week 2 lecture 3 Ao stenosis Flashcards
Parts of the AoV:
Annulus
Cusps
Commissures
Interleaflet triangles
Ao root
Annulus - supports the cusps
Cusps - RCC, LCC, NCC
Commissures - where the cusps come together
Interleaflet triangles - space between the cusps; extensions of the LVOT
Ao root - from the inferior attachment of the Ao cusps to ST junction; includes all of the above parts
Ao sclerosis vs Ao stenosis (AS)
Ao sclerosis
= looks bright (thickening of valve leafles) but opens normally; Ao jet vel <=2.5 m/s
*most old people
Ao stenosis (AS)
= looks bright and doesn’t open well; Ao vel >2.5 m/s
happens bc high press causes microtears and Ca sticks
sometimes Ao sclerosis becomes Ao stenosis
What are the causes of Ao Stenosis (AS)?
- Congenital - bicuspid valve; subvalvular or supravalvular stenosis
- Calcific - age
- Rheumatic - strep throat
Congenitally acquired AS: Bicuspid Valve
- when to look for it?
patient under 50 with AS? look for bicuspid
SAX: count cusps; must assess in SYSTOLE bc raphe
PLAX: look for off centered closure line
most common congenital heart defect (1-2% of population)
bicuspid valves are associated with
- Ao root dilation (dangerous)
- Coarctation of Aorta
- supravalvular Ao stenosis
- VSDs
bc inherently weaker Asc Ao tissues
Also possible to have unicuspid or quadricuspid valve (rare)
Bicuspid valve with raphe vs. without raphe
raphe = seam or union
with raphe
- common, usually btw RCC and LCC
- cusps are unequal in size
- looks tri leaflet in diastole
without raphe
- rare
- two equal sized cusps
Congenitally acquired AS: Subvalvular stenosis
Narrowing or ring in LVOT, or
Septal hypertrophy
= dynamic obstruction bc degree of stenosis depends on loading conditions
- get SAM (Systolic Anterior Motion - MV gets sucked into septum when it is closed)
Congenitally acquired AS: Supravalvular Stenosis
uncommon
- hour glass type dysplasia (abnormal cells) of Ao wall
- hypoplasia (not developed) Asc Ao
- membrane with the central orifice
Acquired AS: Calcific
Most common in elderly - Ca deposits in cusps prevent normal opening in systole
looks CHUNKY and bright
usually no commissural fusion
associated with MAC and CAD
Acquired AS: Rheumatic
Occurs years after untreated strep throat and rheumatic fever
looks THICK and bright (chronic inflammation causes thickening and stiffness)
commissural fusion and triangular systolic orifice
almost always get MS first then AS
Hemodynamic consequences of AS
AS = high afterload so heart has to push harder…
- concentric LVH…. which leads to
- Diastolic Dysf and incr pulmonary press
- Usually systolic function and EF is ok (but get ischemia and sys dysf in end stage disease)
ie untreated AS can cause both sys and diastolic heart failure
Signs and symptoms of AS
Angina
- also have CAD?
- exacuberated by LVH
Syncope (fainting) or presyncope (light headed) on exertion
- related to heart?
heart failure
SOB and fatique
SEM
SEM = Systolic Ejection Murmur
means ?AS (query Ao Stenosis)
SEM just means that the doctor heard a rumbling in systole… could be AS, MR, VSD…
Treatment of AS
Meds - alleviate symptoms
wait as long as possible then replace AoV before heart failure
Surgical:
- bioprosthetic (pig or cow) - lasts 10 yrs
- mechanical valve - incr risk stroke bc on blood thinners
Percutaneous: TAVI
Role of echo in AS
- Presence of AS? progression? Differentiate btw Ao stenosis and Ao sclerosis
- Determine Etiology: Bicuspid, Calcific, Rhuematic
- Assess for LVH… diastolic dysf?
- Measure Ao dimensions… post stenotic dilation?
- Assess for associated lesions:
- AI bc bicuspid and dilated Ao? or bc calcific and closure blocked by chunk of Ca?
- MR bc Ca build up on MV too? - Assess severity of AS (based on Ao jet vel, Mean gradient, AVA, DVI)
Continuity equation
what flows in must flow out
SV LVOT = SV AoV
rem, Q = SV = VTI * CSA
so,
VIT(AoV)CSA (AoV) = VTI(LVOT)CSA(LVOT)
VIT(AoV) - from trace of CW of AoV
CSA (AoV) - ?
VTI(LVOT) - from trace of PW of LVOT
CSA(LVOT) - from LVOT diam measurement
3 steps to do before machine will calculate AVA
- measure LVOT diam; CSA = π*r^2 (this is a source of error
- PW through LVOT; trace the peak and the machine calculates LVOT VTI
- CW through AoV; trace the peak and the machine calculates AoV VTI
Then machine calculates AVA VTI (do not use AVA Vmax!)
normal LVOT VTI
18-22 cm
(same numbers as LVOT diam, but cm not mm!)
normal AVA?
What are values for AVA for mild, mod, severe AS?
3-5 cm^2 (not ASE)
mild >1.5 cm^2
mod 1-1.5
severe <1
What 4 things can you look at to determine the severity of AS?
Ao jet vel
Mean gradient
AVA
DVI
How do you determine AoV jet velocity?
What are values for N and mild, mod, severe AS?
- CW through AoV in multiple windows (5 ch and 3 ch)
- Try PEDOF probe from right parasternal when vel over 3 m/s
- only use highest vel
N <= 2.5 m/s
mild 2.6 - 3
mod 3-4
severe >4
How do you determine the mean gradient?
What are values for mild, mod, severe AS?
- 5 Ch: CW through AoV
- machine will calculate mean gradient between LV and Ao
mild <20 mmHg
mod 20-40
severe >40
What do you do if there is an LVOT obstruction?
Vel is high in LVOT and AoV
Continuity eqn is not valid
(Cannot use AVA)
Instead, assess visually
2D planimetry
SAX - trace the opening of the AoV in mid systole (widest opening) to get AVA
not routine bc many pitfalls - hard to see spot where valve is widest.
Dimensionless Velocity Ratio (DVI) - what is it? What are the values for mild, mod, severe AS?
Vel ratio = Vel (LVOT) / Vel (AoV)
mild >0.5
mod 0.25-0.5
severe <0.25
A smaller number is worse
*not official ASE measurement
Velocity profile and AT for normal versus stenotic
Normal - shorter ejection time and AT
Stenotic - longer ejection time and AT (CW through AoV has more rounded shape); bc door not opening fast
Note: opposite AT pattern to that of pulmonary hypertension RVOT
Subvalvular Stenosis
Similar to LVOT obstruction, continuity eqn will not work (bc high vel through LVOT will continue through AoV and give false readings of health of AoV)
Show stenosis in 2D
Do PW of LVOT if possible
If have to use CW bc high vel, be sure to use generic trace (not AoV) and indicate on report that high vel is from LVOT
Also AS? AoV planimetry?
Supravalvular Stenosis
Show stenosis in 2D
- do PW walk down until you find the step up in vel (3 ch). This proves location
- do CW to get peak vel
Also AS? AoV planimetry?
Low output AS (poor EF)
continuity eqn still works
patient has stenotic valve but normal velocity though valve bc low EF (little blood is being pushed through valve)
Stress echo is used to assess AS in which 2 groups of patients?
- Asymptomatic severe AS at rest - does the AS get worse with exercise? (dynamic AS?)
- Low output AS - used dobutamine to increase contractility and EF, and determine true AVA
