Aortic stenosis rheumatic, gross pathology 20G0014 lores" by CDC/Dr. Edwin P. Ewing, Jr. - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #848.

My DDU point form notes on aortic stenosis…

The rest of my DDU notes are here.

causes

calcific stenosis (especially if bicuspid)

~25% over 65 have sclerosis – typically basal ↑ echoes
10-15% of these progress to obstruction, typically by 70-85yo

further ↑ echogenicity, ↓ systolic opening

congenital (bicuspid, unicuspid)

bicuspid

2/3 of severe aortic stenosis in the <70yo population = bicuspid

can be hard to tell if bicuspid when severe

can only tell in systole due to raphe

bigger anterior leaflet (R+L fusion) in ~80%

R+NCC 2nd, L+NCC 3rd

PLAX

diastolic sagging and systolic doming into aorta, eccentric closure line on M-mode

also dilation of sinuses, ascending aorta

PSAX: assess in systole

unicuspid

attaches at 6 o’clock in PSAX

often diagnosed in childhood

rheumatic

commissural fusion, ↑ echogenicity along leaflet edges, doming
mitral stenosis

other causes of LVOTO

subvalvular

dynamic: hypertrophic cardiomyopathy (HCM)

HCM CW trace

HCM CW trace

fixed

membrane – suspect in young adults with non-stenotic looking valve, TOE shows the membrane

muscular

AS and subvalvular CW trace

AS and subvalvular CW trace

supravalvular

→ so check for gradients above and below valve with PWD if ↑ CWD
high PRF PWD useful in rare patients with both

Overall approach

valve anatomy

supra / subvalvular stenosis

Doppler

Vmax
mean gradient
valve area by continuity

LV

dimensions, volumes
LVH
EF, diastolic function

aorta

diameter at sinuses, mid ascending aorta

AR

vena contracta width
quantitation if > mild

MR

mechanism
severity

pulmonary pressures

B mode

2D

↓ opening
planimetry

problem is 3D structure (need to get narrowest part) + calcific shadowing and reverberation

give anatomic valve area – want functional valve area!

3D

planimetry still not accurate
useful for bicuspid vs tricuspid

DOPPLER ASSESSMENT

values

 NormalMildModSevere
Peak velocity
(m/s)
<2.9 BSE3-3.9>4
2.6-2.9 Otto
Mean gradient
(mmHg)
<2525-40>40
Valve area (cm2 )>2.01.5-21-1.5<1
(Otto: this could be mild in small adults – consider dimensionless index)(Otto: if Vmax < 4 and LV fn ↓ consider low gradient low output AS)
Velocity ratio (Dimensionless index)≥ 0.50.5-0.25≤0.25
other features from Ottoirregular focal thickening but no obstruction → termed sclerosismild LVHlow output, low gradient AS will usually have EF <50% or small LV with normal EF – look at valve calcification ± dobutamine stress echo

maximum aortic jet velocity

key
strongest predictor of outcome
most reliable and reproducible for serial studies
key for deciding on replacement

CWD

including Pedoff probe

higher signal / noise ratio

smaller footprint → optimal angulation / positioning

quality

patient positioning
settings

high wall filters

gain set

scale set ~1 m/s faster than maximum

parallel (cos 0° = 1) – <15° (remember velocity is squared → ↑ error)
jet often eccentric cf plane of valve, long axis of aorta, and CFD
∴ search from multiple windows

apical with steep left lateral decubitus with apical cutout

suprasternal notch, supine with neck extended

even subcostal, L parasternal sometimes!

good jet

well defined peak velocity

audio is tonal, high frequency

mark at edge of dark spectral envelope

d/dx high velocity jets (timing, shape and diastolic flow curves help Δ)

subaortic obstruction

MR, TR

VSD

PS, branch pulmonary artery stenosis

peripheral vascular stenosis eg. subclavian

mean transaortic pressure gradient

equation

simplified Bernoulli equation

Δ Pmax = 4 Vmax2

corresponds to max on catheter derived

Pmean

corresponds to mean on catheter derived

from average of instantaneous gradient along curve

in native valves, can approximate with

Δ Pmean = 2.4(Vmax)2

neither correlates to peak-to-peak catheter gradient

max > peak to peak since aortic peaks later

probably best to use means if comparing different modalities in same patient

considerations

Vmax and Pmean will change with stroke volume
e.g. AR → ↑ SV → ↑ Vmax (may look severe when moderate)
e.g.2. ↓ LV function or MR → ↓ SV → ↓ Vmax despite severe AS
→ value of valve area

continuity equation valve area

SVLVOT = SVAo
assuming flat velocity profile
SV = CSA x VTI
∴ CSALVOT x VTILVOT = CSAAo x VTIAo

∴ AVA = CSAAo = CSALVOT x VTILVOT / VTIAo

simplification

because shape + timing of LVOT and aortic jet curves similar, can use velocities instead of VTIs:

∴ CSAAo = CSALVOT x VLVOT / VAo

issues

technical issues with recordings
outflow tract diameter

mid-systole from white-black interface of septal endocardium to AMVL

PLAX best (axial resolution)

aortic valve assumed circular

not quite on 3D → don’t use for transcatheter prosthetic valve size

value correlates with body size poorly

Δ in a given patients LVOT Ø over time likely error

errors squared

do several measurements and average

outflow tract velocity

2-3 mm sample volume just proximal to region of acceleration (same position as diameter) → start in jet and move back until

smooth curve

little spectral broadening

closing (but not opening) click

adjust transducer position / angle to get fastest curve with these characteristics

peak at edge of most intensive spectral signal, VTI modal, wall filters low enough to define ejection period

velocity ratio (dimensionless index)

essentially the fraction of the “normal” aortic valve area

ALSO ASSESS

other valvular disease

aortic regurgitation

in 80% of patients with predominant aortic stenosis
often mild, moderate
will ↑ Vmax cf AVA still accurate

mitral regurgitation

common because of MAC with calcific AS
will cause ↓ Vmax (2 routes of ejection) but AVA still accurate

other mitral disease

if low SV will ↓ Vmax

left ventricle

thickness

hypertrophies to ↓ wall stress
can trace endocardium and epicardium at end diastole to get LV mass

function

preserved until late
with valve replacement, LV function may recover

HANDLING CONFLICTING FEATURES

Vmax severe but AVA ≤ moderate → consider

VTILVOT: mod-severe AR, ↑ CO, large patient
CSALVOT: overestimated LVOT diameter
Vmax measurement problem: measured too close to valve (really? this is CW, not PWD)

AVA severe but Vmax ≤ moderate → consider

VTILVOT: mod-severe MR or MS, ↓ CO (↓ EF, small chamber), small patient
CSALVOT: underestimated LVOT diameter
Vmax measurement problem: measured too far from valve (really? this is CW, not PWD)

reproducibility

AVA = CSAAo ≈ CSALVOT x VLVOT / VAo

interobserver and intraobserver variability ~3-4% for velocities, higher for LVOT diameter
overall changes > 0.1 m/s in VLVOT, 0.15 cm2 for AVA, or 0.2 m/s for VAo or LVOT diameter, are greater than measurement variability
VAo may not change as AVA ↓ if VLVOT also ↓

low output low gradient AS

physiological valve area can actually ↓ with transaortic volume flow rate ↓ (valve doesn’t open as much) → can get ↓ continuity valve area when stenosis is not severe
need to consider anatomy, other causes of LV dysfunction, response to medical Rx
dobutamine stress echo useful in selected cases

↑ valve area with ↑ transaortic volume flow rate → flexible leaflets, mild to moderate stenosis

lack of contractile reserve → poor prognosis

OUTCOMES

prognosis depends on symptoms

Cover image: Aortic stenosis rheumatic, gross pathology 20G0014 lores” by CDC/Dr. Edwin P. Ewing, Jr.

Tags:
0 Comments

Leave a reply

Your email address will not be published. Required fields are marked *

*

© 2019 Echopraxis

Log in with your credentials

Forgot your details?