-Severe Calcification: prominent acoustic shadow
-Rheumatic: MV>AV
-Subvalvular: fixed (membrane or muscular band) or dynamic (HOCM, mid to late
-Supravalvular: uncommon, congenital (Williams Sd)

-LVOT: PSLA, with anterior mitral leaflet in mid-systole, from inner edge of septal
endocardium to inner edge
-LVOT Vel: PW, apical 5, on LV side of valve, laminar flow curve
-AS Vel: CW, apical 5
-Valve Anatomy: PSLA, PSSA, number of leaflets, raphe presence, cusp mobility,
commissural fusion / calcif.
1- Jet Velocity (m/s): CW, apical and suprasternal - defined as the highest velocity recorded from any window
Color Doppler is helpful occasionally to avoid recording the CWD signal of an eccentric MR jet.
>3 beats should be recorded (>5 beats with irregular rhythms)

Severe AS = Rounded curve                            Mild = peak in early systole                Dynamic subAo = late peaking, early concave  
2- Mean transaortic Pressure Gradient (mmHg):

Simplified Bernouilli Equation

Maximum Gradient                                              
avg. of instantaneous gradient over ejection period

Derived from the Bernouilli equation  assuming that viscous losses and acceleration effects are negligible and by using an
approximation for the constant that relates to the mass density of blood
Also by ignoring the proximal velocity assuming it's < 1 m/s
When the proximal velocity is > 1.5 m/s or the Aortic velocity is < 3 m/s, the proximal velocity should be included:

Sources of error:
-Malalignment of jet and US beam
-Recording of MR jet
-Neglect of an elevated proximal velocity
-Pressure Recovery
PR: where conversion of potential energy
to kinetic energy across a narrowed valve
results in high velocity and drop in pressure.
However, distal to the orifice, flow
accelerates again. Although some of the
kinetic energy dissipates into heat due to
turbulences and viscous losses, some of the
kinetic energy will be reconverted into
potential energy with a corresponding
increase in pressure, the so-called PR. PR is
greatest in stenoses with gradual distal
widening since occurrence of turbulences is
then reduced.

In AS, PR (in mmHg) can indeed be
calculated from the Doppler gradient that
corresponds to the initial pressure drop
across the valve (i.e. 4v2), the effective
orifice area as given by the continuity
equation (EOA) and the cross-sectional area
(CSA) of the ascending aorta (AoA) by the
following equation:
PR = 4v2 × 2EOA/AoA × (1−EOA/AoA).
Thus, PR is basically related to the ratio of
EOA/AoA. As a relatively small EOA is
required to create a relevant gradient,
must also be relatively small
to end up
with a ratio favouring PR. For clinical
purposes, aortic sizes, therefore, appear to
be the key player and PR must be taken into
account primarily in patients with a
diameter of the ascending aorta <30 mm.
It may be clinically relevant particularly in
congenital AS. However, in most adults with
native AS, the magnitude of PR is small
and can be ignored as long as the diameter
of the aorta is >30 mm. When the aorta is
<30 mm, however, one should be aware
that the initial pressure drop from LV to the
vena contracta as reflected by Doppler
measurement may be significantly higher
than the actual net pressure drop across the
stenosis, which represents the
pathophysiologically relevant measurement.

Continuity Equation

-The effective Valve Area is smaller than the anatomic valve area due to
contraction of the flow stream in the orifice, as determined by the contraction
and discharge coefficients for a given orifice geometry.
Although the difference between effective and anatomic valve area may account
for some of the discrepancies between Doppler continuity equation and cath
Gorlin equation valve areas, there's now ample clinical outcome data validating
the use of the continuity equation, supporting the concept
that the effective,
not anatomic, orifice area is the primary predictor of clinical outcome.

-LV dysfunction
results in decreased cusp opening and a small EOA even
though severe stenosis is not present.
LVOT Velocity Apical 5, on the LV side of AV
When AVA changes, look for changes in the different components (LVOT size rarely chges over time

Moderate AS + Moderate AR = Severe combined Valve Disease
4- Planimetry (cm2):
May be an acceptable alternative when doppler estimation of flow velocities is unreliable.
May be inaccurate when valve calcification causes shadow or reverberations
In addition, effective rather than anatomic orifice area is the 1ary predictor of outcome
1-LV Systolic Dysfunction:
When LV Systolic dysfunction is present with severe AS, AS velocity and gradient may be low, despite a small valve area.
= Low-flow low-gradient AS
Effective Orifice Area <1 cm2
LVEF< 40%
Mean Pressure Gradient < 30-40 mmHg

Dobutamine Stress may be helpful to differentiate:
-Severe AS causing LV systolic dysfunction - Needs AVR
-Moderate AS with another cause of LV dysfunction (MI, CMP) (the LV does not generate sufficient energy to overcome the inertia
required to open the aortic valve to its maximum possible extent)

2.5-5 mg/kg/min with an incremental increase Q 3-5 min to a max dose of 10-20 mg/kg/min
STOP when HR rises 20 bpm above baseline or > 100 bpm (max inotropic effect reached)
-Measure LVOT Vel (apical 5) at each stage and biplane EF, AS Vel, mean gdt, valve area
-an increase in valve area to a final >1.0 cm2 suggests that stenosis is not severe
-AS jet > 4.0 or mean gdt > 40 = severe AS (provided that valve area does not exceed 1.0 cm2 at any flow rate)
-Absence of contractile reserve (failure to increase SV or EF by > 20%) is a predictor of a high surgucal mortality and poor long
term outcome although valve replacement may improve outcome in this group

2-LVH: The small LV ejects a small SV so that even when severe stenosis is present the AS velocity and mean gradient may be
lower than expected for a given valve area. many women with small LV sizes also have a small body size and LVOT. However
indexing for body size is controversial (VA does not increase with obesity)

3-HTN: May affect flow and gradient measurements but less AVA measurements

4-AR: 80 % of adults with AS also have AR. When severe AR, measures of AS severity remain accurate including maximum
velocity, mean gradient, and valve area. However, because of the high transaortic volume flow rate, maximum velocity and mean
gradient will be higher than expected for a given valve area.

5-MR: with severe MR, transaortic flow rate may be low, resulting in a low gradient. Valve area calculations remain accurate
-A high velocity MR jet may be mistaken for AS jet as both are systolic directed away from the apex. MR is longer in duration

6-High CO: (HD, anemia, AV fistula, hyperthyroid, liver hemangioma) high gradients in moderate or mild AS

7-Asc Ao: Aortic root dilation is associated with bicuspid AV
CI to BB
Ao A2
Dimensionless Index: < 25% = severe
Some of the variables we can use to determine
prognosis include
peak velocity or extent of
calcification and exercise testing

Causes of valvular AS

Radiation induced:
gives brightness / calcification of
asc ao, AV, aortic annulus, spreads with contiguous
brightness to MV annulus sparing the mitral leaflet tips.
Combined Aortic and Mitral Valve disease
Lysosomal Storage disease: increased LV wall
thickness, pericardial effusion, hyperdynamic LV
function. Bright AV which doesnt seem to be opening at
all. Gradient across the AV 97 mmHg
Low output low gradient: If after a Dobutamine
Stress Test the Gradient increases > 40 mmHg and the
AVA does not change this is severe AS. If both
increase then it's more likely to be moderate AS
Dobutamine Stress Hemodynamics for AS Endpoints:
. 5-20 mcg/Kg/min
. SV(LVOT VTI) plateau
. SV increase 20%
. MG > 30 mmHg
. AVA < 1 cm2

Low Gradient Normal EF
-Increased global afterload (valvulo-arterial impedance)
-Reduced SV Index
So you have preserved EF but a small cavity and small SV index (<35 cc/cm2)
MG < 40 but AVA will be < 1
The natural history is as malignant as high gradient AS with preserved EF.
Operation gives a better outcome over time based on retrospective studies

SEAS study that was looking at simvastatin and ezetimibe in AS looked at
these patients in a prospective fashion and did not see any difference in terms
of outcomes (patients with low AVA, low MG). they thought that the natural
history is similar to moderate AS. A little bit of discrepancy in the literature.
Fibrous Ridge
Discrete fibrous membrane (90%)
Muscular narrowing of LVOT sometimes
Prevalence ~ 6.5% in adult CHD
Can be Iatrogenic after VSD patch repair
Associated AR because of high jet velocity
lesions on AV cusps

Dynamic LVOT Obstruction
. Amyloid Heart Disease
. Hypertensive Heart Disease
. Apical and Mid LV infarction
. Reduced LV chamber size

Fibrous Ridge
. Focal or diffuse narrowing starting at the
sinotubular junction
. Rare involvement of aortic arch and
peripheral vessels
. Frequently associated with
Williams-Beuren syndrome (71%)
. AV abnormalities 50% of patients
(commonly BAV)

Symptoms: CP, pre-syncope
Hourglass narrowing beginning at
sinotubular junction. MG 35 mmHg
Rx: Surgery (Aorta enlargement)
If we put the sample in the
area of flow convergence
we get an overestimated
high LVOT VTI and the
numerator will be large
which will overestimate the