Ebook A practical approach to clinical echocardiography: Part 2

Part 2 book A practical approach to clinical echocardiography presentation of content: Diastolic function, tissue doppler echocardiography current status an, deformation imaging theory and practice, pericardial diseases, ischemic heart disease, congenital heart disease in adults,... And other content.

ˆ IntroductIon

Both ventricles of the heart are bidirectional hemodynamic

pumps and engage in functions of suction (relaxation)

and ejection (contraction) Relaxation aids in filling

during diastole, and therefore, filling parameters denote

diastolic function The phenomena of relaxation and

contraction are interlinked and energy-dependent

Diastole precedes systole, because no ejection is possible

unless there is filling first The processes of relaxation and

filling constitute diastolic function Increased resistance to

filling is the simplest way of defining diastolic dysfunction

Diastolic dysfunction is the first manifestation of a

disease process and explains the symptoms better

Abnormalities of diastolic function are common to

virtually all forms of cardiac disease Noninvasive

evaluation of diastolic ventricular function is based

on Doppler echocardiographic visualization of inflow

and/or ventricular tissue re-extension, although many

more parameters are described

The study of pressure–volume loop during diastole is

the ideal way to understand and assess diastolic function

However, there are several surrogate methods and

parameters in echo-Doppler techniques, which provide

reasonable, reliable and actionable information about

diastolic function In general, diastolic dysfunction may

be characterized by enlargement of upstream chamber

(atrium), alteration in various phases of diastole and

raised filling pressures However, diastolic dysfunction

is dynamic and in early phases, filling pressures are

not increased Assessment of diastolic function in simulated physiological situation, like exercise, may provide enhanced information Diastolic compensatory mechanisms that maintain filling volume are the earliest evidence of dysfunction There is also evidence of regional diastolic wall motion nonuniformity Noninvasive surrogates often reported in clinical studies reflect integrative properties that lack specificity

Diastolic dysfunction is the physiological expression

of morphological cardiovascular disease The healthy myocardium is an active, nonlinear, nonhomogeneous and anisotropic viscoelastic material During diastolic lengthening, normal cardiac muscle behaves like a spring When the spring is more forcefully compressed during systole, diastolic lengthening is higher and vice versa (Fig 12.1)

There is a certain degree of systolic elastance and also

a definite degree of diastolic elastance.1 In several disease states like hypertension, diabetes and left ventricular hypertrophy as also with aging, systolic elastance remains unaffected or may actually increase, and diastolic elastance decreases, which can be studied and assessed by echo-Doppler parameters of diastolic function (Fig 12.2)

On the other hand, when systolic elastance is reduced, diastolic elastance initially increases due to remodeling and diastolic dysfunction denoted by filling pressures, therein, is a manifestation of fluid overload Most systemic

C h a p t e r

Diastolic Function 205

diseases affect the left ventricle (LV) primarily, and

therefore, it is pertinent to discuss largely about the left

ventricular diastolic function/dysfunction

ˆ FActorS contrIButInG to dIAStoLE

• Decline of the myocardial active state following systole

• Passive effects of connective tissue

• Rapid changes in atrial and ventricular pressures

• Transmitral flow

• Interactions with the right ventricle and pericardium

• Atrial systole

ˆ SIGnIFIcAncE oF dIAStoLIc FunctIon

• Identification of preclinical diseases in probands

• Diagnosis of clinical syndrome of heart failure

• Marker of incremental prognosis in diverse cardiac disorders

• Monitoring therapy and follow-up

• Understanding exercise physiology

• Cardiac versus noncardiac dyspnea

• Physiological versus pathological remodeling

• Optimizing devices and drugs response

• Evaluation of intraventricular dyssynchrony

• Study of pericardial diseasesThere is no single definition for diastolic dysfunction;

many features can get altered, and any one change

or their combination is typically called diastolic dysfunction, although the pathophysiology and functional significance varies greatly.2–4 Clinically, the most common manifestation is an elevated end-diastolic pressure and altered filling patterns, but neither of these identifies specific features of diastolic dysfunction (Fig 12.3)

When diastolic dysfunction is detected, it has some morphological, cellular and proteomic connotations These are:

• A change in the extracellular matrix of the myocardium, with the formation of excess collagen tissue5

• At the cellular level, there is reduced phosphorylation

of sarcomeric proteins

• At the proteomic level, an isoform change in important structural macromolecular proteins such as titin.6

Fig 12.1: Left ventricular pressure-volume loop Note that the diastole

is a mirror image of systole

(IVR: Isovolumic relaxation; IVC: Isovolumic contraction; RF: Rapid

filling; AS: Atrial systole).

Fig 12.2: Pressure-volume loop of a normal subject (green color) and that of a subject with diastolic dysfunction (red color) Note the same end-systolic elastance but with reduced end-diastolic elastance.

Fig 12.3: Diastolic dysfunction in clinical sense is raised diastolic

pressures, which means reduced compliance or increased diastolic

stiffness.

Diastole starts with closure of the aortic valve and ends

with onset of ventricular contraction (Fig 12.4) It has

an initial period of ventricular relaxation without filling

(isovolumic relaxation time [IVRT]) and then three phases

of ventricular filling (DFP) The four phases of diastole are:7

1 Isovolumic relaxation phase

2 Rapid filling phase

3 Diastasis

4 Late diastolic filling due to atrial contraction

Diastolic LV function can be assessed in each of the four

phases of diastole—isovolumic relaxation, rapid filling,

slow filling and atrial contraction (Fig 12.5) These four

phases uniquely reflect cardiomyocyte, myocardial or LV

physiology, and are invariably accessible to noninvasive evaluation Diastolic dysfunction is an abnormality that causes impaired relaxation (and decreased ventricular suction), poor filling or loss of atrial contraction.7

There are two phases in systole (Fig 12.6) These are:

1 Isovolumic contraction phase (IVC)

2 Ejection phase

Combined systolic and diastolic function can be assessed by the ratio of IVRT + IVC time/ejection time This ratio has been called myocardial performance index.8Although used for prognosis in various diseased states,

it has not found practical utility for daily use in most echocardiography labs

ˆ ISoVoLuMIc rELAXAtIon tIME

Isovolumic relaxation time, which corresponds to the time interval from aortic valve closure to mitral valve opening,

is difficult to appreciate from simultaneous LV pressure, aortic pressure and wedge pressure recordings but is easily measured by continuous wave Doppler from the simultaneous display of the end of aortic ejection and the onset of mitral inflow (Fig 12.7)

IVRT has a predictable quantitative relationship to constant of isovolumic relaxation and to left atrial (LA) and aortic pressures.8

• Prolonged IVRT indicates poor myocardial relaxation

• A normal IVRT is about 70 ± 12 milliseconds, and approximately 10 milliseconds longer in people above

40 years of age

Fig 12.4: Graphical representation of various phases of the cardiac

cycle of the left heart.

(DFP: Diastolic filling period).

Fig 12.5: Continuous wave Doppler interrogation with sample volume placed between the left ventricular outflow and the inflow showing all four phases of diastole

(IVR: Isovolumic relaxation; RF: Rapid filling; diastasis—slow filling and AC—late filling due to atrial contribution).

Fig 12.6: Doppler signal from left ventricular inflow close to outflow

tract showing all phases of cardiac cycle

(ET: Ejection time; IVC: Isovolumic contraction).

• If IVRT is prolonged (> 110 milliseconds), LA pressure is

not elevated because the delay in mitral valve opening

is related to lower pressure crossover between LV and

LA in the setting of delayed relaxation

• It is safe to conclude that LA pressure is elevated if the

IVRT is short (< 60 milliseconds) in the presence of

cardiac disease

Its clinical value as an index of diastolic LV function

is limited, because it depends on mitral valve opening

pressures and, therefore, is not uniquely related to

LV dysfunction

ˆ rAPId FILLInG PHASE

In early diastole, chamber wall relaxation unmasks stored

elastic strain, allowing the LV to recoil and act as a suction

pump by aspirating blood into the ventricle Normal left

ventricular (LV) filling occurs rapidly early in diastole

caused by a progressive pressure gradient within the

ventricle and with a low LA pressure

Rapid filling phase accounts for 70% of left ventricular

filling It gets shorter in duration with raised filling

pressures and is prolonged in subjects with impaired

relaxation alone.9 When both impaired relaxation and

raised LA pressure coexist, it has variable duration like in

normal subjects Rapid filling phase is denoted by early diastolic (E) mitral flow wave and antegrade diastolic (D) flow wave of the pulmonary veins Variables affecting rapid filling phase are shown in Figure 12.8

ˆ dEcELErAtIon tIME oF EArLY FILLInG WAVE (MItrAL E- And PuLMonArY d-WAVES)

Deceleration time (DT) is the duration between the peak

of early filling wave and where its linear descending slope reaches zero (Fig 12.9) Nonlinear slopes are not measured

Conditions associated with increased LV stiffness are associated with a more rapid rate of deceleration of early filling and a shorter time for this deceleration.10

• It is an index of resistance to early filling with normal values in range of 150–250 milliseconds

• DT denotes chamber stiffness regardless of heart rate, afterload and contractility

• DT of < 150 milliseconds indicates restrictive filling and relatively noncompliant LV (Fig 12.10)

• DT > 250 milliseconds indicates compensatory nism is in place to overcome impaired relaxation

mecha-Prolonging of DT during therapy is a positive sign

of recovery

• There is a close inverse relationship between DT and pulmonary wedge pressure

• DT is affected by age as well as pericardial restraint

As myocardial relaxation becomes less active with

Fig 12.7: Doppler interrogation between left ventricle outflow and

inflow showing measurement of isovolumic relaxation time (IVRT)

At heart rate of 66 beats/min, IVRT is 76 milliseconds in this normal

subject.

Fig 12.8: Variables affecting rapid filling phase in diastole

(PR: P wave to ORS wave interval).

aging or abnormally delayed due to a disease process,

the rate of LV pressure decline during the early diastole

is reduced, and it takes a longer time to reach the

minimal LV diastolic pressure

• Longer DT indicates impaired diastolic reserve

In this situation with abnormal myocardial relaxation,

a reduced diastolic filling period and a lack of atrial

contraction compromise LV filling

During the time of early flow deceleration, there is

rapid flow into the LA from the pulmonary veins DT of

pulmonary vein diastolic wave has same significance as

that of mitral DT (Fig 12.11) A pulmonary vein DT of < 150

milliseconds has much greater specificity for predicting

elevated filling pressures.11

ˆ dIAStASIS

During the slow LV filling phase or diastasis, residual effects of LV relaxation and ‘dynamic’ effects of fast LV inflow have dissipated This phase is used to construct diastolic LV pressure–volume relations from a single cardiac cycle and allows LV stiffness, the slope of the diastolic LV pressure–volume relation, to be derived under so-called static conditions In subjects with impaired relaxation and longer cardiac cycle, residual effects of LV relaxation may persist and positive filling wave during diastasis (L-wave) may be observed (Fig 12.12) Mitral valve L-waves may be evident in healthy patients with relatively low heart rates.12

Fig 12.9: Graphical display of deceleration time (DT) of mitral early

filling wave.

Fig 12.10: Restrictive filling pattern with deceleration time of

85 milliseconds in a patient with dilated cardiomyopathy.

Fig 12.11: Right upper pulmonary vein flow in a patient with atrial

fibrillation Measuring deceleration time of D-wave. Fig 12.12:(L-wave) during diastasis. Pulsed wave Doppler mitral flow showing positive wave

Diastolic Function 209

Importance of L-Wave

• The L-wave may be seen in relatively bradycardic

patients with normal hearts It is usually < 20 cm/s in

velocity

• A pathological L-wave typically is found in patients with

delayed active relaxation with increased LV stiffness

• In the echo laboratory, patients will often have clinical

heart failure, left ventricular hypertrophy with normal

systolic function or LV systolic dysfunction

• A pathological L-wave is suggestive of elevated

LV preload (pseudonormalization)

• A pathological L-wave has prognostic value, in that it is

predictive of future hospitalizations with heart failure

Occasionally, there can be negative L-wave or mid-diastolic mitral regurgitation due to rapid rise in

LV diastolic pressure as a consequence of early filling (Fig 12.13) Its exact significance is not clear

ˆ AtrIAL KIcK or contrIButIon

Late diastolic filling wave is of short duration and occurs due to atrial contraction just before systole starts This accounts for 20–40% of ventricular filling and is absent in atrial fibrillation This gets partly or completely obliterated

in first degree heart block and markedly raised ventricular stiffness Atrial kick is reflected by late diastolic (A) mitral flow wave and atrial flow reversal (Ar) in pulmonary veins

In markedly elevated left ventricular diastolic pressure, atrial contraction may not produce any antegrade flow wave and may be seen to send flow retrogradely in pulmonary veins (Fig 12.14)

ˆ tISSuE MotIon And dIAStoLIc FunctIon

As transmitral flow commences in diastole, the mitral annulus moves longitudinally upward toward the atrium Due to tissue and blood incompressibility, as the annulus rises, the wall thins, and the endocardium is simultaneously displaced radially outward toward the epicardium During filling, the short and long axes change simultaneously (Fig 12.15) Therefore, rate of longitudinal displacement and radial endocardial displacement are good indicators of diastolic function.13 Early diastolic longitudinal excursion rate can be easily obtained from tissue Doppler studies (Fig 12.16)

Fig 12.13: Mid-diastolic negative L-wave in a patient with left ventricular

diastolic dysfunction.

Fig 12.14: Monophasic mitral flow with normal PR interval and heart rate of 69 beats/min in a 90-year-old subject.

Fig 12.15: Graphical display of longitudinal and radial expansion of

the left ventricle during diastole (arrows).

The LV wall motion generates the atrioventricular

pressure gradient resulting in the early transmitral flow

(Doppler E-wave) and associated vortex formation

Substantial residual LV relaxation pressures in

mid-diastole present in some patients with stiff LV can

result in a positive wave called tissue L’-wave14 (Fig 12.17)

ˆ LEFt AtrIAL VoLuME And dIAStoLIc

FunctIon/dYSFunctIon

The measurement of maximum LA volume is an essential

component of the comprehensive assessment of LV

diastolic function.15,16 More recently, LA volumes have

been obtained by 3D echocardiography

The LA volume is usually measured by biplane area–length method (Fig 12.18) In current guidelines, assessment of diastolic function mandates measurement

of LA volume index in every subject Although it has limited role in assessing diastolic function or dysfunction

in acute situations, it has great relevance in chronic stable cardiovascular conditions

• The LA volume can be viewed as a morphological expression of LV diastolic dysfunction

• Left atrial volume is regarded as a ‘barometer’ of the chronicity of diastolic dysfunction

• This simple measure of LA volume provides significant insight into an individual’s risk for the development of adverse cardiovascular events, including myocardial infarction, stroke, atrial fibrillation and heart failure

• Normal values for LA volume are 22 ± 6 mL/M2

• Left atrial volume is graded relative to risk, 28–33 mL/

M2 = mild; 34–39 mL/M2 = moderate; and ≥ 40 mL/M2

regur-Fig 12.16: Biphasic longitudinal expansion of the left ventricle

during diastole E’, early diastolic and A’, late diastolic longitudinal

tis-sue velocity waves.

Fig 12.17: Tissue L’-wave in diastasis (arrow).

Fig 12.18: Estimation of biplane end-systolic left atrial volume by

area–length method.

Diastolic Function 211

• There is a fairly good positive correlation between

LA volume index and grade of diastolic dysfunction

• Maximum LA systolic lengthening and its rate have

also been found to correlate with diastolic dysfunction

(Figs 12.19 and 12.20)

• It is possible to use LA strain during ventricular

systole along with LA pressure or its Doppler

echocardiographic surrogate (E/e′) to calculate

LA chamber stiffness.17

• LA stiffness has good accuracy in identifying patients

in diastolic heart failure

• Change in volume–pressure relationships in left atrium

also indicates change in material properties (ischemia,

fibrosis, etc.) and physiological or pathological remo deling in the LV

Factors extrinsic to the left ventricular myocardium may influence the end-diastolic pressure–volume relationship Changes in intrathoracic pressure (as with spontaneous or assisted ventilation), pericardial constraints and interventricular interactions may each influence ventricular diastolic pressure (when referenced

to atmospheric pressure), which therefore influences this relationship In the absence of these, intrinsic diastolic function governs this relationship Various equations have been derived from mitral flow and tissue expansion rate to predict end-diastolic pressure E/e’ ratio has the strongest relation to pulmonary capillary wedge pressure (PCWP) [r = 0.86, PCWP = 1.55 + 1.47(E/Ea)], irrespective of the pattern and ejection fraction.18

on dIAStoLIc FunctIon

• After estimation of biplane LA volume, one proceeds

to interrogate by pulsed wave (PW) Doppler, four different sites as shown in Figure 12.21

• With the patient supine, apical four-chamber views using a 2.5-MHz transducer are obtained with the sample volume gated at 1.5–5 mm directed between the tips of the mitral valve leaflets and orthogonal to the mitral valve plane

• Continuous wave Doppler is used to record aortic outflow and mitral inflow from the apical view for determination of the IVRT using a sweep speed of

100 mm/s

Fig 12.19: Left atrial (LA) longitudinal lengthening in a normal

subject compared to that of the left ventricle shortening Typically, LA

lengthening is twice or more than that of the LV shortening.

Fig 12.20: Significantly reduced left atrial global strain in the presence

of diastolic dysfunction.

Fig 12.21: Sites for assessing diastolic function in an apical

four-chamber view.

• In apical four-chamber view, ostium of the right upper

pulmonary vein is interrogated by PW Doppler

• M-mode of the color flow propagation velocity across

the mitral valve up to 4 cm into the cavity is obtained

• Doppler tissue imaging (DTI) of the medial and the

lateral mitral annulus and M-mode images are also

recorded DTI is performed at a sample size gated at

2.5 mm

• Effect of Valsalva maneuver is also observed for the

mitral and pulmonary vein flow

• Sometimes, supine exercise is used to study diastolic

function parameters Post exercise E/A ratio as an

independent determinant of severity of exercise

induced dyspnea and impaired exercise tolerance

• Longitudinal strain and untwisting rate of the LV are

also recorded by acoustic speckle tracking

• After obtaining all the measurements, the diastolic

dysfunction, if present, is graded and occasionally it

may be noted as indeterminate if multiparameters give

conflicting results

ˆ MItrAL InFLoW VELocItIES

The mitral inflow velocity profile is initially used to

characterize LV filling dynamics (Fig 12.22)

• E velocity (E) represents the early mitral inflow velocity

and is influenced by the relative pressures between the

LA and LV, which, in turn, are dependent on multiple

variables including LA pressure, LV compliance and

the rate of LV relaxation.19

• A velocity (A) represents the atrial contractile component of mitral filling and is primarily influenced

by LV compliance and LA contractility

• The DT of the E velocity is the interval from peak E to

a point of intersection of the deceleration of flow with the baseline and it correlates with time of pressure equalization between the LA and LV Incomplete or delayed relaxation causes a delay in the transfer of blood from atria to ventricle

• As the early LA and LV filling pressures either evolve toward or away from equivalence, so will the DT either shorten or lengthen, respectively

• Diastolic dysfunction is directly related to the reduction

in early LV relaxation compromising the effective transfer of the blood from the atrial reservoir into the

LV cavity

• Diastolic dysfunction can be categorized into three stages based upon transmitral filling patterns.2–4

Grade I: Impaired relaxation denoted by DT > 250

milliseconds and E/A velocity ratio < 0.8 (Figs 12.23 and 12.24) The American Society of Echocardiography(ASE) and European Association of Echocardiography (EAE) guidelines suggest DT > 200 milliseconds in Grade I

Early in the evolution of ‘diastolic dysfunction’, the delay in emptying (DT > 250 milliseconds) is partially compensated by a more vigorous end-diastolic atria contraction, and, therefore, the E/A ratio is reduced (< 0.8)

Grade II: Pseudonormal pattern with DT of 150–250

milliseconds and E/A ratio between 0.8 and 1.5 ASE–EAE guidelines put DT in range of 160–200 milliseconds

Fig 12.22: Biphasic mitral flow with sample volume at the tips of the

mitral leaflets. Fig 12.23:prolonged deceleration time. Grade I diastolic dysfunction in transmitral flow with

Diastolic Function 213

Pseudonormal pattern needs confirmation by

increased LA volume (> 34 mL/M2) or mitral E-wave

velocity/annular tissue early diastolic velocity > 15

(medial) or > 12 (lateral) or pulmonary vein flow increased

duration of atrial flow reversal wave or Valsalva maneuver

to unearth impaired relaxation in mitral flow

Presence of L-wave or DT < 150 milliseconds could

also provide clue to pseudonormal pattern if E/A velocity

ratio is 0.8–1.5

Grade III: Restrictive flow or reduced compliance

pattern with DT < 160 milliseconds and E/A ratio ≥ 2.0

Others have used DT cut-off limits of < 150 milliseconds

and < 130 milliseconds as well

Mitral Inflow Measurements

Following measurements should be made in each

examination:

• Peak early filling (E-wave)

• Late diastolic filling (A-wave) velocities

• Diastolic filling time

• A-wave velocity–time integral

• Total mitral inflow velocity–time integral (and thus the

atrial filling fraction) with the sample volume at the

level of the mitral annulus

• Mid-diastolic flow is an important signal to recognize

Low velocities can occur in normal subjects, but when increased (≥ 20 cm/s), they often represent markedly delayed LV relaxation and elevated filling pressures

Most confusions arise in so-called pseudonormal pattern, wherein one or the other parameter can be discordant (Fig 12.25) Help can be obtained from using multiple parameters and any of the other abnormality could be construed as abnormal diastolic function especially if the early diastolic annular tissue velocity is significantly reduced.3,4

Restrictive flow is relatively easy to detect and is unambiguous in adult patients with heart disease (Fig 12.26).20 These criteria can not be used in children and young adults who normally have large E-waves and short DT due to very active suction of the LV

Although not supported by the ASE, others have used Grade IV diastolic dysfunction as the one in which either the restrictive pattern is irreversible21 or has monophasic flow pattern with absent A-wave despite sinus rhythm, normal PR interval and usual heart rates (Fig 12.27)

Mitral Inflow: Acquisition and Feasibility

• PW Doppler is performed in the apical four-chamber view to obtain mitral inflow velocities to assess

LV filling

• Color flow imaging can be helpful for optimal alignment of the Doppler beam, particularly when the

LV is dilated

• Performing continuous wave Doppler to assess peak E

Fig 12.24: Grade I diastolic dysfunction denoted by deceleration time

of 278 milliseconds and E/A 0.7.

Fig 12.25: Pseudonormal or Grade II diastolic dysfunction denoted by presence of L-wave (arrow).

(early diastolic) and A (late diastolic) velocities should

be performed before applying the PW technique to

ensure that maximal velocities are obtained

• A 1- to 3-mm sample volume is then placed between

the mitral leaflet tips during diastole to record a crisp

velocity profile

• Optimizing spectral gain and wall filter settings is

important to clearly display the onset and cessation of

LV inflow

• Spectral mitral velocity recordings should be initially

obtained at sweep speeds of 25–50 mm/s for the

evaluation of respiratory variation of flow velocities, as seen in patients with pulmonary or pericardial disease

• If variation is not present, the sweep speed is increased

to 100 mm/s, at end-expiration, and averaged over three consecutive cardiac cycles

• The Valsalva maneuver is performed by forceful expiration (approximately 40 mm Hg) against a closed nose and mouth, producing a complex hemodynamic process involving four phases It helps to identify pseudonormal mitral inflow and irreversible restrictive flow A decrease in E/A ratio ≥ 0.5 is the criterion (Figs 12.28 and 12.29)

In cardiac patients, a decrease of ≥ 50% in the E/A ratio during Valsalva maneuver is highly specific for increased LV filling pressures, but a smaller magnitude of change does not always indicate normal diastolic function

No change in restrictive flow is an ominous sign.21

ˆ MItrAL AnnuLAr VELocItIES

Diastolic tissue velocities measured at the mitral annulus show low-velocity deflections during early filling (e′) and with atrial contraction (a′) with great clarity.22,23 These indicate biphasic longitudinal expansion rate of the LV (Fig 12.30)

• e′ is presumed to correlate closely with LV relaxation indexes and to be relatively preload insensitive

• Similar to mitral E flow, e′ appears to be age-dependent

Fig 12.26: Restrictive (Grade III) flow pattern with short deceleration

time and E/A ratio ≥ 2.

Fig 12.27: Monophasic transmitral flow pattern in a patient with advanced diastolic dysfunction and heart failure due to previous anterior wall myocardial infarction.

Fig 12.28: Valsalva maneuver changing restrictive flow pattern

(left panel) to pattern of impaired relaxation (right panel).

Diastolic Function 215

Fig 12.29: Effect of Valsalva Upper panel shows restrictive flow

pattern, which changes to pseudonormal pattern with an L-wave at the

end of Valsalva maneuver.

Fig 12.30: Annular tissue velocities from lateral edge of the mitral annulus See text for description.

• E depends on LA pressure, residual LV relaxation

pressure and age and because e′ is presumed to

depend only on LV relaxation pressure, dividing E by e′

eliminates LV relaxation pressure and age, so the E/e′

ratio becomes a noninvasive estimate of LA pressure

(Fig 12.31)

• Septal and lateral mitral annular e′ velocities differ

Recent guidelines for the detection of diastolic

dysfunction recommend use of an E/e′ value that is the

average of septal and lateral mitral annular e′

• A value of medial E/e′ > 15 is usually proposed as evidence for elevated LV filling pressure and a value of E/e′ < 8 as evidence for normal LV filling pressure

• There is a wide range of E/e′ values9–12 for which additional investigations are required to obtain a LV filling pressure estimate (Fig 12.32)

• Technical limitations include angle dependency, signal noise, signal drifting, spatial resolution, sample volume and tethering artifacts

Fig 12.31: Upper panel shows mitral inflow pattern and the lower

panel depicts annular velocities from the lateral edge of the mitral

annulus An E/e’ of 7 indicates normal diastolic function as the e’ is

10 cm/s.

Fig 12.32: Upper panel shows restrictive transmitral flow and the lower panel shows annular velocities of septal edge of the mitral annulus An E/e’ ratio of 10 falls in indeterminate zone.

• e′ can be decreased erroneously by mitral annular

calcification, surgical rings or prosthetic valves

• An average of septal and lateral E/e’ ≥ 13 is suggestive

of elevated filling pressures

• A reduced s’ velocity is an indirect index of diastolic

dysfunction, because there is a close correlation

between longitudinal systolic function and early

diastolic function

• In healthy young individuals, septal e′ is ≥ 10 cm/s

and lateral e′ ≥ 15 cm/s at rest But there are

vendor-dependent variations

• e’ < 5 cm/s in cardiac disease is reflection of advanced

diastolic dysfunction

• E/e′ may not work well in patients with severe mitral

regurgitation, intraventricular conduction delay, or

pacemaker

ˆ HoW to oBtAIn AnnuLAr

tISSuE VELocItIES

• PW Doppler tissue imaging is performed in the apical

views to acquire mitral annular velocities

• The sample volume should be positioned at or 1 cm

within the septal and lateral insertion sites of the mitral

leaflets

• It is recommended that spectral recordings be obtained

at a sweep speed of 50–100 mm/s at end-expiration

and that measurements should reflect the average of

three or more consecutive cardiac cycles

• Primary measurements include the systolic (s), early

(é) and late (á) diastolic velocities

• For the assessment of global LV diastolic function, it is recommended to acquire and measure tissue Doppler signals at least at the septal and lateral sides of the mitral annulus and their average

• In patients with cardiac disease, é can be used to correct for the effect of LV relaxation on mitral E velocity, and the E/é ratio can be applied for the prediction of LV filling pressures

• The E/é ratio is not accurate as an index of filling pressures in normal subjects or in patients with heavy annular calcification, mitral valve disease and constrictive pericarditis

• Presence of tissue Doppler wave during diastasis (l’) is suggestive of diastolic dysfunction (Fig 12.33)

• Higher accuracy of a single-cycle E/e′ ratio in predicting mean wedge pressure in patients with atrial fibrillation using a dual Doppler echocardiographic probe has been shown

• Strain rate during IVRT has good correlations with the time constant of LV relaxation and −dP/dt and is not affected by changes in preload Strain rate can be obtained by tissue velocity imaging.24

Practical tips

• In the presence of normal or pseudonormal mitral flow pattern, an E/e’ ratio ≥ 15 obtained from either edge of the mitral annulus suggests Grade II diastolic dysfunction (Fig 12.34)

• In long-standing disease, an E/e’ ratio may not accurately reflect the magnitude of filling pressures but may be indicative of stiff LV (Fig 12.35)

Fig 12.33: Lateral edge mitral annular velocities showing l’ (arrow)

Diastolic dysfunction is also suggested by e’ < a’.

Fig 12.34: Upper panel shows mitral E of 130 cm/s and the lower panel shows septal edge e’ of 7 cm/s E/e’ ratio is 19, indicating Grade II diastolic dysfunction.

Diastolic Function 217

• Greater utility of E/e’ lies in patients with systolic

dysfunction as compared to those with pure diastolic

dysfunction

• In relatively younger patients, this ratio has greater

predictive value for filling pressure and symptoms

(Figs 12.36 and 12.37)

• If E/e’ does not clearly indicate presence of diastolic

dysfunction, an e’/a’ ratio < 1 can be used along with

other data (Fig 12.38)

• In elderly people, all normal-appearing mitral flow

patterns can not be regarded as pseudonormal

An E/e’ may help define the degree of normalcy

(Fig 12.39)

• Fusion of mitral E- and A-waves may make E/e’ calculation difficult (Fig 12.40) Fusion occurs in several conditions listed below

– Sinus tachycardia– Prolonged PR interval– Intraventricular dyssynchrony– Advanced diastolic dysfunction

• In many disease states, post-systolic tissue waves may mask tissue e’, making it difficult to estimate E/e’ ratio (Fig 12.41)

• Annular post-systolic positive waves may convert severe diastolic dysfunction to mild by virtue of changing transmitral flow pattern (Fig 12.42)

Fig 12.35: Upper panel shows transmitral flow, while the lower

panel shows annular velocities at the septal edge in a patient on

maintenance hemodialysis An E/e’ ratio of 34 does not necessarily

imply very high filling pressures in this otherwise stable patient.

Fig 12.36: Left panel shows normal transmitral flow, while mitral annular velocity at septal margin is 5 cm/s and E/e’ ratio of 20 is indicative of elevated filling pressures and most likely cause of dyspnea.

Fig 12.37: Same patient as in Figure 12.36 E/e’ at lateral margin of

the mitral annulus (16.5) is lower than that at the septal margin but

is still way above normal A lateral E/e’ ≥ 12 is indicative of diastolic

dysfunction.

Fig 12.38: An indeterminate E/e’ ratio from the septal edge is mented by absolute e’ of 5 cm/s and e’/a ratio < 1 in suggesting diastolic dysfunction.

compli-Fig 12.39: A 70-year-old healthy woman with normal mitral flow and

a septal edge E/e’ of 11.

Fig 12.40: Improbability of estimating E/e’ ratio due to fusion of mitral E and A in presence of sinus tachycardia and absence of annular e’-wave (upper panel).

Fig 12.41: Post-systolic annular tissue wave masking e’ This could

be called reversed e’.

Fig 12.42: Impaired relaxation pattern of mitral flow (upper panel)

in a patient with advanced heart failure Post-systolic annular waves extending into mid-diastole (lower panel).

• An E/e’ ratio may not be reliable in the presence of

atrial fibrillation, sinus bradycardia and first degree AV

block (Fig 12.43)

• LV diastolic function can be deciphered through

the evaluation not only of the relationship of the

amplitude of E to e′ but also through the evaluation of

the relationship of the timing of the onset of E to the

onset of e′ Normally, mitral inflow is initiated with

rapid LV relaxation and ‘suction’ of blood into the LV

When this occurs, the onset of e′ will be slightly before

or simultaneous with the onset of E.25 If, however,

LA pressure is elevated and LV relaxation reduced, E

velocity onset may precede the onset of e′ (Fig 12.44) These timing relationships have been correlated with

to 12.47) First S-wave is due to atrial relaxation and the

Diastolic Function 219

Fig 12.43: E/e’ ratio of 7 (lateral) in an 84-year-old person with sinus

bradycardia, first degree AV block with heart failure.

Fig 12.44: Mitral E preceding tissue e’ in a patient with Grade II tolic dysfunction.

dias-Fig 12.45: Pulmonary vein flow pattern in a normal subject Patients

with Grade I diastolic dysfunction have similar pattern.

Fig 12.46: Equivalent pulmonary systolic and diastolic wave but with prolonged atrial flow reversal (Ar) suggestive of diastolic dysfunction.

Fig 12.47: Graphical representation of pulmonary vein flow in a

subject with raised left ventricle filling pressure.

second one (S2) due to descent of the mitral annulus during systole D-wave occurs during opened mitral valve

Ar-wave occurs following atrial contraction when blood has option of flowing antegradely into the LV as well as back in pulmonary veins depending upon the relative resistance.26

• The pattern of pulmonary venous flow (systolic vs

diastolic predominance) has been proposed as a dictor of diastolic dysfunction (Figs 12.48 and 12.49)

pre-However, diastolic preponderance is invariable in children and young adults

• Ar velocity > 35 cm/s also indicates raised filling pressures (Fig 12.49)

• Comparison of the duration of flow at atrial contraction across the mitral valve (on the mitral inflow velocity curve) and the duration of reversal flow back into the pulmonary veins (on the pulmonary venous velocity

Fig 12.48: Right upper pulmonary vein diastolic flow velocity and

velocity–time integral is greater than systolic filling fraction in a patient

with significant diastolic dysfunction.

Fig 12.49: Right upper pulmonary vein atrial flow reversal (Ar) velocity

of 50 cm/s indicative of diastolic dysfunction.

Fig 12.50: Atrial flow reversal (Ar) duration of pulmonary vein > mitral

A by > 30 milliseconds is suggestive of elevated LV end-diastolic

curves) has been repeatedly demonstrated to reflect

the left ventricular end-diastolic pressure (Fig 12.50)

• If the duration of atrial reversal flow in the pulmonary

vein exceeds by more than 30 milliseconds the duration

of flow across the mitral valve, raised left ventricular

end-diastolic pressure can be diagnosed with high

specificity

• The major limitations to the use of the pulmonary

venous signals are that these signals are difficult

to obtain and interpret The technical feasibility of

obtaining adequate signals has been reported at < 80%

of unselected patients

• Pulmonary vein flow, when interpretable, is used to refining the grades of diastolic dysfunction (Figs 12.51

to 12.53)

• Longer duration of mitral atrial flow compared to that

of pulmonary vein atrial flow reversal velocity may

be found in Grade I diastolic dysfunction besides in normal subjects

Acquisition of Pulmonary Vein Flow Signals

• Color flow imaging is useful for the proper location of the sample volume in the right upper pulmonary vein

Diastolic Function 221

Fig 12.52: Equivalent pulmonary venous systolic and diastolic flow

fraction (lower panel) but with inspiratory decrease in D-wave (arrow)

is suggestive of normal filling pattern.

Fig 12.53: Upper panel: mitral flow, middle panel: pulmonary flow, lower panel: septal annular velocities There is hardly any S-wave in pulmonary vein flow and E/e’ of 30 indicating advanced diastolic dys- function.

• In most patients, the best Doppler recordings are

obtained by angulating the transducer superiorly such

that the aortic valve is seen

• A 2- to 3-mm sample volume is placed > 0.5 cm into the

pulmonary vein for optimal recording of the spectral

waveforms

• Wall filter settings must be low enough to display the

onset and cessation of the Ar velocity waveform

• Pulmonary venous flow can be obtained in > 80% of

ambulatory patients, although the feasibility is much

lower in the intensive care unit setting

• The major technical problem is LA wall-motion

artifacts, caused by atrial contraction, which interferes

with the accurate display of Ar velocity

• Spectral recordings should be obtained at a sweep

speed of 50–100 mm/s at end-expiration and

measurements include the average of three or more

consecutive cardiac cycles

Pulmonary Vein Flow Parameters

• Measurements of pulmonary venous waveforms

include peak systolic (S) velocity, peak anterograde

diastolic (D) velocity, the S/D ratio, systolic and

diastolic filling fractions, and the peak Ar velocity in

late diastole

• Other measurements are the duration of the Ar

velocity, the time difference between it and mitral

A-wave duration (Ar−A)

• D velocity DT There are two systolic velocities (S1

and S2), mostly noticeable when there is a prolonged

PR interval, because S1 is related to atrial relaxation

S2 should be used to compute the ratio of peak systolic

to peak diastolic velocity

• S1 velocity is primarily influenced by changes in LA pressure and LA contraction and relaxation, whereas S2 is related to stroke volume and PW propagation in the pulmonary arterial tree

• D velocity is influenced by changes in LV filling and compliance and changes in parallel with mitral

E velocity

• Pulmonary venous Ar velocity and duration are influenced by LV late diastolic pressures, atrial preload and LA contractility

• A decrease in LA compliance and an increase in LA pressure decrease the S velocity and increase the

D velocity, resulting in an S/D ratio < 1, systolic filling fraction < 40% and shortening of the DT of D velocity, usually < 150 milliseconds (Figs 12.54 and 12.55)

• However, DT of mitral E and pulmonary vein D may not always be concordant as DT of D-wave tends to be nonlinear more often (Fig 12.56)

ˆ MItrAL FLoW ProPAGAtIon BY coLor M-ModE

Assessment of flow propagation into the LV is another technique that provides better ability to predict filling pressures.27,28

In the normal state, flow rapidly propagates into the

LV (Fig 12.57) Early stage relaxation abnormalities show

a blunting of flow propagation

The propagation velocity (Vp) does not show a

pseudonormalization, and therefore, can be used in all

levels of diastolic dysfunction

Similar to the tissue Doppler velocities, color M-mode

flow propagation has been combined in a ratio with the

mitral E velocity to provide an ‘adjusted’ parameter (E/Vp)

with strong correlation to filling pressures and prognosis

The chief limitations of this tool are lack of consensus

on technique and theoretical concerns that this will be

invalid in small left ventricular cavities

Practical tips

• Acquisition is performed in the apical four-chamber view, using color-flow imaging

• M-mode scan line is placed through the center of the

LV inflow blood column from the mitral valve to the apex, with baseline shift to lower the Nyquist limit so that the central highest velocity jet is blue

• Vp is measured as the slope of the first aliasing velocity during early filling, measured from the mitral valve

Fig 12.54: Upper panel: pulmonary vein flow, lower panel:

transmi-tral flow Restrictive transmitransmi-tral flow is negated by normal pulmonary

venous flow, although atrial flow reversal is 20 milliseconds longer.

Fig 12.55: Pulmonary vein D-wave > S-wave with deceleration time

of 130 milliseconds indicating elevated left ventricular filling pressure.

Fig 12.56: Upper panel shows short deceleration time (DT) of mitral

E, while DT of pulmonary vein D is longer (170 milliseconds) and

non-linear.

Fig 12.57: Mitral flow propagation velocity by M-mode.

Diastolic Function 223

plane to 4 cm distally into the LV cavity, or the slope of

the transition from no color to color

• Vp > 45–50 cm/s is considered normal (Fig 12.58)

• Should other Doppler indices appear inconclusive,

an E/Vp ratio ≥ 2.5 predicts PCWP > 15 mm Hg with

reasonable accuracy (Fig 12.59)

• Patients with normal LV volumes and EFs but elevated

filling pressures can have misleadingly normal Vp

• Peak velocity of early diastolic mitral flow propagation

velocity (Vp) has been used as an approximation for

• Torsion and circumferential strain are normal in patients with isolated diastolic dysfunction (Fig 12.60)

• Assessment of LV torsion has shown that untwisting begins before aortic valve closure and might be an important component of normal diastolic filling.28

• Studies in human subjects using indirect indexes derived from right heart catheterization have suggested a relationship between constant of isovolumic relaxa tion and measures of untwisting

• But the relationship between directly measured diastolic function indexes with micromanometer catheters and untwisting parameters has not been established in human subjects

• Untwisting parameters are related to invasive indexes

of LV relaxation and suction but not to LV stiffness

These data suggest that untwisting is an important component of early diastolic LV filling but not of later diastolic events

Fig 12.58: Vp of 31 cm/s in a patient with heart failure. Fig 12.59: A 43-year-old female with recurrent pulmonary edema

E/e’ of 12.5 (lateral) is inconclusive but E/Vp of 3.3 suggests raised filling pressures.

Fig 12.60: Normal circumferential strain (right panel) in presence of

advanced diastolic dysfunction.

ˆ dIAStoLIc StrESS tESt

Many patients present with exertional dyspnea but have

normal LV filling pressures at rest

In these patients, it is important to evaluate filling

pressure with exercise.30,31

Exercise can be performed using a supine bicycle or

treadmill protocol

Fig 12.61: Diastolic stress test in a normal person There is proportionate increase in mitral E and e’.

Because most patients have limited functional capacity, the workload starts at 25 W and increases in increments of

25 W every 3 minutes

We need to record mitral inflow by pulsed Doppler echocardiography at the level of the mitral tips, mitral annular velocities by spectral Doppler echocardiography and tricuspid regurgitation jet by CW Doppler (Fig 12.61)

Doppler echocardiography provides major insights into the pathophysiology of diastolic LV dysfunction So far, however, no single Doppler echocardiographic index of diastolic LV dysfunction has yielded a robust criterion for elevated LV filling pressures A stepwise strategy with sequential use of multiple Doppler echocardiographic indexes reduces diagnostic sensitivity because it frequently leads to an indeterminate outcome A multiparametric approach with age and clinical situation in mind is the best way of using echocardiography in detection of diastolic dysfunction because it is so complex and dependent upon multitude of variables (Fig 12.62) Because of these persistent shortcomings, clinicians should continue to make critical use of current Doppler echocardiographic estimates of LV filling pressures and should not hesitate

to implement invasive investigations to confirm their

Fig 12.62: A simplified schema to report diastolic function based upon

pulsed wave Doppler mitral flow, annular velocities and pulmonary

vein flow

(DTI: Doppler tissue imaging).

Diastolic Function 225

clinical suspicions Guidelines for assessing diastolic

function by echocardiography are continually being

updated There is reasonable agreement estimating

dias-tolic grade and LA pressure using current guidelines

Further refinements in the definition of mild and moderate

dysfunction may improve agreement There are a number

of limitations to these measurements, including the need

for high-quality signals, adequate flow visualization in the

apical views, experience in acquisition and analysis, and

so on

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Ö Deformation Imaging: Theory and Practice

Ö Rotation, Twist and Torsion

13 Echocardiography: Current Tissue Doppler

Status and Applications

c h a p t E r

ˆ CONCEPT OF TDI

In 1842, an Austrian scientist, Christian Doppler,

presented the concept of measuring distance of planets

from the earth by using what is now called Doppler

effect A century later, at the University of Osaka, Japan,

S Satomura first applied these principles to measure the

blood flow velocities in blood vessels The pioneer of tissue

Doppler imaging is Karl Isaaz, a French man, who was the

first to realize the importance of clinical and diagnostic

potentials of tissue Doppler imaging He hypothesized

that rate and direction of the heart tissue movement can be

obtained by using the tissue Doppler with the assumption

that the movement is parallel to the ultrasound beam

and within the beam Movements of myocardial walls

include components of low velocity and short duration

requiring a high sampling rate Modifications to the filter

settings on pulsed Doppler to image low-velocity,

high-intensity myocardial signal rather than the high-velocity,

low-intensity signal from blood flow allow tissue velocity

estimation Tissue velocities are nearly one-tenth of the

intracardiac flow velocities Measurement of myocardial

tissue motion has created basis for detailed evaluation of

systolic and diastolic cardiac function not only in terms of

velocity, but also in terms of acceleration, displacement

and deformation variables (Fig 13.1)

ˆ LABELING OF TISSUE VELOCITY WAVEFORMS

• Two positive waves of myocardial shortening can

be recorded in systole The first positive wave (S1)

Fig 13.1: Concept of tissue Doppler echocardiography Using a prespecified region for placement of sample volume, a Doppler spectrum is obtained as shown in the Figure depicting velocities in various phases of the cardiac cycle with preordained filter settings Velocities toward the transducer are positive and away from the transducer are negative Temporal resolution of various waves is due

to high frame rates (> 100 frames/s).

Figs 13.2A to D: (A) Tissue Doppler waveforms S1 and S2 are systolic velocities, while e’ and a’ are early and late diastolic velocities There are small biphasic velocities in isovolumic phases, which are normally not named S1 represents longitudinal component, while S2 denotes circumferential component of the systolic velocities Conventionally, tissue velocities are labeled by lowercase letters; (B) Tissue Doppler wave- forms of the actual tracing from the medial edge of the mitral annulus There are two positive (systolic) and two negative (diastolic) waveforms; (C) Lateral edge mitral annular tissue velocity profile showing two distinct systolic waves (S and S2) in a healthy young control It is the S1 that represents contraction of longitudinal fibers that is usually measured; (D) Color Doppler myocardial imaging After acquisition of image containing velocity information, a sample volume of known length is placed (as here at basal inferior septum) and corresponding velocity spectrum is obtained (shown on the right side).

occurs as a result of the longitudinal shortening of

the myocardial tissue during the phase of isometric

contraction The second wave (S2) occurs due to

left ventricle (LV) shortening during LV ejection

(Figs 13.2A to C) Two peak velocities in systolic ejection

are commonly seen in free wall These represent

functional switch-over from subendocardial

longi-tudinal fibers contraction to circumferential fibers

shortening during ejection with a variable delay

• In healthy subjects, the shortening of the longitudinal fibers predominates over that of the circumferential fibers during early systole, whereas the shortening

of the circumferential fibers predominate over that

of longitudinal fibers in the ejection phase However, their relative importance remains ill-defined and, therefore, both systolic waves should be measured and mentioned However, whenever two waves are seen, it is not clear which one should be used As S1 corresponds

Tissue Doppler Echocardiography: Current Status and Applications 231

to contraction of subendocardial longitudinal fibers, it

is better to use it

• Early diastolic velocity, which correlates with active

relaxation, is labeled e’ It is relatively much less

load-dependent

• Late diastolic velocity, which correlates with ventricular

stiffness, is labeled as a’

• There is no consensus on labeling abnormal waves

However, l’ wave is that recorded in diastasis

• A recoil wave can usually be seen after high-velocity

movements during isovolumic contraction, relaxation

or after early diastolic filling, and occurs in a direction

opposite to initial movement

• The rate of LV pressure decline during isovolumic

relaxation (IVR) becomes slower during the

development of most forms of cardiovascular disease

and also becomes slower during normal aging

Prominent and prolonged IVR phase can be often

noticed in diseased states It may be called ‘IVR’.

ˆ TERMS USED IN TISSUE

DOPPLER IMAGING

Velocity: speed of motion with direction (positive or

negative velocity)

Color velocity imaging shows red hue while shortening

and blue while lengthening Velocity is a vector physical

quantity; both magnitude and direction are required to

define it

Displacement: A displacement is the shortest distance

from the initial to the final position of a point In ultrasound

terms, it is time integral of velocity (velocity × time)

Displacement imaging, also called tissue tracking, uses

different hues for degree of displacement TDI measures

only linear displacement

Strain rate: regional myocardial velocity gradient

Strain rate imaging (SRI) has several hues, for example,

green color denotes no strain rate, while orange–red

hue indicates negative strain rate; blue color indicates

positive strain rate (color hues are reverse of tissue velocity

imaging (TVI)]

Strain: Integral of strain rate and time over a fixed

region measured in percent Strain imaging has different

hues, for example, white means no strain

Acceleration: Rate of velocity over a region (velocity/

time) ‘Deceleration’ is called a ‘negative acceleration’

Momentum: Integral of mass and velocity, rarely used

in TDI, although more common in flow Doppler studies

Deformation: Change in shape and size of an elastic

object when a force is applied Strain and strain rate are examples of deformation imaging

TDI or TVI: An imaging technique that provides

qualitative and quantitative information about regional velocities using pulsed wave Doppler with good temporal resolution

Spectral pulsed TDI is online velocity determination

from a single point by placing a small sample volume It has the advantage of online measurements of velocities and time intervals and an excellent temporal resolution (8 milliseconds)

Color Doppler myocardial imaging (CDMI): An

imaging technique that provides qualitative or quantitative information about spatial velocities using fast Fournier algorithm of color flow mapping Peak velocities measured

by this technique are approximately 20–30% lower than that of TDI, because these are mean velocities rather than peak values (Fig 13.2D)

Merely by turning on a knob, one can convert it to

displacement imaging or deformation imaging or tissue synchronization imaging.

Curved anatomical M-mode TVI: High resolution

semiquantitative technique to study regional tissue velocities and velocity-derived parameters In M-mode tracing, the derivative of the position versus time graph of

an object is equal to the velocity of the object

ˆ TECHNICAL DETAILS OF TDI

TDI is an assessment of myocardial motion using Doppler ultrasound imaging, often with color coding

The fundamental units are velocity observed from the echocardiographic transducer as a frame of reference

Most systems have TDI software, which automatically brings on tissue velocities once a sample volume is placed

in that image after activating the software TDI information

is embedded in gray-scale images or the images are colored

• Velocities are obtained from the selected sample volume (single or multiple point velocity in reference

to the position of the transducer), which can be of variable dimension A sample volume of 2–5 mm is optimum for spectral Doppler, while CDMI has a wide but well-defined area (6–12 mm) from where velocities can be obtained ex post facto

• Tissue velocities are usually < 25 cm/s

• A high sampling rate is essential for a proper rendering

of TVI signals (but introduces noise)—too low frame

rates result in underestimation (< 70 frames/s) To

ensure the optimal signal-to-noise ratio, temporal

filtering should be used with caution (usually 200

frames/s), governed by the awareness of the interplay

between sampling rate and temporal filters

• The influence of unfavorable insonation angle may

affect tissue Doppler measurements resulting in

underestimation of the true myocardial velocities

• Default gain settings of 50% saturation should be used

to measure velocities accurately Overgaining results

in overestimation of tissue velocities by approximately

20% Intervendor settings differences also should be

noted

• In clinical practice, annular velocities are used most

often because these are more reproducible (Fig 13.3)

Usually, septal or lateral edges of the mitral annulus are

interrogated and can be used separately or by averaging

the two Multiple points of the annulus can also be

used to enhance accuracy but are cumbersome and

are not recommended The results of averaging mitral

annular velocities obtained from the four myocardial

walls do not differ from the average of using velocities

measured at the septal and lateral sites

• Color Doppler myocardial velocities are obtained ex

post facto and can be obtained from multiple sites

either in M-mode or two-dimensional (2D) format

(Figs 13.4 to 13.6)

• Color Doppler obtained velocities are 20% to 30% lesser than the pulsed wave Doppler velocities but provide mean velocity estimation from several sites simultaneously

• Temporal resolution is maximum in M-mode tissue velocities, followed by pulsed wave TDI and then CDMI (Fig 13.5B)

• TDI is used for assessing regional longitudinal function It is possible to obtain radial velocities, which are mostly used for pattern reading and understanding myocardial mechanics

• Systolic and early diastolic velocities decrease with aging and hence normal values are age-dependent when used in isolation

• Tissue velocities have a base-to-apex gradient and are usually nearly absent close to the apex Typical annular tissue s’ and e’ velocities are ≥ 8 cm/s in healthy subjects while a’ is less than e’

• Lateral annular velocities are higher than medial annular velocities (Fig 13.6)

• Tricuspid annular and right ventricular (RV) free wall velocities are usually higher than mitral annular and

LV free wall velocities by approximately 20–30%

• Tissue velocities have greatest utility for estimating subclinical systolic and diastolic dysfunction and prognosis All waves have implications Even s’ + e’ have been used for prognosis High temporal resolution provides information about the behavior of the tissue region over the entire cardiac cycle

• The isovolumic myocardial motion variables are

of considerable clinical interest since they appear

to be early markers of pathological phenomena like ischemia-induced disturbances in myocardial function Post-systolic prominent positive velocities usually indicate nonspecific myocardial diseased state and are not specific to ischemia (Fig 13.7)

• Occasionally, there is a negative wave between e’ and a’ during diastasis This is called L’-wave L’-wave is mostly seen when heart rate is slow and represents elevated diastolic pressures (Fig 13.8)

• TDI sometimes show phenomena that are of physiological significance but are not present in flow Doppler interrogation, for example, phasic or pan-cyclic temporal or velocity alternans suggestive of advanced myopathic process (Figs 13.9A and B)

• Accurate measurement of myocardial tissues velocities

is of considerable clinical interest since it is accepted

Fig 13.3: Spectral pulsed wave tissue velocities from the medial

edge of the mitral annulus Velocities obtained from here are most

stable and commonly used for serial studies This is because angle of

insonation is optimal.

Tissue Doppler Echocardiography: Current Status and Applications 233

Figs 13.4A to D: (A) Color Doppler myocardial imaging from interventricular septum Note velocity spectrum derivation from multiple points in

a single cardiac cycle The tissue velocities decrease from base to apex; (B) Color Doppler myocardial imaging from interventricular septum

Note velocity spectrum derivation from multiple points in a single cardiac cycle The tissue velocities decrease from base to apex; (C) Right

ventricular free wall shows base-to-apex gradient of peak systolic velocities and diastolic velocities in a normal adult (D) Color Doppler displacement

imaging of the interventricular septum Average displacement of a myocardial wall is approximately 8 mm with a base-to-apex gradient Note that

the apical segment (red curve) is nearly stationary while the basal segment moves a distance of 13.8 mm in systole.

that decreased peak systolic and early diastolic

velocities indicate failing myocardial function

Attention should be paid to the site and size of sample

volume, frames rates, gain and angle of insonification

• Longitudinal systolic dysfunction (s’ velocities) might

be compensated by an increase of the radial function

Therefore, in early disease states, there is no correlation

between systolic velocities and ejection fraction and the

two provide complimentary but different information

• Before TDI measurements, it is wise to perform cardiac

event marking defining aortic valve opening and

closure and mitral valve opening and closure

• Age, heart rate and LV dimensions account for between

20% and 70% of the variability seen in LV systolic and

diastolic velocities Instead of relying upon normative data from literature, each center should develop its own normal values

• Mitral annular velocity measurement cannot be used

in patients with severe mitral annular calcification, prosthetic ring or prosthetic mitral valve

• Apical segments cannot be assessed using TDI because

of limited movement of the apex and unfavorable angle

of incidence of apical myocardial motion with respect

to the transducer position

• Although TDI has become synonymous with ‘velocity measurement’, in many cases it is not the frequency shift (Doppler shift) of the received signal that is measured, but the phase shift (when the received signal

arrives) This is used to study cardiac asynchrony and

cardiac phase-related myocardial performance index

(isovolumic phase duration/ejection phase duration)

and tissue alternans (Figs 13.9A and B)

ˆ MYOCARDIAL VELOCITIES IN SHORT AXIS

Myocardial velocities in the short axis are acquired

from the posterior wall and the interventricular septum

(Fig 13.10) Short-axis TDI implies the possibility of

measuring a combination of longitudinal, radial and circumferential, rather than the pure circumferential motion

• Posterior wall waves resemble the waveforms of the longitudinal plane with two systolic (S1 and S2) and three diastolic waves (IVR, E’ and A’)

• The motion of the interventricular septum is more complex as it is shared between the two ventricles Moreover, there is a hinge point in the septum, proximal to which it moves away from the LV cavity in

Figs 13.5A and B: (A) M-mode color Doppler myocardial imaging in the apical four-chamber view of the left ventricle Bright orange or red color velocities are positive, while blue ones are negative Note lack of any motion at the apex Also note temporal heterogeneity of the septal wall in this 50-year-old female with hypertrophic cardiomyopathy due to myofiber disarray The walls are traced by curved anatomical M-mode method; (B) M-mode Doppler myocardial imaging of the basal right ventricular free wall Orange color are positive velocities, while blue are negative velocities Note the excellent temporal resolution Positive velocity after early diastolic wave is due to recoil and is normal.

Fig 13.6: Color Doppler myocardial velocities from basal septum

compared to basal lateral wall Note that the velocities from the lateral

wall are higher.

Fig 13.7: Tissue Doppler imaging of medial mitral annulus showing prominent post-systolic positive wave (pst) A negative component

of similar magnitude is present during isovolumic relaxation Post- systolic wave indicates non-specific myopathic process but one induced by stress are specific for ischemia.

Tissue Doppler Echocardiography: Current Status and Applications 235

systole and toward the LV cavity in diastole The part of

the septum distal to it moves in the opposite direction

• The tissue velocities in the later part of the septum

shows two inward movements in systole, the first (S1)

being due to isometric contraction, and the second

(S2) due to ventricular ejection S2 wave in short axis is

bigger than in long axis

• The diastolic waves show a biphasic wave in early

diastole (e’) and a wave of atrial contraction (a’)

• The systolic and diastolic waves occur earlier in the

septum as compared to the posterior wall and are

consistent with the pattern of electrical activation of

the septum This information can be used to detect

ventricular pre-excitation

• The reason for the biphasic motion of the septum

in early diastole is not known It may be because

of translational and/or RV influences (Fig 13.11)

ˆ INTERNAL DEPENDENCY OF VELOCITIES

As systole is coupled with diastole, systolic velocities are related to diastolic tissue velocities s’ velocity denotes longitudinal systolic function, while e’ denotes myocardial relaxation a’ is a reflection of ventricular stiffness

• Systolic velocity (s’) is positively correlated to the early diastolic velocity (e’) Increased longitudinal contraction is able to improve early diastolic LV filling through the effect of elastic recoil and vice versa

Fig 13.8: Tissue Doppler imaging of the lateral edge of the mitral annulus Note prominent L’-wave at a heart rate of 61 beats/min I’-wave is

independent of E’ or A’ magnitude.

Figs 13.9A and B: (A) Tissue Doppler imaging of the medial edge of the mitral annulus Note temporal alternans during diastole (tissue diastole

in milliseconds is shown in each beat) Also note prominent post-systolic positive wave Both alternans and positive isovolumic velocities are

indicative of advanced myopathic process; (B) A 14-year-old female child with heart failure (idiopathic dilated cardiomyopathy) Tissue Doppler

imaging at mitral annulus shows pan-cyclic Doppler alternans, which usually precedes flow alternans and is more specific than the latter Note

alternation of peak velocities as well as duration of each wave There is fusion of e’ and a’ in alternate cardiac cycle due to shortened tissue

diastole.

• There is a negative correlation between early diastolic

(E’) and late diastolic (A’) velocities except in end-stage

disease, where both decrease (Fig 13.12)

• Therefore, S’ and A’ are independent predictors of

myocardial properties while e’ is dependent upon S

• E’/A’ and S’ are more robust parameters of abnormal

physiology

• Limited data exist on isovolumic phase velocities and

their significance at rest Stress-induced prominent

post-systolic positive velocities may be specific markers

of ischemia and correlate with extent of perfusion

defects Prominent post-systolic velocities have also been called delayed longitudinal contractions

• Regional myocardial tissue velocities, however, represent the net effect of the contractile and elastic properties of the area under investigation and traction and tethering effects from other regions Tissue motion can be resolved by velocities but difference between active or passive motion can not be made out For this, myocardial velocity gradient imaging (deformation imaging) is used

• e’/a’ ratio increases with increasing physiological stress and exercise in healthy subjects Abnormal response could signify disease process or aging

• e’ is relatively independent of the effect of heart rate, preload and afterload but is affected by age

ˆ FUNDAMENTAL BASIS OF TDI

Heart as an organ continues to surprise us The intricate layout of muscle fibers from inside to outside, from right

to left and from base to apex is designed for mechanical efficiency of extreme proportions at low energy consumption (Fig 13.13) TVI is one of the techniques that has helped us in understanding this complexity Heart is a complex mechanical organ that undergoes cyclic changes

in multiple dimensions that ultimately effect a change

in chamber volume that results in ejection of blood In simple terms, it is called multidimensional motion or movement Primary motion of heart muscle secondary

to electromechanical coupling provides passive motion

to blood Movement of blood or flow has been studied

Fig 13.10: Myocardial tissue velocities from the posterior wall in short

axis. Fig 13.11:the left ventricular short axis Note the biphasic motion in the posterior M-mode depiction of the color-coded tissue velocities of

wall in isovolumic phases Of note is the bidirectional and bilayered pattern of contraction and relaxation in the interventricular septum.

Fig 13.12: Septal annular pulsed wave Doppler tissue velocity pattern

in an elderly subject Both S’ and E’ are decreased (5–6 cm/s), while A’

is increased (> 10 cm/s) This pattern indicates combined systolic and

diastolic dysfunction.

Tissue Doppler Echocardiography: Current Status and Applications 237

for long by use of the Doppler principle Application

of the Doppler principle to the heart tissue motion is

called tissue Doppler echocardiography (TDI) or tissue

velocity imaging This requires a simple modification

of the settings used for flow velocity studies Regardless

of imaging technique, the holy grail of heart motion or

action called ‘ejection fraction’, which is a sum total of

the heart motion, is unable to provide information on the

underlying myocardial mechanical activity Also, ejection fraction reflects the sum contribution of several regions only during systole and does not provide information on regional function Regional function assessed visually is subjective and prone to error The most difficult part of regional function by conventional imaging method has been the study of diastolic function and isovolumic phase function with temporal and spatial evaluation Focal estimation of the regional function has been the subject

of much research Tissue Doppler imaging (TDI) is one

of the earliest such methods Modifications to the filter settings on pulsed Doppler to image low-velocity, high-intensity myocardial signal rather than the high-velocity, low-intensity signal from blood flow allows segmental

or regional assessment by ultrasound The TDI method depicts myocardial motion (measured as tissue velocity)

at specific locations in the heart Tissue velocity indicates the rate at which a particular point in the myocardium moves toward or away from the transducer Integration

of velocity over time yields displacement or the absolute distance moved by that point Although myocardial velocity curves can be constructed either online from spectral pulse TDI or offline from 2D color TDI, the latter approach is preferable, because multiple segments can be compared within the same heart beat Further estimation

of myocardial velocity gradient by TDI over a fixed region provides strain rate (rate of shortening or lengthening;

Figs 13.14 and 13.15)

Fig 13.13: Myo-architecture of the left ventricle from base to apex

Subendocardial fibers (green line) descend toward the apex and then

make a figure of 8 as these ascend upwards as subepicardial fibers

(red line) Arrows represent circumferential component of the

motion, while other parts represent longitudinal motion.

Fig 13.14: Mean velocity gradient over a segment of fixed length obtained by color Doppler myocardial imaging yields strain rate curves

as shown on the left side of the diagram It is expressed as number/

second.

Fig 13.15: Tissue Doppler-derived strain rate imaging of the

basal septum in the apical four-chamber view over a fixed segment of

12 mm length Systolic strain rates are negative (rate of longi tudinal

shortening, esr), while diastolic strain rates are positive (rate of

diastolic lengthening) Note prominent post-systolic negative strain

rate (pssr), which usually indicates diseased segment.

Time integral of the strain rate gives information about

strain (amount of shortening, thickening or lengthening)

Strain is dependent on preload, afterload, heart rate

as well as state of contraction It correlates best with

dP/dt and to some extent with ejection fraction (Figs 13.16

and 13.17)

The validity of this approach for calculating strain has

been confirmed by the use of sonomicrometry and

tagged-magnetic resonance imaging as reference methods

Tissue velocity per unit time provides regional

myocardial acceleration All these above mentioned

parameters provide incremental assessment of the

function of regional and global heart muscle in health and

disease TDI provided the greatest impetus to the study of

these parameters based upon non-Doppler methods when

limitations of TVI became obvious in certain situations

Despite its obvious limitations, angle dependency,

inability to differentiate active versus passive motion and

nondiagnostic information about radial or circumferential

motion, it has found great utility in diagnosis, prognosis and

guiding therapy of a large number of clinical conditions

Tissue velocity and strain data appear to be of optimal value

if the images are acquired carefully, analysis is meticulous

and the interpretation is judicious and balanced In short,

tissue velocity and strain echocardiography allow detailed

interrogation of regional and global mechanics and offer

substantial incremental information on myocardial

function compared with conventional echocardiography

Both techniques characterize fundamental concepts in cardiac physiology and represent a paradigm shift in the application of echocardiography in clinical practice

ˆ TISSUE DOPPLER DATA PROCESSING FOR DEFORMATION IMAGING

• Strain rate is calculated with a sample volume distance

of 8–12 mm

• A 16-segment model of the left ventricle is used, i.e each wall is subdivided into an apical, mid and basal segment

• Strain rate curves are obtained from the center of the segment and velocity curves are obtained from the basal end

• Wall motion is manually tracked to keep midwall position Three heart cycles are temporally averaged to improve the signal-to-noise ratio of the curves

• Displacement and strain curves are calculated by integrating velocity and strain rate data, respectively, and are baseline-corrected

• TVI and SRI curved M-modes can also be obtained from all walls

• Timing of aortic and mitral valve opening (AVO, MVO) and closure (AVC, MVC) is derived from the echo recordings

• TVI parameters are positive if the region of interest moves toward the transducer (for longitudinal velocities usually systole) and negative if it moves away

Fig 13.16: Diagram depicting strain spectrum from mid-septum

obtained by integrating myocardial velocity gradient and time over a

fixed segment length Strain is derived from color Doppler myocardial

imaging.

Fig 13.17: Tissue Doppler imaging-derived strain spectrum from basal septum Systolic strain is depicted in negative values (-11%) There is additional -3% post-systolic strain Post-systolic strain has same significance as post-systolic velocity.

Tissue Doppler Echocardiography: Current Status and Applications 239

from it SRI parameters are negative in shortening

and positive in lengthening myocardium (Figs 13.18

to 13.20)

ˆ CLINICAL UTILITY OF TDI

TDI has found clinical application in a large number of

clinical situations Of these, the important ones are listed

below:

• Assessment of LV diastolic function and filling

pressures

• Heart failure with normal ejection fraction (HFnEF)

• Assessment of early LV systolic dysfunction

• Constrictive pericarditis versus restrictive myopathy

cardio-• Physiological versus pathological hypertrophy

• Assessment of RV function

• Phenomenon of aging

• Study of exercise physiology

• Utility in stress echocardiography

• Study of atrial function

• Correlation with genomics in hypertrophic myopathy (HCM), Fabry disease, etcetera

cardio-• Prognosis in various disease states

• Study of muscle mechanics

• Detection of intraventricular dyssynchrony

Left Ventricular Filling Pressure and Diastolic Function

The early diastolic velocity of the longitudinal motion of the mitral annulus (e’) reflects the rate of myocardial relaxation (Fig 13.21) In normal subjects, e’ increases as transmitral gradient increases with exertion or increased preload, whereas in patients with impaired myocardial relaxation, e’ is reduced at baseline and does not increase

as much as in normal subjects with increased preload

Lateral annulus early diastolic velocity is usually higher than septal annulus e’ As e’ increases with increasing transmitral gradient in healthy individuals, so that E/e’ is similar at rest and with exercise (usually < 8)

Fig 13.18: Strain rate spectrum derived from basal lateral wall

Negative waveform during systole is integrated with time to obtain

peak systolic strain Note early diastolic strain rate, which is more than

systolic strain rate and correlates with diastolic function.

Fig 13.19: Anatomical M-mode description of strain rate of the interventricular septum Negative strain rate is shown red–orange, while blue color indicates positive strain rate Green indicates no strain rate.

Fig 13.20: Integration of strain rate with time to obtain strain of right

ventricular free wall Peak longitudinal strain is normally around -20%

in left ventricular free wall and around -30% in right ventricular free wall

(RVFW) and its peaks at end systole in health and in diastole in

dis-ease Peak systolic strain of -17% of RVFW suggests RV dysfunction.

Decreased e’ is one of the earliest markers for diastolic

dysfunction and is present in all stages of diastolic

dysfunction However, not everyone with impaired

myo-cardial relaxation has physiologically significant diastolic

dysfunction Because e’ velocity remains reduced and

mitral E velocity increases with higher filling pressure,

the ratio between transmitral E and e’ (E/e’) correlates

well with LV filling pressure or pulmonary capillary wedge

pressure (PCWP) The PCWP is ≥ 20 mm Hg if E/e’ is

≥ 15 and normal if E/e’ is < 8 Because PCWP has been

shown to be a prognostic indicator in patients with

heart failure (HF), it is reasonable to expect E/e’ to be

a similarly powerful prognosticator in various cardiac diseases However, e’ is affected by adjacent wall motion abnormality

Kasner et al who have conducted extensive research correlating invasive versus noninvasive diastolic function using diastolic pressure–volume loops versus early diastolic tissue velocities have found e’ and a’ both to

be robust and reliable methods of assessing diastolic dysfunction in health and disease A combined data showing e’ < a’ and E’ ≤ 8 cm/s at lateral edge of mitral annulus correctly identifies 93% of the patients with invasively proven diastolic dysfunction

The recent guidelines have included E/e’ in grading

of diastolic dysfunction and have made the following observations:

• Mitral annular septal E/e’ ≥ 15 and lateral E/e’ ≥ 12 are indicative of significant diastolic dysfunction (Fig 13.22)

• An average (septal + lateral edge) E/e’ ≥ 13 can also be used as a marker of diastolic dysfunction

• E/e’ ≤ 8 is indicative of normal diastolic function

• E/e’ of 9 to 14 is of borderline significance needing corroboration by other factors (Fig 13.23)

• Overall, E/e’ is the best predictor but does not have adequate discriminative power in isolation in predicting filling pressures

TDI and Exercise Physiology: Heart Failure with Normal Ejection Fraction

Heart failure with normal ejection fraction is present

in > 50% of all HF patients The mortality and morbidity

Fig 13.21: Pulsed Doppler lateral edge mitral annular velocities in a

66-year-old subject with coronary artery disease A ratio of e’/a’ < 1

and e’ 12 cm/s suggests normal left ventricular filling pressures and

normal diastolic function.

Fig 13.22: Mitral annular velocities from medial edge (above) and transmitral pulsed wave Doppler flow pattern Transmitral flow pattern can be normal or pseudonormal; however, reduced e’ (7 cm/s) and E/e’ ratio of 20 indicates Grade II diastolic dysfunction.

Fig 13.23: Pulsed wave mitral flow Doppler (above) and medial mitral

annular tissue velocities (below) in a 58-year-old hypertensive subject

E/e’ is 10 and but e’ < a’ suggests presence of diastolic dysfunction.

Tissue Doppler Echocardiography: Current Status and Applications 241

of these patients may be quite elevated, and making the

diagnosis accurately is important The gold standard

for assessing diastolic function remains the pressure–

volume relationship, but it requires an invasive approach,

ideally with a conductance catheter system Doppler

echocardiography and tissue Doppler imaging have been

studied and validated in patients with systolic dysfunction

and congestive HF and have been shown to be reliable in

assessing filling pressures Kasner et al have shown TDI to

be more accurate than conventional Doppler for detecting

impaired diastolic function in patients with HFnEF

• In general, the lateral annular velocities are more

closely related to the LV relaxation and compliance

indexes as determined by pressure–volume loop

analysis than the septal annular velocities

• TDI indexes e’lat and e’/a’lat correlate more closely with

LV stiffness than any conventional echocardiography

index

• Similarly, the dimensionless E/e’ index shows the

best correlation with indexes of diastolic parameters

obtained by pressure–volume loop measurements

• Patients with HFnEF and E/e’lat > 8 have significantly

increased LV stiffness

• Both E/e’lat > 8 and E’/a’lat < 1 detect HFnEF patients

with diastolic abnormalities equally well, but e’/a’lat

showed lower sensitivity, yielding more false-negative

results than E/e’lat

• Combination of E/e’lat and e’/a’ can detect diastolic dysfunction in 93% of the patients with HFnEF (Fig 13.24)

García et al and Meluzin et al have demonstrated that the peak systolic mitral annular velocity (s’) belongs to the most useful parameters for identifying HFnEF, having even a higher predictive value than the peak early diastolic mitral annular velocity (e’) The following potential predi-ctors of HFnEF have been suggested by Meluzin et al.:

• Exercise s’ < 10 cm/s with a sensitivity and specificity

is the earliest sign of LV systolic dysfunction

Because the LV apex is stationary, simple M-mode measurement of mitral annulus excursion provides a useful and sensitive measure of ventricular function, which is rapidly affected by ischemia The amplitude of long-axis motion during systole also correlates well with left ventricular ejection fraction (LVEF), which is also true for the right ventricle

• Mitral and tricuspid annular systolic excursions have been measured by M-mode echocardiography to assess

LV longitudinal function M-mode measurements of the mitral or tricuspid annulus amplitude are more laborious than measuring the peak systolic and diastolic velocities by TDI, and the time course of this movement is less readily obtained by M-mode

• Peak myocardial systolic velocity averaged from six sites around the mitral annulus correlates well with LVEF, and a cut-off of > 7.5 cm/s had a sensitivity of 79%

and a specificity of 88% in predicting normal global LV function

Fig 13.24: Lateral mitral annular velocities in a 33-year-old

hyperten-sive female with dyspnea e’ lat (6 cm/s) and e’/a’ (< 1) both are

sug-gestive of heart failure with normal ejection fraction with nearly 93%

accuracy.

• Similar data with color Doppler myocardial velocities

from four basal segments have defined a cut-off limit

of 5 cm/s for ejection fraction of 50%

• The peak systolic velocity is also a sensitive marker

of mildly impaired LV systolic function, even in those

with a normal LVEF or apparently preserved LV systolic

function, such as ‘diastolic heart failure’, or in diabetic

subjects without overt heart disease

• Reduced TDI velocities are present also in subjects

with HCM mutations at a time of subclinical disease

when cardiac hypertrophy is not present Therefore,

TDI can be used for early identification of HCM

• In a group of asymptomatic patients with severe mitral

regurgitation but normal ejection fraction, Agricola

et al showed that TDI of the lateral mitral annulus

systolic velocity could predict those who would develop

LVEF reduction after mitral valve surgery (Fig 13.25)

Similar observations have been made in patients with

HF, post-transplant patients, etc

• Peak annular or basal systolic velocities are strong

predictors of outcome in several conditions Wang et al

followed a cohort of 518 subjects (353 with cardiac

disease and the rest normal) for 2 years after measuring

the average mitral annular velocities from four sites

(septal, lateral, anterior and inferior) from color-coded

TDI Cardiac mortality was significantly higher when

both s’ and e’ were ≤ 3 cm/s [hazard ratios (HRs) 7.5

and 5.3, respectively]

• There is a viewpoint that reduced s’ (< 8 cm/s) itself in clinical syndrome of HF correctly characterizes cardiac origin of dyspnea regardless of ejection fraction or E/e’

TDI in Constrictive Pericarditis and Restrictive Cardiomyopathy

Constrictive pericarditis presents like a syndrome of

HF with essentially normal myocardial function except

in advanced state wherein, subepicardial fibers may get involved Pericardial constraint restricts transverse motion of the heart, but longitudinal motion is preserved There is also some degree of RV dysfunction because of compression However, it is the study of the left ventricle that gives clues about constriction in a patient with HF with normal LVEF but elevated filling pressures In these patients, e’ is preserved or even accentuated even though transmitral flow is restrictive (Fig 13.26)

Therefore, E/e’ ratio is normal in constrictive pericarditis while it is increased in other varieties of HF syndrome This phenomenon has been labeled annulus paradoxus (Fig 13.27) Several studies have reported that mitral annular e’ ≥ 8 cm/s can differentiate constrictive pericarditis from restrictive cardiomyopathy with a sensitivity and specificity of > 90% A recent study has suggested an average of > 5.5 cm/s basal segment e’ velocity to have 93% sensitivity in diagnosing constrictive pericarditis In some patients with constriction, regional

Fig 13.25: Medial edge mitral annular velocities in a 64-year-old

patient with asymptomatic severe mitral regurgitation Note normal

diastolic velocities but lower S’ velocity suggestive of subclinical

systolic dysfunction There is paradoxically increased E’ with

decreased S’ This indicates that despite higher preload (increasing

E’), left ventricular systolic function is depressed.

Fig 13.26: Tissue Doppler imaging of lateral edge of the mitral annulus in a 42-year-old surgically proven case of constrictive pericarditis Note prominent e’ (> 26 cm/s) along with normal peak systolic velocity (14 cm/s) Accentuated e’ is due to marked longi- tudinal expansion as transverse expansion is limited by the thick pericardial shell.

Tissue Doppler Echocardiography: Current Status and Applications 243

mitral annular velocities may be decreased because of

concomitant myocardial disease, direct subepicardial and

midmyocardial scarring, compromise of coronary arterial

flow or pericardial calcification It is, therefore, proposed

that tissue Doppler imaging from more than one wall of

the left ventricle would provide a more representative

global measure of longitudinal LV mechanics

Idiopathic restrictive cardiomyopathy as a clinical

syndrome resembles constrictive pericarditis However,

e’ is markedly reduced and annulus paradoxus is absent

(Fig 13.28)

Another tissue Doppler phenomenon mentioned

in constrictive pericarditis is called ‘annulus reversus’

Normally, septal edge mitral annular e’ is lower than the lateral or free edge In patients with constrictive pericarditis, the lateral wall gets tethered to the thick pericardium reducing its movements and hence e’ recorded is lower on the lateral edge (Fig 13.29)

Another tissue Doppler phenomenon observed in constrictive pericarditis is multiple diastolic polyphasic waveforms in the interventricular septum like diastolic fluttering observed during gray-scale imaging (Fig 13.30)

It has relatively high specificity for diagnosing constriction

Significance of TDI in Right Ventricular Function

It is difficult to estimate right ventricular function because of its complex geometry However, RV function has prognostic significance in coronary artery disease, pulmonary hypertension, congenital heart disease and in postoperative cases

The primary function of the RV free wall is to move the atrioventricular valve ring toward the apex

As compared with the evaluation of annular excursions, the Doppler tissue imaging approach is quicker, simpler and measurements can be made online within a very short time interval

Tricuspid annular velocities may be widely used clinically because they can be obtained in nearly all patients, and systolic velocities are independent of age

Fig 13.27: E/e’ of 6 in a 42-year-old patient with surgically proven

constrictive pericarditis Normal E/e’ in a subject with clinical syndrome

of heart failure is called annulus paradoxus Also respiratory variation

in transmitral flow is noted.

Fig 13.28: A 62-year-old male with idiopathic restrictive myopathy and atrial fibrillation Upper panel shows transmitral Doppler flow, while the lower panel shows medial edge mitral annular veloci- ties Note markedly decreased e’ (first of the two negative waveforms) and an E/e’ of 35 Prominent biphasic waveform during isovolumic contraction shows a prominent negative component and a positive component before s’.

cardio-Fig 13.29: Left and upper panel shows tissue velocities of the

medial mitral annulus, while the right lower panel shows the lateral

edge velocities, which are lower than at the medial edge (annulus

reversus).