Diastolic Dysfunction: Nuts, bolts & who cares ?

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• Diastolic Dysfunction Nuts, bolts who cares ?
• Kunjan Bhatt MD
• Austin Heart

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Background

• For patients gt 65 years old, CHF is the most
  common diagnosis at discharge.
• The population is aging
• In the early 1900s, 4 population was gt 65.
• By 2010, 1/3 population will be gt 65.

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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.

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Background

• Classically, weve 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.

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• Lets Clarify some misconceptions

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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 gt 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 gt SHF

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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?

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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. Its
  patronizing to patients who have rip-roaring CHF
  with preserved LV function.
• Spectrum of disease. LOAD DEPENDENT!!
• This is why Im giving the talk!

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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.

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Causes of Diastolic dysfunction ? Heart Failure

• Hypertension
• Hypertension
• Hypertension
• Hypertension
• Hypertension
• Hypertension
• Hypertension

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Other Causes of abnormal Diastolic filling

• Cardiomyopathy
• Hypertrophic
• Restrictive
• Infiltrative
• CAD
• Valvular heart disease
• Diabetes
• Obesity
• Sleep Apnea
• Constrictive Pericarditis

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Determinants of Diastolic filling
Quinones ASE Review 2007
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Topics for Discussion

• Brief Review of Diastolic physiology
• MV inflow patterns
• IVRT Isovolumic Relaxation time
• DT Deceleration time
• Velocity of propagation
• Tissue Doppler of the MV annulus
• E/E
• Atrial Fib and Sinus Tachycardia
• Diseases of the Pericardium
• The who cares factor

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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

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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
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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

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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. Its 20 LV filling.

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• MV Inflow Patterns

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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

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MV PW inflow patterns
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MV inflow pattern limitations
Advantages Disadvantages
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• DT and IVRT

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IVRT Isovolumic relaxation time

• Time interval between aortic valve closure and
  mitral valve opening. Usually obtained from
  Apical view with Doppler sample between AV and MV

• It will lengthen with impaired LV relaxation and
  decrease with with increase in LV filling
  pressures.
• Normal 70 90 ms.

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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.

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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)

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IVRT DT Strengths and Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008 51 679 - 689
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• Velocity of Propogation
• (color M-mode of MV inflow)

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Velocity of propagation of mitral inflow

• Normally, there is a intraventricular pressure
  gradient.
• Apical lt 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.

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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.
• gt 50 cm/s normal
• lt 50cm/s abnormal
• Load dependent.
• Hard to do accurately

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Velocity of propagation of mitral inflow

• Vp has been used to estimate filling pressures
  (PCWP)
• 1. E/Vp gt 1.5 ? PCWP gt 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.

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MV inflow propagation velocity Strengths and
Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008 51 679 - 689
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• LA Volume

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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, its an index)
• A4C and A2C traced LAs
• Shortest length

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LA volume

• Divide the LA volume by BSA!!
• A-L method is used most commonly (we dont like
  calculus)
• 22 /- 6 ml / m2 (normal)
• 28-34 - mild
• 34-40 - moderate
• gt40 - severe

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LA volume Strengths and Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008 51 679 - 689
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• Pulmonary Vein Profile

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Pulmonary venous flow

• Normally 4 different waves seen S1/S2/D/A
• Normal S dominance.
• Young people can have a D dom normally

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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 S2gtS1
• Distinction only identifiable in about 30
  people, normally.

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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

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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.

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PV profiles in diastolic dysfunction.
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Pulmonary Vein flow Strengths and Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008 51 679 - 689
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• Tissue Doppler
• (heres where it gets ugly)

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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

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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

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QUESTION

• WHAT ARE THE 3 profiles seen on Tissue Doppler?

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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 gt 6 cm/s
• Can perform segmental or regional functional
  assessment
• E Early Diastolic velocity
• 2 sites are typically measured medial and
  lateral Normal Range
• Em gt 10 cm/s
• El gt 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)

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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

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Tissue Doppler Normal Profiles
Lateral gt 15 cm/s
Medial gt 10 cm/s
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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 its low doesnt
  increase as much with exertion or inc. preload

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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

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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

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Who cares about Tissue Doppler? (beyond the Echo
Nerd Herd)

• E/E can guesstimate PCWP
• gt15 ? wedge gt 20
• lt 8 normal
• 8 - 15 ??
• E/E has been validated in clinical studies as a
  marker of elevated PCWP (gt 15).

• Elevated E/E is predictive of poor outcomes in
  MI
• Significantly decreased E associated with higher
  mortality.

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E/E is a robust clinical marker

• What the ratio means?
• gt 15 ? elevated filling pressures
• lt 8 ? Nl
• 8 15 ? ???

Nagueh et al, JACC 1997 30 1527 - 1533
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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

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Lets Review
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Normal MV inflow

• E/A 0.9-1.5
• DT 160-240 ms
• IVRT 70-90 ms
• Vp gt 50 cm/s
• S dominant PV pattern

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Stage I

• DT gt 240 ms
• E/A lt 0.9
• IVRT - gt 90 ms
• LAVIgt28 ml/m2
• Elt10
• Vp lt 50 cm/s
• S dominant PV pattern

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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

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How do I differentiate between Stage II and
normal?

• Valsalva shouldnt 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 (Em lt10,
  El lt 15).
• Left atrial volume With elevated filling
  pressures, the left atrium will remodel and
  enlarge (LA Volume Index gt 28 ml / m2)
• Velocity of propagation - gt 50 cm/s (normal) or lt
  50 cm/s (abnormal)
• D dominant pulmonary veins

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Stage II

• Valsalva
• ???

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The 4 Phased Valsalva Maneuver

• 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.

Nishimura et al. Mayo clinic proceedings.
200479 577-578.
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Stage III Restrictive,reversible

• DT lt 160 ms
• IVRT lt 70 ms
• E/A gt 21
• E lt 5cm/s
• Vp lt 50 cm/s
• LAVI gt 35 ml / m2
• DgtgtS (PV Pattern)

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Stage III Restrictive, reversible

• Valsalva
• ???

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Stage IV restrictive irreversible

• DT lt 130ms
• E/A gt 2.5
• E lt 5 cm/s
• Vp lt 50 cm/s
• IVRT lt 70ms
• LAVI gt 40
• No valsalva change
• DgtgtS (PV pattern)

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What about other causes of CHF with preserved LV
function

• TEE 5C view

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Causes of pericardial constriction

• Prior Cardiac surgery
• Idiopathic
• Pericarditis
• Prior Radiation
• Collagen Vascular
• Infection (TB)

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Constrictive Pericarditis

• Everything weve 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

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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

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Echo criteria to diagnose Pericardial Constriction

• 1)Disassociation between intrathoracic and
  intra-pericardial pressures. (normally theyre
  related)
• 2)Exaggerated ventricular interdependence (i.e.
  the filling of one, significantly impacts the
  filling of the other)

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Doppler Findings in Constrictive Pericarditis

• Respiratory variation of gt25 in mitral E
  velocity

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Doppler Findings in Constrictive Pericarditis

• OH Figure 17-29

• Increased DFR with expiration in the hepatic vein.

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Other features of constriction

• Tissue doppler that is gt 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 gt 1.5 and DT lt 160 ms.
• E/E is inversely proportional to the PCWP (as
  opposed to myocardial diseases).

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• WHO CARES?

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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 gt
  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

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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, youll favorably alter
  patient care. Thats the bottom line.

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• Thank you !
• (for not falling asleep)