1. Diastolic Dysfunction: Nuts, bolts & who cares ?
Kunjan Bhatt MD
Austin Heart

2. 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.

3. 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.

4. 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.

5. Let’s Clarify some misconceptions…

6. Misconception #1
Diastolic dysfunction is uncommon as is Diastolic congestive heart failure.
Fact #1
Everyone and their mother over the age of 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

7. 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?

8. 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!

9. 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.

10. Causes of Diastolic dysfunction  Heart Failure
Hypertension

11. Other Causes of abnormal Diastolic filling
Cardiomyopathy
Hypertrophic
Restrictive
Infiltrative
CAD
Valvular heart disease
Diabetes
Obesity
Sleep Apnea
*** Constrictive Pericarditis

12. Determinants of Diastolic filling
Quinones ASE Review 2007

13. 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”

14. 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

15. 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

16. 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

17. 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.

18. MV Inflow Patterns

19. 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

20. MV PW inflow patterns

21. MV inflow pattern limitations
Advantages Disadvantages

22. DT and IVRT

23. 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.

24. 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.

25. 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)

26. IVRT + DT: Strengths and Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008; 51;

27. Velocity of Propogation
(color M-mode of MV inflow)

28. 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.

29. 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

30. 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.

31. MV inflow propagation velocity: Strengths and Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008; 51;

32. LA Volume

33. 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

34. 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)
mild
moderate
>40 - severe

35. LA volume: Strengths and Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008; 51;

36. Pulmonary Vein Profile

37. Pulmonary venous flow Normally 4 different waves seen – S1/S2/D/A
Normal S – dominance.
Young people can have a D dom normally

38. 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.

39. 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

40. 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.

41. PV profiles in diastolic dysfunction.

42. Pulmonary Vein flow: Strengths and Weaknesses
Strengths Weaknesses
Lester et al, JACC 2008; 51;

43. (here’s where it gets ugly)
Tissue Doppler
(here’s where it gets ugly)

44. 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

45. 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

46. WHAT ARE THE 3 profiles seen on Tissue Doppler?
QUESTION
WHAT ARE THE 3 profiles seen on Tissue Doppler?

47. Tissue doppler S’ – systolic velocity of the MV annulus.
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)

48. 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

49. Tissue Doppler – Normal Profiles
Lateral > 15 cm/s
Medial > 10 cm/s

50. 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

51. 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’

52. Tissue Doppler STRENGTHS WEAKNESSES
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

53. Who cares about Tissue Doppler? (beyond the Echo Nerd Herd)
E/E’ can guesstimate PCWP
>15  wedge > 20
< 8 – normal ??
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.

54. 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:

55. Assessment of Diastolic filling in A-fib and Sinus Tachycardia
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’

56. Let’s Review

57. 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

58. Stage I DT > 240 ms E/A < 0.9 IVRT - > 90 ms LAVI>28 ml/m2
Vp < 50 cm/s
S – dominant PV pattern

59. 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

60. 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

61. Stage II
Valsalva


62. 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:

63. 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)

64. Stage III – Restrictive, reversible
Valsalva


65. 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)

66. What about other causes of CHF with preserved LV function
TEE 5C view

67. Causes of pericardial constriction
Prior Cardiac surgery
Idiopathic
Pericarditis
Prior Radiation
Collagen Vascular
Infection (TB)

68. 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

69. 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

70. 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)

71. Doppler Findings in Constrictive Pericarditis
Respiratory variation of >25% in mitral E velocity

72. Doppler Findings in Constrictive Pericarditis
OH Figure 17-29
Increased DFR with expiration in the hepatic vein.

73. 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).

74. WHO CARES?

75. 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

76. 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.

77. (for not falling asleep)
Thank you !
(for not falling asleep)