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DEEPAK NANDAN. ANATOMY Area-2.6-3.5 cm². Structure 3 cusps,3 commissures supported by fibrous annulus Arantius nodule 3 sinuses.

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Presentation on theme: "DEEPAK NANDAN. ANATOMY Area-2.6-3.5 cm². Structure 3 cusps,3 commissures supported by fibrous annulus Arantius nodule 3 sinuses."— Presentation transcript:

1 DEEPAK NANDAN

2 ANATOMY Area-2.6-3.5 cm². Structure 3 cusps,3 commissures supported by fibrous annulus Arantius nodule 3 sinuses

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4  Qualitative diagnosis  Thin and delicate  Plax-opening and closing  Basal short axis view-Y-inverted Mercedes Benz sign

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9  Maximum jet velocity ◦ BERNOULLI’s equation ◦ Multiple windows ◦ Parallel alignment ◦ Colour doppler ◦ Angle correction

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11  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

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14  Discrepancies ◦ Tech poor doppler recording ◦ Non parallel interrogation angle ◦ Pressure grad depends on flow rate & valve narrowing –AR/LV dysfunction

15  Continuity equation:- SV (lvot)= SV (Ao) SV=CSAxTVI CSA (lvot) xTVI (lvot)=CSA (Ao) x TVI (Ao) AVA=CSA x TVI (lvot) / TVI (Ao)

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18  Correlates well with invasive data (GORLINS)  Adv compared to Berrnoulli co-existing AR Left ventricular dysfunction

19  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

20  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)

21  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

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23  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

24  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

25 AVAMACS N > 2cm2N > 15 mm < 0.75 cm2 < 8 mm > 1 cm2 > 12 mm gray area 8 – 12 mm

26  Ao valve resistance- flow independent measure of stenosis severity Resistance=(∆P/∆Q)mean x1333 Resistance=28√gradient( mean)/AVA

27  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 AV Less dependent on the flow >25%--- poor outcome

28  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

29  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

30  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

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32  Mitral annulus  The leaflets  Chordae tendinae-papillary muscle  Underlying ventricular wall

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34 Annulus

35  Anterior- three scallops  Posterior- three scallops  Scallop 1-lateral most  Scallop 3-medial most

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38  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

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40  Maximal excursion of leaflet tips  Tubular channel

41  Commissural fusion⇒doming/bowing  Chordal thickening ⇒ abnormal motion  Progressive fibrosis⇒stiffening ⇒calcification

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43  Doming of the mitral valve (hockey stick AML)  Funnel shaped opening of mitral valves  Focal thickening and beading of leaflets  calcification

44 early diastolic doming motion of the AML, restriction of tip motion. Pliable, little fibrosis, calcification, or thickening. Dilated LA

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50  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

51 1. Funnel-shaped Actual limiting orifice at the tip 2. Instrumentation setting ‘’blooming” of the echoes due to increased gain

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55  Increased echogenicity of leaflets  Decreased E-F slope >80mm/s⇒MVA =4-6cm² <15mm/s⇒MVA <1.3cm²  Paradoxical anterior motion of PML

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57  Trans mitral pressure gradient single most imp factor in determining the severity & relation to symptoms & functional status Depends on Volume status Heart rate

58 Early trans mitral flow volume Cardiac output High output states Mitral reguritation Mean pressure gradient Average MVA Cardiac output Peak pressure gradient

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61  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

62  PHT=½ Peak=V½  V½=Vmax/√2  V½=V max/1.414  V½=Vmax x.707  MVA=220/PHT

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64  Post BMV- accuracy ↓  Aortic regurgitation- over estimates MVA  Severe LVH- ↓LV compliance  Prosthetic mitral valve- not validated

65  Independent of Cardiac output Mitral regurgitation

66  Pressure half time=29% of Deceleration time  MVA=220 ÷ (0.29 × DT)  MVA=759 ÷ DT

67  Left atrial dilation  Atrial fibrillation  Spontaneous echo contrast  LA thrombus  Secondary pulm htn-TR

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69  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

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72  Individuals with score≤8 –excellent for BMV  Those with score≧12-less satisfactory results

73 THANK YOU


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