C6: AV stenosis Flashcards
where is the sinotubular junction
where the sinus of valsalva becomes the AO
is it common to see post stenotic dilation of the AO from AS
yes
where are the Aortic commissures
where the leaflets attach to the annulus
where do most age related calcifications of the AV start
AO commissures and works its way along the free edge to the center of the valve
define stenosis
formation of a high velocity jet through a narrowed orifice
define AO stenosis
incompetent opening of the AV during systole leading to a high velocity jet… leaflets will be tethered and thickened
do value leaflets calcify, or tether, first?
calcify
3 levels of obstruction of AS
1 supravalvular - membrane of shelf in AO.. usually congenital
2 valvular - calcific, congenital, rheumatic
3 subvalvular - membrane or muscular IVS (hypertrophic cardiomyopathy)
what is the most common cause of AS
valvular
do the LVOT and AV velocities usually peak at the same time
no, LVOT peaks first
what does the instantaneous peak measure
the pressure gradient at one point in time, the LVOT and AV pressure wont both be at their peak at one point in time so the difference b/w them will be greater
this is what we measure on echo
what does the peak to peak method of measuring press different than instantaneous peak
it measures the press gradient b/w the peak press of the LVOT and AV, its more accurate than instantaneous peak
Done in the cath lab
describe the effect of afterload on the LV
LV systolic pressure will rise, to keep SV norm, theres an increase in inotropy which causes concentric LVH due to the pressure overload
symptoms of AS
SOB fatigue chest pain/palpitations syncope arrthythmias signs of CHF
would a patient have symptoms w/ mild-moderate AS
not usually
w/ AS, what will you hear w/ auscultation
when and where
when:
harsh ejection murmur during systole
systolic ejection click and a crescendo-decrescendo murmur
where:
right upper sternal border that may radiate to CCAs
if you have a murmur from AS is it likely you will also hear a regurg murmur?
yes, if the valve doesn’t open well, then its likely it doesnt close well either
3 primary manifestations of severe AS
angina pectoris:
made worse by LVH, also caused by poor profusion of CA and the compress of coronary arteries from high cavity press, prolonged contraction and impaired relaxation
syncope or presyncope:
usually w/ exertion…. heart has reduced ability to maintain cerebral perfusion press w/ AS
CHF
what is presyncope
symptoms you feel before passing out
3 etiologies of AS
calcified AS (degenerative): also called age related AS, thickening starts at the underside of the cusps, can be associated w/ bicuspid AV
congenital:
bicuspid (more common type of congenital), uni, or quad
rheumatic:
thickening starts at cusp edges
which etiology of AS is the most common
calcific/degenerative
What % of adults over 65 will have some degree of AO sclerosis
25%
What is the precursor to AO stenosis
Sclerosis
W/ AO sclerosis will there be an increase in blood velocity?
Why or why not
No, its not yet restrictive
What % of patients w/ AO sclerosis will develop AS
10-15%
Describe the pathology of calcification AS
It’s an extension of what pathology
There are lipid deposits, inflammation and calcifications that cause the leaflets to stick together
atherosclerosis
what is the pathogenesis of calcific AS
endothelial damage causes the endothelial cells to lose the ability to produce gasses that prevent clotting and inflammation…. in time this leads to necrosis, calcifications and narrowing
causes of endothelial damage
force from high velocity blood flow, high BP, age
6 roles of echo in AS
- determine the etiology of the lesion (congenital, degenerative, rheumatic)
- exclude other sources of LVOT obstruction
- assess LV size, systolic and diastolic function
- assess degree of LVH
- estimate severity of stenosis
- identify associated valve lesions
where should the diastolic closure line of the AV be found on M mode
middle of the AO annulus
how might AS appear of M mode
- Ao closure line not in the middle of the AO annulus
- ‘extra lines’ seen where the AO root is located due to calcium deposites
- AV won’t open fully
can it be hard to see the valves on M mode w/ calcific AS
yes
what can cause morphology changes on the AV
atherosclerosis
calcium
commissural fusion
post-stenotic dilation
is the AV is very stenotic, can it be hard to tell how many cusps it has
yes
describe the changes seen w/ AV sclerosis
- some thickening and calcifications of the cusps
- slight reduction of cusp excursion
- CW doppler velocity of AV norm or slightly elevated
CW velocity of AV <2.5 m/s
describe the changes seen w/ AV stenosis
- obvious thickening and calcifications of the cusps
- obvious reduction of cusp excursion
- CW doppler velocity elevated through AV
CW velocity of AV >2.5 m/s
what is AV sclerosis
atherosclerosis on the AV
will you always have sclerosis before stenosis
yes
when a bicuspid AV is open, what shape does it make
football
does a bicuspid AV usually occur with a dilated AO root and ascending AO
yes
what type of AS is most common in patients under 50
congenital, bicuspid AV
does bicuspid AV effect one gender more than the other
yes, males
familial inheritance rate for bicuspid AV
What % of the general population has a bicuspid AV
9%
1-2%
describe the structure of a bicuspid AV
- multiple configurations possible
- bicuspid w/ or w/ raphe
where is cuspal fusion most likely to occur w/ a bicuspid AV
85% RCC and LCC
15% RCC and NCC
what is a raphe
seam that joins 2 cusps together
2D assessments w/ a bicuspid AV
eccentric closure line/non central coaptation
systolic doming of the larger cusp
norm leaflet excursion
concentric LVH
LV dilation
LA dilation
thickened leaflets
can you see a raphe if the AV is closed
no
another term for raphe
rudimentary cusp
what view in a bicuspid AV best seen
how can we diagnose a raphe
PSAX
you need to show the football shaped opening in systole in PSAX to diagnose this
anomalies associated w/ bicuspid AV
congenital membranes (sub or supravalvular) supravalvular narrowing subAO LVOT obstruction
where should you look for a supravalvular narrowing
ascending/descending AO
AO arch or junction
subAO LVOT obstruction is associated w/ which condition
HCM- hypertrophic cardiomyopathy
describe rheumatic AS, 2 types
how does it cause AS
inflammatory condition caused by beta-hemolytic steptococci
acute
chronic
causes scarring and leads to rheumatic AS
w/ rheumatic AS, where does the thickening of the AV start
leaflet tips
what is involved in the acute phase of rheumatic AS
-endocardial vasculitis (inflammation of the endocardium, most important) - swelling that leads to valve damage
-inflammation of the myocardium, pericardium, synovial joints, lungs and pleura
(these may or may not lead to scarring)
endocardial vasculitis most often affects which valves
Mitral - most common- 75-80%
AV - 20-25%
PV, TV - 5%
2 possible outcomes of endocardial vasculitis
resolve completely
or lead to progressive scarring
which type of rheumatic HD do we most commonly see
chronic
what is a 2D parameter that can be used to assess AS
AV planimetry
AV planimetry in done in which views
what are we looking for
PLAX, PSAX… trace the orific in mid-systole
of cusps
mobility and commissural fusion
valve calcification
what parameters are usually used to assess AS
why
hemodynamic parameters
AV planimetry is not as accurate, especially w/ calcific valves
what is the continuity rule
the volume of flow prox and distal to a narrowing must be equal, so blood flow speeds up in the narrowing
how does the continuity rule apply to SV
formula
SV of the LVOT = SV of the AV
LVOT (pie (r^4) x VTI) = AV (pie (r^4) x VTI)
3 items you need for AVA continuity equation
LVOT diameter
LVOT VTI w/ PW
AV VTI w/ CW
Use the highest AV VTI (or velocity) from all views
where should the LVOT PW be taken
same spot at the LVTO diameter
how are area and velocity of a stenotic valve related
inversely
eg, area reduction of 3 times, will cause velocity through that area to be tripled
is alignment to the AV usually more lateral than the apex
yes
is the mean or peak gradient more important for AS
mean
when the AV CW velocity is over 2.5 m/s, which 4 views should you assess velocities from
Which velocity and VTI is used to calculate
apical
R suprasternal or R supraclavicular (pedoff probe)
R parasternal
subcostal
Highest numbers are used, unless patient has arrthyhmias, then average values over the 5 beats
when would you get a good AV velocity from a subcostal view
if the jet is eccentric
why do we assess many locations if the AV velocity is >2.5m/s
highest velocity can be found at any of the 4 locations
how does the peak velocity method assess AS
cons of this method
-it gives you an AVA uses only a single point from both the LVOT and AV
- unable to incorporate velocity over time
- will over estimate stenosis if the waveform is narrow w/ a high peak velocity
which method is more accurate for AS, peak velocity or VTI
VTI
how does the VTI method assess AS
pros of this method
Gives you an AVA using velocity time integral which incorporates all of the velocities in the ejection period
- incorporated the parabolic shape of the waveform
- doesn’t over estimate degree of stenosis
which is more stenotic, a parabolic waveform, or a narrow waveform w/ high velocity
parabolic
what is the velocity ratio
formula for AV
a different way to quantify the degree of stenosis of a valve… the ratio can also be done using VTI
VR = velocity of LVOT/velocity of AV
or
VTI = VTI LVOT/VTI AV
how are the degree of a stenosis and velocity related
directly
AV jet velocity for mild AS
severely abnorm value
2.5 - 2.9 m/s
> 4 m/s
AV mean gradient (CW) value for mild AS
severe AS
Mild: <20 mmHg
severe: >40 mmHg
AV area value for mild AS
severe AS
mild: >1.5 cm^2
severe: < 1 cm^2
indexed AVA to BSA value for mild AS
severe AS
mild: > 0.85
severe: <0.6
LVOT/AV velocity ratio value for mild AS
severe AS
mild: >0.5
severe: <0.25
what does a velocity ratio of <0.25 indicate
the velocity of the blood increases 4 fold when moving from the LVOT through the AV
describe the spectral waveform of subAO stenosis compared to severe AS
subAO stenosis: late peaking profile and fast DT - dagger sign…. very high velocity
severe AS: acceleration time and DT are the same so you have a symmetrical waveform
example of a subAO stenosis
SAM - systolic anterior motion of the MV leaflet
compare the timing and duration of the AS and MR
AS: starts later and ends sooner than MR - stenosis never occurs during the isovolumic periods
MR: occurs during the isovolumic period (no gap b/w outflow and inflow)
if the AV velocity indicates severe AS but the area does not, what might be causing this?
how can you fix this
technical errors - LVOTd or LVOT VTI overestimated (re measure)
large body size - calculate indexed AVA
high transAO flow - significant AR, pregnancy, tachycardia, fever, etc )used AVA for severity)
how can you overestimated the LVOT VTI
measuring the velocity too close to the AV when the blood is starting to pick up speed
if the AV velocity is normal but the area indicates severe AS, what might be causing this?
how can you fix this
technical errors - LVOTd or LVOT VTI underestimated (re measure)
small body size - calculate indexed AVA
low transAO flow
low EF: dobutamine stress echo
norm EF: patient may have significant MR or low indexed SV… use AVA for severity in both cases
