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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.

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background
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.
background1
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.
background2
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.
misconception 1
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
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
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
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
Causes of Diastolic dysfunction  Heart Failure
  • Hypertension
  • Hypertension
  • Hypertension
  • Hypertension
  • Hypertension
  • Hypertension
  • Hypertension
other causes of abnormal diastolic filling
Other Causes of abnormal Diastolic filling
  • Cardiomyopathy
    • Hypertrophic
    • Restrictive
    • Infiltrative
  • CAD
  • Valvular heart disease
  • Diabetes
  • Obesity
  • Sleep Apnea
  • *** Constrictive Pericarditis
determinants of diastolic filling
Determinants of Diastolic filling

Quinones ASE Review 2007

topics for discussion
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”
normal diastolic function
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
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 function1
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 function2
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 inflow pattern limitations
MV inflow pattern limitations

Advantages Disadvantages

ivrt isovolumic relaxation time
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.
dt and ivrt
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
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
IVRT + DT: Strengths and Weaknesses

StrengthsWeaknesses

Lester et al, JACC 2008; 51; 679 - 689

slide27

Velocity of Propogation

(color M-mode of MV inflow)

velocity of propagation of mitral 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 inflow1
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 inflow2
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
MV inflow propagation velocity: Strengths and Weaknesses

Strengths Weaknesses

Lester et al, JACC 2008; 51; 679 - 689

la volume index
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
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
LA volume: Strengths and Weaknesses

Strengths Weaknesses

Lester et al, JACC 2008; 51; 679 - 689

pulmonary venous flow
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
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 profile1
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 profile2
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.
pulmonary vein flow strengths and weaknesses
Pulmonary Vein flow: Strengths and Weaknesses

Strengths Weaknesses

Lester et al, JACC 2008; 51; 679 - 689

slide43

Tissue Doppler

(here’s where it gets ugly)

tissue doppler
Tissue doppler
  • Measuring tissue velocity and NOTblood 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
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
QUESTION

WHAT ARE THE 3 profiles seen on Tissue Doppler?

tissue doppler1
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
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 (akineticvs scar).
    • Relates to Tissue velocity gradients
tissue doppler normal profiles
Tissue Doppler – Normal Profiles

Lateral > 15 cm/s

Medial > 10 cm/s

tissue doppler2
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 doppler3
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 doppler4
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
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
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
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’
normal mv inflow
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
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
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
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 ii1
Stage II

Valsalva



the 4 phased valsalva maneuver
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. 2004;79: 577-578.

stage iii restrictive reversible
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 iv restrictive irreversible
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)
causes of pericardial constriction
Causes of pericardial constriction
  • Prior Cardiac surgery
  • Idiopathic
  • Pericarditis
  • Prior Radiation
  • Collagen Vascular
  • Infection (TB)
constrictive pericarditis
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
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
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
Doppler Findings in Constrictive Pericarditis

Respiratory variation of >25% in mitral E velocity

doppler findings in constrictive pericarditis1
Doppler Findings in Constrictive Pericarditis
  • Increased DFR with expiration in the hepatic vein.
  • OH Figure 17-29
other features of constriction
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 about diastolic dysfunction
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
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.
slide77

Thank you !

(for not falling asleep)