Evaluation of Diastolic
Dysfunction by
Echocardiography
Brandon Kuebler, MD
Pediatric Cardiology Fellow
Wednesday, February 09, 2011
Assessment of Diastolic Ventricular
Function
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Defining diastole
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Methods to assess diastole
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Patterns of diastolic disease
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Age-related changes
When does diastole occur?
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Is it around tea time?
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No
Required for every heart beat
Systole
Diastole
Phases of Diastole
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Isovolumetric relaxation
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Rapid filling
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E-wave
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2/3 LV filling
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Diastasis
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Atrial contraction
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A-wave
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1/3 LV filling
Factors Affecting Diastole
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Ventricular function
AV valve function
Rate of relaxation
Ventricular compliance
Atrial systolic function
Preload
Heart rate and rhythm
Pulmonary Venous Inflow
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Apical 4-chamber view
Identify RUPV or LUPV
inflow parallel to beam
Pulsed-wave sampling
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Alternatives views:
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Place Apical 4 w PW in Distal PV
1-2 cm distal to orifice
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Parasternal
Suprasternal
Subcostals
Pulsed-wave Pulmonary Vein Inflow
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Identify peak S and D velocities
Measure atrial reversal (AR) duration
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AR presence is variable. It is indicative of abnormal elevated LA pressure
in a neonate, but may be normal in a child with more compliant
pulmonary veins. The duration of flow reversal is more helpful in
relation to atrial systole
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Note: S-wave may be biphasic owing to differences of
atrial relaxation and mitral valve annular displacement
Should take the highest of the peaks
Mitral Inflow
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Apical 4-chamber view
Align Doppler beam to
be parallel to mitral
inflow
Pulsed-wave sampling at
tips of MV leaflets
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Decreased velocity if
sampled within LA
Pulsed-wave Mitral Valve Inflow
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Peak E and A velocities, ratio E/A
Mitral A-wave duration (to compare with PV AR
duration)
Mitral deceleration time(from peak of E-wave to base)
Mitral Doppler VTI (and valve area)
Mitral Valve Doppler Evaluation

In a 5 chamber view
Continuous-wave
across tips of MV
through LVOT
 Obtain mitral inflow
& LV outflow
 Measure
Isovolumetric
Relaxation Time
(IVRT)
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Tissue Doppler
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Measures displacement of myocardium while
avoiding blood flow detection throughout the
cardiac cycle
For our purposes:
Mitral valve annular junction
 Septal annular junction
 Tricuspid annular junction
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Mitral and tricuspid data is relatively volume
load independent, including respiratory cycle
TDI Methodology
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Using Doppler pulsed
cursor, 3-5 mm
Set Nyquist limits to 1530 cm/s
Using lowest wall filter
Set dynamic range to 3035db
Sweep speed of 100-150
mm/s
TDI Pulsed-wave
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Ea ( or E´), Aa ( or A´), Sa ( or S´) waves
IVRT and Isovolumetric Contraction Time (IVCT)
Important to maintain a parallel line of annular motion
with the imaging beam
Color M-mode Flow Propagation
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Estimate of ventricular filling to correlate with LV
relaxation, even at increased LA pressures
Not affected by preload
Varies with changes of lusitropic conditions
Correlates in ischemic heart disease
Color M-mode Flow Propagation
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In apical 4 chamber view
Align M-mode cursor
through LV apex and
orifice of MV
Apply Color Doppler
Switch to M-mode
acquisition
Decrease Nyquist limit
until color inflow shows
line of aliasing
Color M-mode Flow Propagation
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Demonstrated by Garcia et al., JACC 1999, that in both dogs
with occluded IVC and in adults undergoing CABG, under
partial CPB, measures were not affected
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Although, MV E waves and associated measures were impacted by each
scenario
In dogs, under various doses of dobutamine and esmolol, there were
expected changes of Vp correlating to measured changes of LVEDp
Calculations using Vp
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Border et al, JASE 2003
20 pts age 6.6yrs ± 6yrs
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Indicated L heart cath w/o
MV stenosis/arrhythmia
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Found E/ Vp > 2.0,
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LVEDp >15mmHg
Sensitivity 100%
Specificity 77%
PPV: 70%
NPV: 100%
Calculations using Vp(FPV)
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Gonzalez-Vilchez, JACC 1999
Adults in ICU w Swan’s
20 test, 34 study patients
Estimated PCWP = 4.5(103/[2•IVRT]+FPV)-9
Simplified to:
 103/[2•IVRT]+FPV
 Value ≥5.5, correlates to PCWP > 15mmHg (r=0.89)
Calculations using Vp
Use of TDI and Color M-mode in
Infants
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Study by Larrazet et al, Pediatric Critical Care
Medicine, 2005
Studied infants 3-8 months of age, immediately
post-operatively for VSD/AVCD repair w LA
line in place
For LA pressure > 10mmHg
E/Ea > 15 – Sensitivity 94%, Specificity 72%
 E/Vp >2.0 – Sensitivity 83%, Specificity 89%
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LA Volume
In adults, atrial dilation has correlated as a risk for first CV event
(a-fib, stroke, CHF)
 Defined as: women ≥ 30cm2/m2, men ≥ 33cm2/m2
 Not routinely measured in children,
but recent norms established

8/3π[(A1)(A2)/(L)] obtained from Apical 2 & 4 chamber views
LA Volume in Children
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Data collected by 3D Echo and separated by
BSA
0.5-0.75m2 :
 0.75-1.0m2 :
 1.0-1.25m2 :
 1.25-1.5m2 :
 >1.5m2 :
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19.6 mL/m2
21.7 mL/m2
22.0 mL/m2
24.5 mL/m2
27.4 mL/m2
No normative values for RA established in kids
Tricuspid and Right Heart
Evaluation

Usual measures performed on MV, are
influenced by variable preload through the
respiratory cycle.

With inspiration amongst children
Peak E may increase by 26%
 Peak A may increase by 20%
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Tricuspid and Right Heart
Evaluation
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SVC inflow invariably does not have AR amongst
healthy children
AR-wave usually seen with:
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Reversal with ventricular systole
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Right atrial hypertension
Tricuspid stenosis
Significant tricuspid regurgitation
Loss of AV-synchrony
Restrictive physiology
Decreased flow of systemic veins or TV inflow with
Exhalation seen with Tamponade

MV E-wave decreases by >25% during onset of INhalation
Tricuspid and Right Heart
Evaluation

In a restrictive, non-compliant RV, which acts
essentially as a conduit for the PA
Forward flow may be seen in PA with atrial systole
 Only in settings with low PVR or absence of distal
stenoses
 May be seen in those with history of Tetralogy or
Pulmonary valve abnormalities

Classification of Diastolic
Dysfunction
Classification of Diastolic
Dysfunction
Abnormal LV Relaxation
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The ability of the LV myocardial filaments to
actively uncouple after systole, is delayed

Ventricular compliance is unaffected

IVRT is prolonged, as time needed to decrease
LV pressure < LA pressure is extended
Abnormal LV Relaxation
Insert fig
8.14
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LA-LV pressure difference in
early diastole narrowed –
max E-wave velocity
decreased
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LV relaxation is slower, so Ewave is prolonged

A-wave increased as a
compensatory to complete
LV filling
Insert
fig 8.15
Abnormal LV Relaxation
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Infamous “L-wave” seen in MV inflow pattern
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Described by Keren in 1986
Presence of LA-LV pressure gradient in diastasis
Occurs with MARKEDLY delayed LV relaxation
Abnormal LV Relaxation …
and LA Hypertension
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Also called “Pseudonormalization”
Result of worsened ventricular compliance with
transmitted increase of atrial pressure
Ultimately, relative pressure difference between
LA-LV is similar to normal, just at higher
pressure
Pulmonary vein inflow pattern helpful to
distinguish this from normal
Abnormal LV Relaxation … and LA
Hypertension

TDI has been shown to be relatively
independent of preload
Abali et al, JASE 2005, studied 100+ adult males
after 500mL blood donation, found no differences in
TDI measures or Color M-mode, Vp
 Eidem et al, JASE 2005, found that children with
chronic LV preload (VSD’s) and preserved systolic
and diastolic function, did not have changes in TDI

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Those with chronic afterload (AS) demonstrated decreases
of TDI measures
Abnormal LV Relaxation … and LA
Hypertension
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Nagueh et al, JACC 1997
125 adults, 60 cathed for PCWP, separated
Normal from Impaired Relaxation from
Pseudnormalized (EF low in this group)
Found E/Ea >10 correlated to PCWP of
>12mmHg

Sensitivity 91%, Specificity 81%
Nagueh et al, JACC 1997
Could predict mean PCWP= 1.24(E/Ea ) +1.9
TDI in Pseudonormalization
Nagueh et al, JACC 1997, 30; 1527-33
Color M-mode in
Pseudonormalization
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Helpful to differentiate normal MV inflow
patterns from ‘pseudonormalization’
Decreased rate of flow propagation (Vp)
correlate with delayed relaxation, even with
elevated LA pressure
Measures are preload independent
Measure of MV peak E velocity to rate of flow
propagation, E/ Vp > 2.0 predicts LVEDp
>15mmHg (sensitivity 100%, specificity 77%)
Restrictive Physiology/Decreased
Ventricular Compliance
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Ventricle is significantly stiff, non-compliant, that with small
increases of volume, pressures increase disproportionately

On MV inflow, the E-wave is accelerated with short deceleration
time due to rapid rise of ventricular pressure and the end of
inflow

A-wave is remarkably small, if not absent all together, as atrial
systole minimally generates a pressure gradient across the AV
valve
 Instead prolonged reflux in PV observed
Restrictive Physiology/Decreased
Ventricular Compliance
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IVRT shortened due to atrial hypertension with
early opening of MV and ventricular filling
Measures through childhood
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Infants
Very limited early diastolic flow
 Significant contribution from atrial systole
 Limited tolerance to changes in preload
 Improved compliance around 2 months
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Childhood
Limited variability of measures (Inflow/TDI)
through childhood and adolescence
 Noted changes with increasing IVRT likely
associated with age-related decreased HR

Tables of normative values for
children are available
Tables of normative values for
children are available
Let’s apply our data
52.4 cm/s
57.0 cm/s
Let’s apply our data
144 cm/s
72 cm/s
2.0
130
108 ms
90 ms
Let’s apply our data
13.1 cm/s
11
Vs= Vp x Li
Vs = strength of early filling
Vs Strength of Filling
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In a recent article by Stewart et al., JACC Imaging 2011
Found that in addition to a decreased filling velocity
(Vp) with diastolic dysfunction, the velocity further
slowed closer to the MV than the apex (Li)
Vs= Vp x Li
Found this measure to have better correlation to goldstandard than Vp alone
Would like to see used with other measures to further
strengthen accuracy and separation of abnormal states
Looking at Vp
69 cm/s
E/Vp= 2.0
Estimated
PCWP = 4.5(103/[2•IVRT]+FPV)-9
4.5(103/[2•60]+69)-9
= 15 mmHg
Simplified
version = 103/[2•IVRT]+FPV
103/[2•60]+69
= 5.2
To summarize our non-invasive data
E/Vp= 2.0
So by our echo data…
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I would classify this patient as having
 RESTRICTIVE
PHYSIOLOGY
He just so happened to have been cathed
just before I obtained these measures…
I did not know these results
Disease states
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Hypertrophic cardiomyopathy
Chronic disease states
HOCM
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Abnormalities of E/Ea, color M-mode flow
propagation, and diastolic strain rates have
correlated with abnormal relaxation and predict
LV filling pressures.
TDI (DTI) has been found to be predictive of
adverse outcomes
E/Ea >12 predicted risk for SCD, Cardiac Arrest,
and VT
 Those without, events had range 7.4-11.2
 Those with symptoms had ratio higher compared to
those without (11.9 vs 8.1)
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Distinguishing HOCM from Athletic
Heart
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Diastolic TDI annular patterns, IVRT, and LA
volume have identified HOCM in absence of
pathologic changes
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Early diastolic TDI velocities (Ea)
Athletes: normal to increased
 HOCM: consistently decreased, often Ea/Aa <1.
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Children with Chronic Dz’s
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Renal failure
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Those on dialysis had changes on echo compared to normal
controls:
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Increased LV mass with preserved systolic function
Evidence of diastolic dysfunction: higher E’s, lower Ea’s and
therefore increased E/Ea ratios
Obesity
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Demonstrated changes with Ea (↓) and Aa (↑) velocities
where the ratio Ea/Aa was < controls
Demonstrated changes with strain rate imaging also noted
Children with Chronic Dz’s

Obstructive sleep apnea
Evidence of diastolic dysfunction correlated with
severity of sleep apnea
 Measures improved with effective therapies
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Anthracycline toxicity
Demonstrated changes with Ea (↓) and Aa (↑)
velocities, Ea/Aa ratio is ↓↓↓
 Persists over time, even without evidence of systolic
dysfunction
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Congenital Heart Disease

Aortic Stenosis
Measures are more pronounced in more severe
disease
 Does not resolve immediately with relief of
obstruction
 Changes/improvement correlate more with degree
of ventricular hypertrophy
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Congenital Heart Disease

Single ventricles
Demonstrated impaired relaxation, decreased peak E
velocities, presence of mid-diastolic filling waves,
decreased E/A velocity ratio
 Different pulmonary venous inflow patterns due to
different sources of pulmonary antegrade blood flow
 In well functioning single ventricles, biphasic
pulmonary venous inflow still seen (mid-systolic
peak, and late diastolic peak)
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Congenital Heart Disease
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Single ventricles

With decrease ventricular systolic function
Decreased systolic flow in PV
 Increased late diastolic flow in PV
 Seems to correlate with changes in EF

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Serial studies in HLHS
No differences in early stages within 1st year of life
 Need more longitudinal studies
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Congenital Heart Disease

TGA

Atrial Switches (Senning/Mustard)
Found to have decrease IVCT, and sensitive to changes of
systemic RV dysfunction in adolescents and young adults
 Measures of TDI are lower than normals, as expected
 More data needed for the population, esp Arterial
Switches
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References

Frommelt, P. (2009). Diastolic Ventricular Function Assessment. In WW Lai, LL Mertens, MS
Cohen, T Geva (Eds), Echocardiography in Pediatric and Congenital Heart Disease (1st Edition, p95-118).
Hoboken, USA: Wiley-Blackwell.
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Garcia MJ, et al. Color M-mode doppler flow propagation velocity is a preload insensitive index
of left ventricular relaxation: animal and human validation. JACC 2000; 35: 201-8.
Nagueh SF, et al. Doppler tissue imaging: a noninvasive technique for evaluation of left
ventricular relaxation and estimation of filling pressures. JACC 1997; 30: 1527-33.
Eidem BW, et al. Impact of chronic left ventricular preload and afterload on doppler tissue
imaging velocities: a study in congenital heart disease. J Am Soc Echocardiogr 2005; 18: 830-8.
Larrazet F, et al. Tissue doppler echocardiographic and color M-mode estimation of left atrial
pressure in infants. Pediatr Crit Care Med 2005; 6: 448-53.
Gonzalez-Vilchez F, et al. Combined use of pulsed and color M-mode doppler echocardiography
for the estimation of pulmonary capillary wedge pressure: an emperical approach based on an
analytical relation. JACC 1999; 34: 515-23.
Border WL, et al. Color M-mode and doppler tissue evaluation of diastolic function in children:
simultaneous correlation with invasive indices. J Am Soc Echocardiogr 2003; 16: 988-94.
Abali G, et al. Which doppler parameters are load independent? A study in normal volunteers
after blood donation. J Am Soc Echocardiogr 2005; 18: 1260-5.
Stewart KC, et al. Evaluation of LV diastolic function from color M-mode echocardiography. J
Am Coll Cardiol Img 2011; 4: 37-46.
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