Ebook The EACVI Echo handbook: Part 2

(BQ) Part 2 book The EACVI Echo handbook presents the following contents: Heart valve disease, cardiomyopathies, right heart function and pulmonary artery pressure, pericardial disease, cardiac transplants, critically ill patients, adult congenital heart disease, cardiac source of embolism (soe) and cardiac masses, diseases of the aorta, stress echocardiography, systemic disease and other conditions.

CHAPTER 7

Heart Valve Disease

7.1 Aortic valve stenosis 201

Should aortic valve area be indexed? 208

What to do in the presence of arrhythmia? 208

Discrepancy between echo and cath lab 209

Aortic valve area planimetry 210

Velocity ratio (dimensionless index: DI) 211

Modified continuity equation (CE) 211

7.4 Tricuspid stenosis (TS) 240

Role of echo 240 Assessment of TS severity 241 Grades of TS severity 243

7.5 Aortic regurgitation (AR) 244

Role of echo 244 Aortic valve anatomy/imaging 246 Mechanism of dysfunction (Carpentier's classification) 247 Assessment of AR severity 249

Integrating indices of AR severity 261 Monitoring of asymptomatic patients with AR 262 Chronic/acute AR: differential diagnosis 263

7.6 Mitral regurgitation (MR) 264

Role of echo 264 Mechanism: lesion/deformation resulting in valve dysfunction 265

Dysfunction (Carpentier's classification): leaflet motion

abnormality 267

Mitral valve anatomy/imaging 269

Mitral valve analysis: transthoracic echo (TTE) 270

Mitral valve analysis: transoesophageal echo (TOE) 272

Probability of successful mitral valve repair in MR 274

Assessment of MR severity 275

Consequences of MR 285

Integrating indices of MR severity 286

Chronic/acute MR: differential diagnosis 287

Monitoring of asymptomatic patients with primary MR 288

Exercise echocardiography in MR 289

7.7 Tricuspid stenosis regurgitation (TR) 290

Role of echo 290

Tricuspid valve anatomy/imaging 291

Tricuspid valve imaging 292

Mechanism: lesion/deformation resulting in valve dysfunction 293

Assessment of TR severity 295

Consequences of TR 303

Integrating indices of TR severity 305

Persistent or recurrent TR after left-sided valve surgery 306

7.8 Pulmonary regurgitation (PR) 307

Role of echo 307

Pulmonary valve (PV) anatomy/imaging 308

Assessment of PR severity 308

Integrating indices of PR severity 312

7.9 Multiple and mixed valve disease 313

Physiologic regurgitation/mechanical valves 328 Pathologic regurgitation in PrVs 330

Aetiology of high Doppler gradients in PrVs 332 Associated features 336

Aortic valve prosthesis 336 Follow-up transthoracic echocardiogram 336

7.11 Infective endocarditis (Ie) 338

Role of echo 338 Anatomic and echo findings 339 Diagnosis of vegetation 340 Diagnosis of abscess 341 Role of 3D echocardiograpy 342 Indications for echocardiography 342 Echocardiographic prognostic markers 343 Echocardiography in IE: follow-up 344 Indications for surgery—native IE 345 Infectious complications 346 Prediction of embolic risk 347 IE: specific situations 348 Prosthetic valve IE (PrVIE) 348 Indications for surgery—PrVIE 349 Cardiac device-related IE (CDRIE) 350 Indications for surgery—CDRIE 351 Right-sided IE 352

◆ calcifications located in the central part of each cusp (no

commissural fusion) resulting in a stellate-shaped systolic

Fig 7.1.1 Aortic stenosis aetiology (top: 2D imaging;

bottom: 3D imaging) A: Degenerative tricuspid valve, B: Bicuspid valve, C: Rheumatic AS Imaging AV: PTLAX and PTSAX views

Features to report: number of cusps, raphe, mobility, calcifications, commissural fusion

Calcifications

Raphe

Commissural fusion

three parameters which should be concordant

◆

aortic orifice measured using CW Doppler

◆

recording as peak velocity

◆

continuity equation (Fig 7.1.2)

TVIAV)

◆

◆

from the apical 5CV just proximal to the valve

◆

◆ TVIAV: time–velocity integral of the jet crossing the aortic

orifice recorded with CW Doppler

◆

measurement of the LVOT diameter is considered not

reliable DI = (TVILVOT / TVIAV)

Fig 7.1.2 The continuity equation

CSALVOT

LVOT Diameter

TVILVOT

TVIAVAortic valve area =

×

the AV orifice (Fig 7.1.3)

◆

septal endocardium to the anterior mitral leaflet)

◆ Diameter is used to calculate a circular cross-sectional area

(CSALVOT = π × (D2/4)) that is assumed to be circular (Fig 7.1.5)

◆

elliptical (Fig 7.1.6)

Fig 7.1.3 LVOT diameter measurement Blue arrow:

0.5–1.0 cm of the AV orifice Red arrow: insertion of aortic cusps

Fig 7.1.6 Elliptical LVOT due

to upper septal hypertrophy

carefully into the LVOT if required to obtain laminar flow

curve (Fig 7.1.7AB)

◆ Low wall filter setting

Fig 7.1.7A AP 5CV LVOT velocity recording

LVOT:

Smooth curve with narrow borders

Valve: aliasing

Fig 7.1.7B LVOT velocity recording

velocity range at peak velocity

LVOT velocity: pitfalls

◆ V1 cannot be ignored if > 1.5 m/s and modified Bernoulli

gradients but is more problematic for calculation of mean

◆ Multiple acoustic windows (e.g apical, suprasternal, right

parasternal) (Fig 7.1.12AB)

Fig 7.1.12B Right parasternal view with Pedof probe (feasibility: 85%)

obstruction Mild obstruction, the peak is in early systole

AS jet velocity: underestimation

◆

jet results in underestimation of AS velocity and gradients

AS jet velocity: overestimation

◆

◆

measurement of higher velocity in AF without averaging peak

velocities)

m/s m/s

AS

AS signal starts after QRS onset

MR has a longer duration, starts with MV closure till MV opening

MR

Fig 7.1.13 CW Doppler MR jet signal

◆ Inclusion in measurement of fine linear signals at the peak of

the curve (due to transit time effect and not to be included)

(Fig 7.1.14)

◆

◆ Pressure recovery (if ascending aorta diameter at STJ < 30 mm

use the ‘energy loss coefficient' = ELCo = (EOA × Aa/(Aa –

EOA))/BSA, where Aa is the aorta diameter

Should aortic valve area be indexed?

◆ In obese patients, valve area does not increase with excess

body weight, and indexing for BSA is not recommended

What to do in the presence of arrhythmia?

◆

◆ Do not use TVI of a premature beat or of the beat after it

◆

◆ Atrial fibrillation: average the velocities from three to five

consecutive beats (Fig 7.1.15)

Fig 7.1.14 CW Doppler AS jet Fine linear signals (arrow)

Fig 7.1.15 CW Doppler AS jet in a patient with atrial fibrillation

Fig 7.1.16 Top: AS CW Doppler signal vs catheterization data Bottom: evaluation of global LV load

MPG = mean aortic pressure gradient using CW Doppler;

PR = pressure recovery; SAP = systolic arterial pressure;

impedance

Total Load

AVA AOA LVOT

Valvulo - Arterial Impedance (Zva)

LVSP

Flow axis

LVSP SVi = SVi = SVi Zva =

LV pressure

PR

0

SAP

Fig 7.1.18 AS AVA planimetry (TOE)

Modified continuity equation (CE)

3D echo assessment of SV (Figs 7.1.20, 7.1.21, Box 7.1.2)

◆

methods to calculate AVA

◆

Box 7.1.1 Formula to calculate DI (Fig 7.1.19)Velocity ratio = TVILVOT / TVIAV

3D Full Volume of the LV

Fig 7.1.21 CW AS jet velocity

TVI AV = 79.6 cm

◆ global longitudinal function is more sensitive to identify intrinsic myocardial

dysfunction (i.e GLS < 16%, Fig 7.1.22)

Table 7.1.1 AS classification (report also blood pressure at the time of examination)

Aortic valve area (AVA), cm 2 Normal ≥ 1.5 ≥ 0.8 cm 2 /m 2 1−1.5 0.6−0.8 cm 2 /m 2 < 1 < 0.6 cm 2 /m 2

Box 7.1.2 Modified CE using 3D echo

AVA = 59/79.6

Left atrial (LA) size

Concentric hypertrophy

Concentric remodelling

( ) ( )

( ) ( )

Fig 7.1.23 LV remodelling/mass evaluation

given valve area but the continuity equation remains valid

◆

severe combined aortic valve disease

pressure ++ (recommendation for surgery class IIaC)

◆

surgery class IIbC)

responsible for the low gradient

opening (weak opening forces)

Dobutamine stress echocardiography (DSe)

beta-blockers ≥ 24 hours before is usually recommended

◆ Changes in mean aortic pressure gradient (MPG) and AVA Fig 7.1.24 dobutamine infusion in a patient with flow reserve Changes in LVOT TVI and AV TVI under

and fixed severe AS Note the increase in SV and MPG

Baseline

13 LVOT Time Velocity Integral (cm)

Preserved LVeF and low-gradient AS

Paradoxical low-flow, low-gradient AS

◆

◆ Definition (Fig 7.1.26)

AVA < 1 cm2 (< 0.6 cm2/m2)

+ LV ejection fraction (EF > 50%)

+ Mean Ao pressure gradient < 40 mm Hg+ SV index < 35 mL/m2

Flow reserve No flow reserve

True severe AS Pseudo-severe AS Indeterminate AS

Final AVA > 1.0 cm 2

AVA<1 cm2MPG<40 mmHg SVi<35mL/m2LVEF>50%

Rule out small body size

Additional features of paradoxical low flow

Zva >4.5 mmHg/ml/m2EDD<47 mm EDVi<55 ml/m 2

RWTR>0.50 GLS<16%

Rule out pseudo-severe AS

dobutamine/exercise stress echo, calcium score by CT, BNP

Present

consider low-flow, low-gradient

AS with preserved LVEF

Absent

consider inconsistencies

in guidelines criteria

Safeguard

- LVOT is proportional to BSA

- theoretical LVOT diameter

= (5.7 × BSA) + 12.1

Consider paradoxical low-flow severe AS

Fig 7.1.26 Stepwise approach to the differential diagnosis of paradoxical low-flow, low-gradient severe AS and LVEF > 50% CMR: cardiac magnetic resonance; CT: computed tomography; BNP: brain natriuretic peptide

Assessment of the presence, severity, and consequence of PS

Aetiology (cause of the valve disease)

outlet RV, complete atrioventricular, univentricular heart

◆

◆ acquired: rheumatic (rare), carcinoid disease, compression by tumour (internal

RVOT or external), deterioration of a bioprosthesis/homograft (Ross surgery)

Not possible, except with 3D but not validated

Pressure gradient (Fig 7.2.2)

Functional valve area

◆

aware of subvalvular stenosis)

◆ PVA: TVIPV/ ((RVOT/2)2 × 3.14) × TVIRVOT

Fig 7.2.2 CW Doppler of PV flow

Colour Doppler aliasing level

pulmonary branch, PV gradient may be different from RV

enlargement, and RA enlargement

◆ Dilated pulmonary artery (Fig 7.2.6)

Grades of PS severity (Table 7.2.1)

Table 7.2.1 Grades of PS severity

Fig 7.2.5A RV hypertrophy (SAX) Fig 7.2.5B RV hypertrophy (AP 4CV) Fig 7.2.6 Dilated pulmonary artery (arrow)

Aetiology (cause of the valve disease)

◆

◆ Primary MS (morphological changes of the MV): rheumatic disease (predominant

cause of MS, commissural fusion, multivalve involvement), degenerative

(calcifications), congenital (very rare in adults), malignant carcinoid disease,

mucopolysaccharidoses, systemic lupus erythematosus,

rheumatoid arthritis, methysergide therapy, post-radiation

therapy

◆

◆ Secondary/functional MS (mitral valve is morphologically

intact): 1) LV inflow obstruction related to extrinsic

compression of the MV (usually in the presence of a

non-diseased valve), 2) intermittent flow obstruction created by a

voluminous LA mass (myxoma/LA thrombus)

Morphology assessment in rheumatic MS

(Box 7.3.1, Tables 7.3.1 and 7.3.2)

◆

◆ Thickening of leaflets edges—first change in RMS, significant

if ≥ 5 mm (Fig 7.3.1)

◆

◆ Fusion of commissures—pathognomonic (Fig 7.3.2

PMC: posteromedial commissure, ALC: anterolateral

commissure; AML: anterior mitral leaflet; PML: posterior

mitral leaflet)

◆

◆ Chordae shortening and fusion—contributes less to MS,

more to associated MR (Fig 7.3.3 Systolic apical displacement

(red arrow) of the leaflet closure line in relation to the mitral

annular plane (green dotted line) due to systolic restriction of

the leaflets Carpentier IIIa MR can be suspected)

◆

◆ Calcific deposits

◆

Box 7.3.1 Morphology assessmentMorphology assessment is crucial for therapeutic decision making, best assessed by TOE, can be completed by

a 3D echocardiographic study Several morphological scores (Wilkins and Cormier) can be used to predict the feasibility of PMC

Fig 7.3.1 TTE PTLAX: Free edge thickening of AML (arrow) transthoracic

Ao LA

Fig 7.3.2 TTE PTSAX zoom mode at the MV opening:

Commissural fusion (arrows)

PMC AML ALC

PML

Fig 7.3.3 TTE modified PTLAX showing the subvalvular apparatus with chordae thickening

Fused & shortened chordae

◆ if doubt regarding the presence of calcific deposits by echo, it

can be confirmed by fluoroscopy

Reduced leaflet mobility

◆

◆ diastolic doming of anterior mitral leaflet (AML) in PSLA

view, most specific echo sign for RMS (Fig 7.3.4)

◆

◆ 'fish-mouth' appearance of the MV in diastole in the PSSA

view (Fig 7.3.5)

◆

◆ ‘hockey-stick' appearance of the AML created by the

leaflet edges thickening + the diastolic doming of the AML

(Fig 7.3.6)

◆

◆ ‘funnel shape', complete loss of mobility, in the late stages of

RMS, frequently associated with Carpentier IIIa MR

Fig 7.3.4 TTE PTLAX: Diastolic doming of the AML (dotted line)

AML

LA

Fig 7.3.5 TTE PTSAX: ‘Fish-mouth'- like opening of the mitral valve in a patient with RMS

AML

PML

Fig 7.3.6 TTE PTLAX: ‘Hockey

stick' appearance of

the AML in diastole

AML

PML

Fig 7.3.7 Wilkin's score: Interpretation

Correlates with good results after PMC

Does not preclude PMC in selected cases

Is associated with poor results after PMC

> 12

≤ 8

Table 7.3.1 Wilkin's score

1 Highly mobile valve Only

leaflet tips have restricted

2 Leaflet mid and basal

segments have normal

mobility

Mid segments of the leaflet are normal but there is considerable thickening of the edges (5–8 mm)

Scattered areas of brightness confined to leaflet's edges

Thickening of chordae extending

to one of the chordae length

3 Valve continues to move

forward in diastole mainly

from the basal segments

Thickening of the leaflets on all segments (edges, mid and basal segments) between 5–8 mm

Table 7.3.2 Cormier score

Echocardiographic group Mitral valve anatomy

Group 1 Pliable non-calcified anterior mitral leaflet and mild subvalvular disease (thin chordae ≥ 10 mm long)

Group 2 Pliable non-calcified anterior mitral leaflet and severe subvalvular disease (thickened chordae < 10

mm long)

Group 3 Calcification of mitral valve of any extent, whatever the state of subvalvular apparatus

level, going up towards the base of the mitral annulus, in a

parallel plane to the MV opening plane (Fig 7.3.8A)

◆

◆ scanning stops at the level of the MV leaflet tip's plane (will

allow definition of the smallest opening orifice)

◆

giving a ‘fish-mouth' appearance of the MV orifice in diastole

◆ measure at least five cardiac cycles in atrial fibrillation

Fig 7.3.8 Image acquisition and measurement

of the MVA by planimetry with 2D TTE

B

MVA Planimetry = 1.0 cm 2

A

◆ allows optimization of the position of the sagittal plane in

relation to MV orifice, increasing accuracy of measurement

◆

lateral plane is adjusted to transect the edges of the MV leaflets

in diastole (Fig 7.3.9)

◆

3D zoom mode or full volume acquisition focused on the MV

◆

◆

reformat of the 3D data (Fig 7.3.10C)

◆

3D image (yellow dotted tracing, Fig 7.3.10D)

Limitations of the planimetry

◆

orifice

◆

◆ too close to the mitral annulus plane or transecting the mid

portion of the MV leaflets → overestimates MVA (Fig 7.3.8A)

◆

◆ oblique in relation to the real MV orifice → excludes one of

the commissures from the image plane → overestimates MVA

Fig 7.3.9 3D TTE—biplane modality

Trans-mitral diastolic pressure gradient (Fig 7.3.11,

Box 7.3.2)

◆

◆ Maximum pressure gradient (PPG) across the valve is related

to the high velocity jet in the stenosis through the simplified

◆

◆ Mean pressure gradient (MPG) is calculated by averaging the

instantaneous gradients over the flow period

◆ Re-evaluation is mandatory after adequate heart rate control

(adjustment of betablocker treatment, optimal HR < 80 bpm)

◆

◆ Always report the HR at which gradient was measured

(important for follow-up studies and disease's progression)

Fixed MV area

Increase in trans-mitral diastolic PG

Increased transvalvular flow (i.e MR, anaemia, etc.)

Increased heart rate (i.e rapid AF, sinus tachycardia)

Increased LA compliance (i.e LA dilatation) Decreased LV compliance (i.e stiff LV) or increase in LV EDP (i.e severe AR)

Decrease in trans-mitral diastolic PG

Fig 7.3.11 Trans-mitral diastolic pressure gradient

Box 7.3.2 Trans-mitral diastolic pressure gradientNot reliable in the first 24–72 h after

percutaneous mitral commissurotomy (PMC) However, it yields prognostic value

in follow-up studies after PMC and should always be reported

Trans-mitral diastolic PG image acquisition (Box 7.3.3)

Box 7.3.3 Trans-mitral diastolic PG image acquisition

◆

allow optimal alignment with the flow)

◆

optimal alignment of the CW Doppler is needed Angle (θ)

between the direction of the flow and CW Doppler line

< 20° to avoid underestimation of PG (Fig 7.3.12A)

◆

prevent signal aliasing) can be used by taking care of an

adequate position the sample volume at the level of the

minimal valve opening plane (into the stenotic orifice)

◆

◆ Baseline is shifted and velocity scale adjusted so that

velocities fill but fit the vertical axis of the tracing

◆

◆ To avid beat-to-beat variation of the signal, patients should

suspend respiration during image acquisition

Box 7.3.4 MeasurementOptimal sweep speed 100–150 mm/s Measurement is done at the black–white

interface (Fig 7.3.12B)

◆

◆ Careful tracing of the outer edge of the signal is done, avoiding the fine linear echoes at the peak of the curve—due to the transit time effect

MG = 8.63 mmHg

HR = 61 bpm

Fig 7.3.12 Colour Doppler-guided detection To avoid underestimation

of PG (A) and measurement (B)

A

B

trans-mitral PG and the time point at which this gradient

attains the half of its maximal value

LVEDP lowers PHT → underestimate MVA

◆ short diastolic filling time (i.e first degree AV block)

Pressure half-time (PhT) measurement (Fig 7.3.13)

◆

MV PHT = 275 ms MVA by PHT = 0.8 cm2

Fig 7.3.13 MVA assessment by PHT Notice that sample volume is position at the level of the minimal valve opening

edge of the diastolic slope is clearly defined

the slowest of the slopes (Fig 7.3.14)

◆

Continuity equation, the Doppler volumetric method

mild AR or MR is present, but PISA method is applicable

◆

steady-state process, the rate at which volume enters a

system is equal to the rate at which volume leaves the system

Fig 7.3.14 MVA assessment by PHT Use the slowest slope to evaluate the PHT

LVOTd = 2.3 cm CSALVOT = π* LVOTd 2 /4

LVOT flow = MV orifice flow

Fig 7.3.15 MVA by the continuity equation

A

C

B

D

direction of flow in order to detect a correct PISA radius

◆

frame where the flow convergence, the jet expansion into the

LV, and the proximal isovelocity surface area are best seen

◆

detect the highest velocity, flow alignment is guided by colour

Doppler

Box 7.3.5 Equations for the Doppler volumetric method

Blood volume at LV inflow in diastole = Blood volume at LV outflow in systole

TVILVOT = time velocity integral of the LVOT

MVA = mitral valve area

TVIMV = time velocity integral of the trans-mitral flow

CSA LVOT = π × D2/4, where D is the LVOT diameter

Box 7.3.6 Equations for the PISA method

2πr2 × Va = MVA × VmaxMVA = 2πr2 × Va/VmaxMVA = 2πr2 × Va/Vmax × (α/180)

◆

◆

◆ 2πr2 is the surface of the hemisphere corresponding

to the velocity of aliasing

r PISA = 0.85 cm

Va = 0.54 m/s

Fig 7.3.16 MVA estimation using the PISA method

MV stenosis is considered haemodynamically significant if MVA < 1.5 cm 2

An MVA < 1.0 cm 2 designates a severe MV stenosis (Table 7.3.3)

Table 7.3.3 Recommendations for classification of MS according to current guidelines

(report heart rate at the time of examination)

Direct findings

Supportive findings

Pulmonary artery pressure < 30 mmHg 30–50 mmHg > 50 mmHg

* in patients in sinus rhythm and heart rate < 80 bpm

prompt the initiation of anticoagulation in MS patients (recommendation class IIa, level of evidence C)

RV dysfunction and failure

◆

patient with MS, but it reflects a higher mortality rate

MS (i.e mild to moderate MS in a patient describing exertional dyspnoea)

◆

changes in trans-mitral pressure gradient and pulmonary artery pressures during exercise

in selecting patients with significant MS at higher risk for future cardiovascular events

Echo criteria for PMC

TOE evaluation is mandatory in patients considered for PMC

difficulties related to transseptal puncture)

Unfavourable echo characteristics

→ is indicative of procedure abortion

Evaluation after PMC (before hospital discharge)

The following features are evaluated (usually by TTE)

◆

Fig 7.3.17 2D TTE evaluation before and after PMC

Wilkins score = 6 MV Vmax = 1.87 m/sMPG = 8.63 mmHg

HR = 61 bpm

MV Vmax = 1.64 m/s MPG = 4.13 mmHg

HR = 55 bpm Opening of the

commissure

A, before PMC

B, after PMC