ECHOCARDIOGRAPHIC ASSESSMENT OF STENOTIC
VALVULAR LESIONSDEEPAK NANDAN
ANATOMY
Area-2.6-3.5 cm².
Structure 3 cusps,3 commissures supported
by fibrous annulus Arantius nodule 3 sinuses
AORTIC VALVE
Qualitative diagnosis
Thin and delicate
Plax-opening and closing
Basal short axis view-Y-inverted Mercedes Benz sign
2D-IMAGE
Maximum jet velocity
◦ BERNOULLI’s equation
◦ Multiple windows
◦ Parallel alignment
◦ Colour doppler
◦ Angle correction
Doppler assessment
MIPG=4 xV²(maximal jet velocity)m/s
MPG=4x(∑V1²+V2²+…Vn²)/n
MPG=∆P(max)/1.45 +2
MPG=2.4(Vmax)²
Pressure gradients-Instantaneous vMean
Discrepancies
◦ Tech poor doppler recording
◦ Non parallel interrogation angle
◦ Pressure grad depends on flow rate & valve narrowing –AR/LV dysfunction
Bernoulli's VS invasive
Continuity equation:-
SV (lvot)= SV (Ao)
SV=CSAxTVI
CSA (lvot) xTVI (lvot)=CSA (Ao) x TVI (Ao)
AVA=CSA x TVI (lvot) / TVI (Ao)
Aortic valve area
Correlates well with invasive data (GORLINS)
Adv compared to Berrnoulli
co-existing AR
Left ventricular dysfunction
Rarely are all 3 leaflets imaged perpendicular
Triangular shape- measurement error
Deformities n irregularities- further exacerb
AV- superior-inferior rapid moments
0.25 cm2 margin
AVA-Direct planimetry
Ao valve area≈Ao flow rate
Dist- true severe valvular stenosis (vs) mild to mod stenosis with LV dysfn
Stepwise infusion of dobutamine(5—30µg/kg/min)
DOBUTAMINE ECHO
Flexible valves:- AVA ↑ when SV ↑
True stenotis:- AVA↔ when SV ↑
Flexible valves:-Vmax(lvot)/jet ↑
True stenosis:-Vmax(lvot)/jet↔
Safe& clinically useful, limitation- non response to dobutamine
Stress findings of severe stenosis AVA<1cm² jet velocity>40m/s mean gradient>40mm of Hg
Lack of contractile reserve- failure of LVEF to ↑ by 20% is a poor
prognostic sign
Maximal aortic cusp separation (MACS) Vertical distance between right CC and non CC
during systole Stenotic AV → decreased MACS
Limitations Single dimension Asymmetrical AV involvement Calcification / thickness ↓ LV systolic function ↓ CO status
M- mode
AVA MACS
N > 2cm2 N > 15 mm
< 0.75 cm2 < 8 mm
> 1 cm2 > 12 mm
gray area 8 – 12 mm
Ao valve resistance- flow independent measure of
stenosis severity
Resistance=(∆P/∆Q)mean x1333
Resistance=28√gradient( mean)/AVA
OTHER APPROACHES
Left ventricular stroke work loss(SWL)
SWL (%) = (100 ×∆ P mean) / (∆P mean + SBP)
Principle-LV expends work during systole to keep the AV open and to eject blood into the aorta
Depends on the stiffness of AVLess dependent on the flow
>25%--- poor outcome
LVOT overestimated
LVOT TVI recorded too close to valve
Hgh transAo flow rate
mod-sev AR Hgh output state Large body size
LVOT underestimated
LVOT TVI-too far frm val
Small body size Lw transAo flw rate low EF small vent
chamber mod-sev MR mod-sev MS
Discrepencies in AS severity assessmentSevere AS by gradient Severe by area
Valve anatomy, etiology Exclude other LVOTO Stenosis severity – jet velocity mean pressure gradient AVA – continuity eq LV – dimensions/hypertrophy/EF/diastolic fn Aorta- aortic diameter/ assess COA AR – quantification if more than mild MR- mechanism & severity Pulmonary pressure
APPROACH
Av ↑in MPG per yr = 0 to 10mm/yr mean 7mm Hg AVA ↓ by 0.1 to ∓ 0.19cm²
Jet vel < 3m/s – rate of symptom onset needing MVR is 8 % /yr
3-4m/s – 17%/yr
>4m/s – 40% /yr
NATURAL HISTORY
MITRAL STENOSIS
Mitral annulus
The leaflets
Chordae tendinae-papillary muscle
Underlying ventricular wall
Mitral valve-anatomy
Annulus
Leaflets Anterior- three scallops
Posterior- three scallops
Scallop 1-lateral most
Scallop 3-medial most
LEAFLETS & SCALLOPS
Antero lateral PM- chordae to AL half of both leaflets
Dual blood supply
Postero medial PM- chordae to PM half both leaflets
RCA blood supply
Chordae and papillary muscles
2d echo-features Maximal excursion of leaflet tips Tubular channel
Commissural fusion⇒doming/bowing
Chordal thickening ⇒ abnormal motion
Progressive fibrosis⇒stiffening ⇒calcification
RHEUMATIC MS
Doming of the mitral valve (hockey stick AML)
Funnel shaped opening of mitral valves
Focal thickening and beading of leaflets
calcification
Mitral stenosis 2D
early diastolic doming motion of the AML, restriction of tip motion. Pliable, little fibrosis, calcification, or thickening. Dilated LA
2D-Planimetry
2D short axis imaging of diastolic orifice -planimetry
Smallest orifice at the leaflet tips
Inner edge of the black/white interface traced
Correlates well with hemodynamic assessment
1. Funnel-shaped
Actual limiting orifice at the tip
2. Instrumentation setting
‘’blooming” of the echoes due to increased gain
Technical factors
M-mode assessment
Increased echogenicity of leaflets
Decreased E-F slope >80mm/s⇒MVA =4-6cm² <15mm/s⇒MVA <1.3cm²
Paradoxical anterior motion of PML
Doppler assessment Trans mitral pressure gradient single most imp factor in determining the
severity & relation to symptoms & functional status
Depends onVolume statusHeart rate
Early trans mitral flow volume Cardiac output High output states Mitral reguritation
Mean pressure gradient Average MVA Cardiac output
Peak pressure gradient
Pressure half time
Measure of rate of decay of mitral valve gradient
Time in ms at which initial instant pr gradient declines to one half
Time interval from V max to the point where velocity has fallen to Vmax/√2
PHT=½ Peak=V½
V½=Vmax/√2
V½=V max/1.414
V½=Vmax x .707
MVA=220/PHT
Limitation Post BMV- accuracy ↓
Aortic regurgitation- over estimates MVA
Severe LVH- ↓LV compliance
Prosthetic mitral valve- not validated
Independent of
Cardiac output Mitral regurgitation
PHT
Pressure half time=29% of Deceleration time
MVA=220 ÷ (0.29 × DT)
MVA=759 ÷ DT
Deceleration time
Left atrial dilation
Atrial fibrillation
Spontaneous echo contrast
LA thrombus
Secondary pulm htn-TR
Secondary features of MS
Echo approach to MS Valve morphology Exclude other causes of clinical
presentation MS severity Mean transmitral pr gradient 2D valve area PHT valve area Assos MR LA enlargement Pulmonary art pressure Co-existing TR severity TEE for LA clot
Individuals with score≤8 –excellent for BMV
Those with score≧12-less satisfactory results
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