Transcript Diastolic Dysfunction – MV inflow

Diastolic Dysfunction:
Nuts, bolts & who
cares ?
Kunjan Bhatt MD
Austin Heart
Background
• For patients > 65 years old, CHF is the
most common diagnosis at discharge.
• The population is aging
– In the early 1900s, ~ 4% population was >
65.
– By 2010, 1/3 population will be > 65.
Background
• Among the elderly, cardiovascular disease
is the MOST common cause of mortality
and morbidity.
• In the US, 5 million people have CHF. ½
these cases are from CHF with preserved
LV function.
Background
• Classically, we’ve sought out causes of
CHF as a result of systolic dysfunction.
• Now we are discovering that ½ cases of
CHF is being caused by diastolic
dysfunction, where LV systolic function is
preserved.
Let’s Clarify some
misconceptions…
Misconception #1
Diastolic dysfunction is uncommon as is Diastolic
congestive heart failure.
• Fact #1
– Everyone and their mother over the age of 40-50 has
E/A reversal, during resting 2D echo. The actual
incidence is ~25-30% in individuals > 45 years.
– Over the past 10 years, incidence of Diastolic CHF has
increased.
• 70 y.o pts’ incidence of CHF: SHF = DHF
• 80 y.o pts’ incidence of CHF: DHF > SHF
Misconception #2
• Discussions of Diastolic dysfunction cause
people to vasovagal, fall asleep, and bore
them ½ to death. Diastolic dysfunction is
simple, SEE?
– E/A normal  great! Normal Diastolic function!
Stop pestering me!
– E/A reversed  whoop-dee-do. Abnormal
diastolic dysfunction. Can we stop talking about
this now?
FACT #2
• This is actually ½ true – this subject is
great to put most people to sleep.
• HOWEVER, Diastolic dysfunction
classification should not be normal or
abnormal. It’s patronizing to patient’s who
have rip-roaring CHF with preserved LV
function.
• Spectrum of disease. LOAD DEPENDENT!!
• This is why I’m giving the talk!
Misconception #3
• Diastolic dysfunction = Diastolic CHF
• Not quite!
• Fact #3
– Diastolic dysfunction characterizes abnormal
relaxation of the LV, and for the purposes of
this talk, an echo finding.
– Diastolic CHF describes a clinical syndrome of
CHF in patient with preserved LV function.
Causes of Diastolic dysfunction
 Heart Failure
• Hypertension
• Hypertension
• Hypertension
• Hypertension
• Hypertension
• Hypertension
• Hypertension
Other Causes of abnormal
Diastolic filling
• Cardiomyopathy
– Hypertrophic
– Restrictive
– Infiltrative
•
•
•
•
•
•
CAD
Valvular heart disease
Diabetes
Obesity
Sleep Apnea
*** Constrictive Pericarditis
Determinants of Diastolic filling
Quinones ASE Review 2007
Topics for Discussion
1. Brief Review of Diastolic physiology
2. MV inflow patterns
3. IVRT – Isovolumic Relaxation time
4. DT – Deceleration time
5. Velocity of propagation
6. Tissue Doppler of the MV annulus
7. E/E’
8. Atrial Fib and Sinus Tachycardia
9. Diseases of the Pericardium
10. The “who cares factor”
Normal Diastolic function
• Occupies about 2/3 of the cardiac cycle.
Takes longer than systole
• Active process, requires energy
• Abnormalities of diastolic function ALWAYS
precede those of systolic function.
– Ex: Acute MI
Normal Diastolic filling
1. Isovolumic Relaxation
2. Early rapid diastolic
filling phase
3. Diastasis
4. Late diastolic filling
due to atrial
contraction
Quinones, ASE Review 2007
Normal Diastolic function
• When LV pressure
•
•
•
becomes less than LA
pressure, MV opens
Rapid early diastolic filling
begins.
Driving force is
predominantly elastic
recoil and normal
relaxation.
~80% LV filling during this
phase
Normal Diastolic function
• As a result of rapid filling,
•
•
LV pressure rapidly
equilibrates with and may
exceed LA pressure.
Results in deceleration of
MV inflow.
Late diastolic filling is from
atrial contraction. It’s ~
20% LV filling.
MV Inflow Patterns
MV inflow Patterns
• 5 stages – Normal and Stages I – IV
diastolic dysfunction
• Stage I – Impaired relaxation
• Stage II – Pseudo-normal
• Stage III – Restrictive Filling, reversible
• Stage IV – Restrictive Filling, irreversible
MV PW inflow patterns
MV inflow pattern limitations
Advantages
Disadvantages
DT and IVRT
IVRT – Isovolumic relaxation
time
• Time interval between • It will lengthen with
aortic valve closure
and mitral valve
opening. Usually
obtained from Apical
view with Doppler
sample between AV
and MV
•
impaired LV relaxation
and decrease with
with increase in LV
filling pressures.
Normal = 70 – 90 ms.
DT and IVRT
• DT - Peak of the E
•
•
wave – time interval
for the E wave
velocity to reach 0.
PHT = 0.29 * DT
IVRT – time interval
of AV closure to MV
opening.
Deceleration time
• Nl = 160 – 220 ms
• Deceleration time increases, if there is abnormal
•
•
relaxation. It decreases in elevated LV filling pressures
The LV can also relax vigorously from tremendous elastic
recoil such as young healthy people (short DT but
normal)
Conversely, if there is a decrease in LV compliance or a
significant increase in LA pressure  DT decreases
(pathologic – suggests elevated filling pressures)
IVRT + DT: Strengths and
Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
Velocity of Propogation
(color M-mode of MV inflow)
Velocity of propagation of mitral
inflow
• Normally, there is a
intraventricular pressure
gradient.
– Apical < Base
• This gradient decreases with
a decrease in myocardial
relaxation
• Color M mode displays color
coded mean velocities from
the annulus to the apex over
time.
Velocity of propagation of mitral
inflow
• Color flow baseline needs to be
•
•
•
•
•
•
shifted to lower the nyquist
limit.
The central highest velocity jet
should be blue.
Trace the slope of the first
aliasing line.
> 50 cm/s normal
< 50cm/s abnormal
Load dependent.
Hard to do accurately
Velocity of propagation of mitral
inflow
• Vp has been used to estimate filling
pressures (PCWP)
1. E/Vp > 1.5  PCWP > 15 mmHg
2. PCWP = 4.5 [1000/(2 x IVRT) + Vp] – 9
3. PCWP = (5.27 x E/Vp) + 4.6
• Falsely high in restrictive Cardiomyopathy
and HOCM.
MV inflow propagation velocity:
Strengths and Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
LA Volume
LA Volume Index
• EASY TO DO!!
• The new echo GOLD
STANDARD for LA size.
• LA 2D dimension extrapolates
that LA enlarges in an AP
diameter. Erroneous
assumption.
• Correlates much better with
the true gold standard which is
MRI.
• Has been called the HbAIC of
cardiac disease. Robust marker
of clinical outcomes
• WHAT DO YOU NEED:
– BSA (remember, it’s an
index)
– A4C and A2C traced LA’s
– Shortest length
LA volume
• Divide the LA volume by
•
•
BSA!!
A-L method is used most
commonly (we don’t like calculus)
22 +/- 6 ml / m2
(normal)
– 28-34 - mild
– 34-40 - moderate
– >40 - severe
LA volume: Strengths and
Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
Pulmonary Vein Profile
Pulmonary venous flow
• Normally 4
different waves
seen – S1/S2/D/A
• Normal S –
dominance.
• Young people can
have a D dom
normally
Pulmonary Vein Profile
• PVs1 – early in systole and
•
relates to atrial relaxation. A
decrease in LA pressure
promotes forward flow.
PVs2 – mid systole.
Represents the increase in
pulmonary venous pressure.
– Normally the S2>S1
• Distinction only identifiable
in about 30% people,
normally.
Pulmonary Vein Profile
• PVd – occurs after
•
opening of the MV and in
conjunction with decrease
in LA pressure
Pva – increase with atrial
contraction. May result in
a flow reversal into the
PV. Depends upon
– LV diastolic pressure
– LA compliance
– HR
Pulmonary Vein Profile
• Think of PVd and Pva as
extensions of MV inflow E and
A.
• The peak velocity and DT
correlate well with those of
mitral E velocity because the
LA acts as a passive conduit
for flow during early diastole.
• DT becomes shorter as PCWP
increases.
• Both Pva velocity and duration
increase with higher LVEDP.
PV profiles in diastolic
dysfunction.
Pulmonary Vein flow: Strengths
and Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
Tissue Doppler
(here’s where it gets ugly)
Tissue doppler
• Measuring tissue velocity and NOT
blood flow
• Speed of tissue is ~ 1/10 of arterial blood.
– Arterial blood velocity ~ 150 cm/s
– Venous Blood velocity ~ 10 cm/s
– Myocardial Tissue velocity ~ 1 – 20 cm/s
• Speed usually expressed in cm/s
Tissue Doppler – What we
change on echo Machines
• Doppler instruments are altered to
reject the high velocity of blood
• Requires a high frame rate
• DECREASE GAIN!
• Lower aliasing velocities
QUESTION
WHAT ARE THE 3 profiles seen on
Tissue Doppler?
Tissue doppler
• 3 velocity profiles are seen – systolic (S’), Early Diastolic (E’) and
late diastolic (A’)
• S’ – systolic velocity of the MV annulus.
– Normally should be > 6 cm/s
– Can perform segmental or regional functional assessment
• E’ – Early Diastolic velocity
– 2 sites are typically measured – medial and lateral – Normal Range…
– E’m – > 10 cm/s
– E’l > 15 cm/s
• A’ –
–
–
–
Late diastolic velocity.
Atrial contraction
Correlates with LA function
Increases in early diastolic dysfunction
decreases with LA dysfunction (later diastolic dysfunction)
TDI - applications
• Beyond E’ and E/E’, mostly in research…
• Evaluation of Thick Walls
– LVH, HCM, Infiltrative CM, Restrictive CM, & Athlete's
Heart
– Normal TDI and strain vs abnormal TDI and strain
• Assessment of viability (akinetic vs scar).
– Relates to Tissue velocity gradients
Tissue Doppler – Normal Profiles
Lateral
> 15 cm/s
Medial
> 10 cm/s
Tissue Doppler
• E’ velocity is essential for classifying the diastolic
•
•
•
filling pattern and estimating filling pressures.
Helpful to differentiate myocardial disease from
pericardial disease
Normally E’ increases with an increase in the
transmitral gradient (exertion or increase
preload)
In Diastolic Dysfunction – it’s low & doesn’t
increase as much with exertion or inc. preload
Tissue Doppler
• E’ decreases with aging (precedes even E/A
•
•
•
reversal)
Load independent! Reproducible
One of the earliest markers for diastolic
dysfunction
Correlates with filling pressures, especially when
used as a ratio
– E/E’
Tissue Doppler
STRENGTHS
1. Can be obtained in most
patients
2. Early marker of diastolic
dysfunction
3. Not influenced by
changes in heart rate
4. Primarily load
independent in disease
states
WEAKNESSES
1. Influenced by local
changes in wall motion
(infarction)
2. Not accurate in significant
MV disease –
- MAC
- MVR
Who cares about Tissue
Doppler?
(beyond the Echo Nerd Herd)
• E/E’ can guesstimate
•
PCWP
– >15  wedge > 20
– < 8 – normal
– 8 - 15 ??
E/E’ has been validated in
clinical studies as a
marker of elevated PCWP
(> 15).
• Elevated E/E’ is predictive
•
of poor outcomes in MI
Significantly decreased E’
associated with higher
mortality.
E/E’ is a robust clinical marker
What the ratio
means?
> 15  elevated
filling pressures
< 8  Nl
8 – 15  ???
Nagueh et al, JACC 1997; 30: 1527 - 1533
Assessment of Diastolic filling in
A-fib and Sinus Tachycardia
• A fib:
– No A wave from Mv inflow and blunted PVs
wave
– DT time measurement is tricky, variable
– Can use E/E’
– Can use DT of the PVd wave
• Sinus Tachycardia
– E and A waves may fuse.
– Use E/E’
Let’s Review
Normal MV inflow
• E/A = 0.9-1.5
• DT = 160-240
ms
• IVRT 70-90 ms
• Vp > 50 cm/s
• S – dominant
PV pattern
Stage I
• DT > 240 ms
• E/A < 0.9
• IVRT - > 90
ms
• LAVI>28 ml/m2
• E’<10
• Vp < 50 cm/s
• S – dominant
PV pattern
Stage II
• Looks the same like
•
•
normal – hence the
name “pseudonormal”
Many of the
parameters are the
same as Normal LV
inflow.
PV – S blunting or D
dominant PV
How do I differentiate between
Stage II and normal?
• Valsalva – shouldn’t change normal but pseudonormal should look like Stage
I. Also Stage III should look like stage I
• E’ (Tissue Doppler) – Normal is normal. Lower velocities with
diastolic dysfunction (E’m <10, E’l < 15).
• Left atrial volume – With elevated filling pressures, the left atrium
will remodel and enlarge (LA Volume Index > 28 ml / m2)
• Velocity of propagation - > 50 cm/s (normal) or < 50 cm/s
(abnormal)
• D – dominant pulmonary veins
Stage II
Valsalva

The 4 Phased Valsalva
Maneuver
Nishimura et al. Mayo clinic proceedings. 2004;79: 577-578.
PHASES
• I - AO pressure
increases (increase in IT
pres.)
• II – AO and PP decrease
because dec. in preload.
Reflex tachycardia.
• III – AO pressure
decreases more in
response to release of IT
pressure
• IV – recovery period.
Preload, AO, PP +
increase.
Stage III – Restrictive,reversible
• DT < 160 ms
• IVRT < 70 ms
• E/A > 2:1
• E’ < 5cm/s
• Vp < 50 cm/s
• LAVI > 35 ml / m2
• D>>S (PV Pattern)
Stage III – Restrictive,
reversible
Valsalva

Stage IV – restrictive
irreversible
•
•
•
•
•
•
•
•
DT < 130ms
E/A > 2.5
E’ < 5 cm/s
Vp < 50 cm/s
IVRT < 70ms
LAVI > 40
No valsalva change
D>>S (PV pattern)
What about other causes of CHF
with preserved LV function
TEE 5C view
Causes of pericardial
constriction
• Prior Cardiac surgery
• Idiopathic
• Pericarditis
• Prior Radiation
• Collagen Vascular
• Infection (TB)
Constrictive Pericarditis
• Everything we’ve spoken about for diastolic
•
•
•
•
dysfunction DOES NOT APPLY HERE.
Not uncommon
Escapes clinical and echo detection
Pericardial Thickness may be normal in
1/5th of cases
Calcification of the pericardium may only
occur in ~ 20% pts on CXR
Constrictive Pericarditis – some
Echo findings
• Thickened pericardium (~ 80%)
• Abnormal ventricular septal motion
• Flattening of the posterior wall during
diastole
• Respirophasic variation of Ventricular
cavity size
• Dilated IVC
Echo criteria to diagnose
Pericardial Constriction
1)Disassociation between intrathoracic and
intra-pericardial pressures. (normally
they’re related)
2)Exaggerated ventricular
interdependence (i.e. the filling of one,
significantly impacts the filling of the
other)
Doppler Findings in Constrictive
Pericarditis
Respiratory variation of >25% in mitral E velocity
Doppler Findings in Constrictive
Pericarditis
• OH Figure 17-29
• Increased DFR with expiration in the hepatic vein.
Other features of constriction
• Tissue doppler that is > 7 cm/s (annulus
paradoxus)
– Unless the myocardium is involved, myocardial relaxation is
intact.
– Septal annular velocities are normal or even increased (not close
to the pericardium like the lateral annulus)
• PW MV inflow that looks like restrictive filling
pattern 
– E/A > 1.5 and DT < 160 ms.
• E/E’ is inversely proportional to the PCWP (as
opposed to myocardial diseases).
WHO CARES?
Who cares about diastolic
dysfunction?
• Steady rise in prevalence of CHF with preserved LV
•
•
•
function.
By the 7th decade, incidence of diastolic CHF = systolic
CHF
By the 8th decade, incidence of diastolic CHF > systolic
CHF
The survival of patients with the clinical
syndrome of heart failure is similar in those with
persevered versus those with a reduced LV
ejection fraction
Summary
• Diastolic Dysfunction is a real, dynamic process.
• Much information can be gained on LV filling
•
•
pressures without a drop of blood (no cath)
Prognostic information and therapeutic options
stem from the results (myocardial, pericardial).
You are in the front line to look for this stuff.
Keep a sharp look out, you’ll favorably alter
patient care. That’s the bottom line.
Thank you !
(for not falling asleep)