
• Calcified usually in older adults

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Congenital Bicuspid AoV

• Often no symptoms until in 20s
• M-mode eccentric valve closure line

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Bicuspid AoV- 2D

• Thickened cusps increases with age
• Eccentric closure PLAx
• Football or cat eye shape in systole
• Examine for raphe
• Doming in systole
• Diastolic doming may be present (prolapse)

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Note doming. Can you see post-stenotic
dilatation of the aortic root in one frame?
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AS concepts

• AS creates a pressure overload of the LV
• afterload the resistance the ventricles must
  overcome while ejecting blood (RPrp p. 93)
• Physiologic response of LV to afterload
  concentric LVH
• LVH worsens as AS progresses
• Late in dz, LV systolic dysfx occurs LVE at
  end-systole reduced contractility

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Afterload-see Reynolds Prep
Afterload is determined by 3 things. Ask what is
making it hard for the LV to eject blood?
narrowing of semilunar valve? (AS or PS) high
arterial blood pressure (systemic HTN or
PHTN?) increased viscosity of the blood?
(polycythemia) also coarctation of aorta
renal artery stenosis can cause
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Force-Velocity relationship

• Force- the load the ht fibers must produce to
  eject
• Velocity- the rate of fiber shortening during
  systole
• increase in afterload generally decreases cardiac
  performance

As afterload increases, performance
decreases. Reducing afterload improves cardiac
performance.
Rprp. Pp 93,156, 296-7, 314
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Effect of Systolic Function

• If nml/wnl then increase in gradient across AoV
  will be proportionate to the degree of stenosis
  (spectral Doppler)
• Low CO state tends to underestimate severity
• Poor LV fx due to MI
• High CO state tends to overestimate severity
• Pregnancy, significant AI
• again, the whole picture should make sense

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Complications

• LV pressure overload LVH
• Increased LVEDP
• B-bump on MV M-mode
• Increased LA pressure
• LVE systolic dysfx late in disease
• Increased risk for
• embolic events
• infective endocarditis
• serious arrhythmias
• sudden death

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Echo Analysis of AS

• 2D is superior to M-mode
• Color Doppler-
• helps define orifice - helps locate stenotic jet
• helps locate/assess associated regurgitations
• Spectral Doppler-
• to estimate AVA
• change in spectral profile Peak in mid-sys VS
  late peaking

- multiple views are important for all of these

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Estimating AS severity

• 2D- cusp thickening, mobility, doming measure
  LVOT diameter, LV size/fx
• CF Doppler to locate AS jet help with cursor
  placement
• Spectral Doppler to obtain Pk Mn Vels
• of both LVOT aortic valve flow
• Plug data into the Continuity equation

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Modified Continuity Equation
(Use either VTI or velocity from V1
V2) AVA 0.785 x LVOTd² x LVOTVTI
AoVVTI OR AVA 0.785 x LVOTd² x PkV
LVOT Pk Vel AoV
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LVOT diameter

• Use PLAX view in early-mid systole
• Maximize LVOT image
• Inner edge to inner edge at border of aortic
  cusps with IVS AMVL
• See Reynolds p. 338-339

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What the heck is VTI?(and how do I get it??)

• Velocity time integral
• A measure of stroke distance (cm)
• Trace the spectral envelope PW or CW
• Value is displayed in text area unit is cm

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Proper placement for LVOT
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Pitfalls of AVA calc

• Difficult to know where to take your PW Doppler
  sample in the LVOT
• a rule of thumb is to find peak AoV flow, then
  back up the SV into the LV about 1cm
• moving target!
• measure at least 3 beats in NSR, at least 5 in
  irregular rhythm

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Example AVA
Assume the following measurements - LVOT
diameter 1.8cm - LVOT pk vel (V1) 1.0
m/s - Aortic pk vel (V2) 3.5 m/s Using the
modified continuity equation, the AVA ?
AVA 0.785 x (LVOT)² x V1 V2
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AVA
This example uses velocities to estimate the
AVA. AVA 0.785 x ________ x ________
_______ 0.785 x (3.24) x 1 3.5
2.54 3.5 0.73 cm² What is your
estimate of this severity?
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AVA gradient criteria

• Peak Pr. Gradient
• Mild 16-36 mmHg
• Mod 36-64 mmHg
• (modly sev 50-64)
• Severe gt 64 mmHg

• Mean Pr. Gradient
• Mild lt 30 mmHg
• Mod 30-50 mmHg
• Severe gt 50 mmHg

assuming normal LV systolic fx
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AVA criteria
Valve area normal gt 3-5 cm² mild 1.1 1.9
cm² moderate 0.75 1.1 cm² severe lt 0.75
cm² slight differences among authors
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Aortic Valve Planimetry

• For anatomic area, PSAX
• Use zoom
• Early systole
• Difficult if calcification causes shadowing

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LVOT/AoV ratio
Can help determine if patient has severe AS (lt
0.75cm²) V1 V2 ratio ratio of lt 0.2
is c/w severe AS (in approx. 2.0cm LVOT
diameter)
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Body Surface Area (BSA)
A calculation that can easily be done by entering
the patients height weight into the U/S
system at the same time you enter the name, acct.
number, etc. The larger the patient, the larger
the BSA. A larger person may be symptomatic at
an AVA that measures gt 0.75 cm². A smaller
person may be asymptomatic at an AVA measuring lt
0.75 cm²
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Comparison to Cath Data

• Most cath labs report a peak-to-peak aortic
  gradient
• -the difference between the peak LV pressure and
  the peak Ao pressure
• -usually lower than peak instantaneous gradient

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Cath gradient definitions

• Peak-to-peak (last slide)
• Mean- measures pressure gradient over time. Used
  to assess valvular stenosis
• Doppler cath mean gradients should show close
  correlation
• Peak instantaneous- measured at peak pressure
  difference between 2 chambers

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Remember!

• Mean gradients obtained by cath or by Doppler
  should show close correlation
• Poor correlation between cath peak-to-peak
  compared to mean or peak instantaneous gradient
  obtained by Doppler.

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Aortic Regurgitation (AI)

• Leaking of blood back into the LV
• increased preload
• Called AR or AI
• Typical murmur high-pitched, blowing, diastolic
  decrescendo (murmur heard at LSB)
• Severe AI murmur low, diastolic rumble at apex
  called Austin-Flint murmur

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Causes of AI- numerous

• Chronic AI
• AS, other valvular dz
• Bicuspid aortic valve
• Prosthetic aortic valve
• Atherosclerosis
• Rheumatic heart disease
• Sinus of Valsalva aneurysm
• Aortic dilatation (varying etiology)
• others

• Acute AI
• Infective endocarditis
• Dissection
• Trauma (loss of commissural support)
• 
  

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Symptoms of AI

• Dyspnea- shortness of breath (SOB/SOA)
• Fatigue
• Palpitations - CP - Dizziness - syncope
• Over time- Signs of CHF (left heart failure)
• Paroxysmal nocturnal dyspnea-
• Dyspnea on exertion (DOE)
• Untreated may result in right heart failure
  (jugular vein distention, hepatomegaly, LE edema)
  

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Chronic AI

• Chronic AI LV volume overload (increased
  preload) (LVVO pattern physiologic response)
• Eventual failure of systolic LV function
• Patient may be asymptomatic for a long time
• Assess chamber sizes, LV volume and systolic fx
• Remember Starling Curve

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Acute AI

• Significant acute AI LV pressure volume
  overloads
• Assess M-mode for
• Increased LVEDP causes LV pressure to exceed Ao
  pressure
• premature closure of MV
• Premature opening of aortic valve
• Assess MV Doppler signal
• DT lt 140ms
• Increased E/A ratio
• These indicate increased LVEDP

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Cath lab diagnosis

• Cardiac cath used to be method of choice for
  assessing AI, now echo
• Doppler assessment may differ from cath unless
  patient is in similar status at both times

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M-mode findings

• Fine diastolic fluttering of AMVL
• LV volume overload pattern
• Early closure MV (C pt on/before onset QRS)
• Early opening AoV (on/before onset QRS)
• Color M-mode

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2D echo findings

• ?reason for AI incomplete closure?
• Fine diastolic flutter of AMVL
• LVVO pattern
• LV may be spherical shaped increased mass
  little if any LVH late in course
• Check LV size systolic function
• Check LA size increases in later stages

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Color Doppler of AI

• Use multiple views to assess severity of AI
• Color Doppler can be used to subjectively assess
  AI visually
• AI jet width/LVOTW ratio
• lt 25 mild AI
• 65 severe AI

Reynolds Pkt, Table 6, 7 pg. 44
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CFD in PSAX for AI

• JSAA/LVOTA ratio
• Mild lt 4
• Mod 4-24
• Mod-sev 24-59
• Severe 60

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Other techniques

• Color M-mode
• Vena contracta width
• Mild lt 0.3 cm
• Severe gt 0.6 cm
• Jet width
• Mild lt 4 mm
• Severe gt 10 mm
• Regurgitant volume
• Effective regurgitant area

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Spectral Doppler of AI

• AI deceleration time P½T can give some
  estimate, but are not always reliable
• Generally, the steeper the AI slope, the more
  severe the AI

P1/2T lt 200ms may indicate significant AI
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Views for Doppler of AI

• Spectral Doppler
• Apical 5 chamber is one of the best to use for
  AI
• Apical LAX

• CFD
• SSN flow reversal in D Ao may be seen
• Brief early reversed flow is normal
• Holodiastolic reversed flow is c/w moderate to
  severe AI
• Subx hard to get good line-up, but may give clue

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References
DeWitt, Susan. Echocardiographythe Notebook, 5th
edition. Feigenbaum, Harvey. Echocardiography,
6th edition. Otto, Catherine. Textbook of
Clinical Echocardiography, 3rd edition. Reynolds,
Terry. The Echocardiographers Pocket Reference,
3rd edition Reynolds, Terry. Cardiovascular
Principles, A Registry Review Preparation.