1. HEMODYNAMICS OF DIASTOLIC HEART FAILURE
DR VIVEK PILLAI,
SENIOR RESIDENT IN CARDIOLOGY,
MCH- KOZHIKODE
59 slides

2. DEFINITION.
As per the consensus document by the European Working Group HFnlEF is defined as
-1) signs and symptoms of congestive heart failure.
-2)LVEF > 50% and a non dilated LV(<97 ml 3).
-3)Evidence of elevated LV filling pressures.
The last criterion is fulfilled in three ways-
-a)invasive hemodynamics with PCWP> 12 mm Hg or LVEDP > 16 mm Hg.
- b)unequivocal echo evidence of elevated filling pressure-E/e’ > 15.
-c) equivocal echo evidence(E/e’ > 8 but < 15 and a positive BNP(NT-BNP> 220pg/ml or BNP > 200 pg/ml).

3. Factors influencing diastolic filling.
RV – LV Interaction

4. Hemodynamic basis of symptoms and signs.
-Exertional dyspnea-frequently an early event in diastolic Hf- caused by pulmonary congestion.
Elevated LV filling pressures→ transmission into LA→transmitted into pulm. Vasc bed→pulm. Congestion and dyspnea.
later on this mechanism operates in the recumbent position and at rest-giving rise to orthopnea.
Stiff ventricle may give rise to an S4 on auscultation.

5. Diastolic heart failure- a continuum.

6. NORMAL DIASTOLE
-Diastole- means to send apart. What constitutes normal diastolic function?-Normal diastolic function allows the ventricle to fill adequately during rest and exercise, without an abnormal increase in diastolic pressures. Best defined as the time period beginning at the end of ventricular ejection( closure of semilunar valves) and extending to closure of the AV valves.

7. 1) isovolumic relaxation phase. 2)rapid filling phase.70- 80% filling.
Phases of diastole
1) isovolumic relaxation phase.
2)rapid filling phase % filling.
3)slow filling phase( diastasis)- 5% of LV filling.
4) atrial filling phase %.

8. Early diastolic filling is driven by the LA-LV pressure gradient.
LA-LV pressure gradient depends on a number of factors-
a)rate of relaxation of the LV.
b)LV diastolic stiffness.
c)LV elastic recoil.
d) LV contractile state.
e)LA pressures.

9. f) ventricular interaction. g)pericardial constraint. h) LA stiffness
f) ventricular interaction. g)pericardial constraint. h) LA stiffness. i) pulmonary vein properties. j)mitral orifice area.

10. LV RELAXATION.
Is an active , energy dependent process,begins during the ejection phase of systole , continues into the isovolumic relaxation and rapid filling phase.
Enhanced LV relaxation thus ↑es the LA-LV pressure gradient, without ↑ing LA pressures, and enhanced filling during exercise without the need for elevated LA pressures.

11. INVASIVE MEASUREMENT OF RELAXATION.
The time constant of relaxation(ᵼ) describes the rate of LV pressure decay during isovolumic relaxation.
Measurement of tau requires high fidelity manometer tipped LV catheters.

12. Weiss equation P=P0*e-t/τ(P0 is the LV pressure at end ejection.)
τ=-(1/slope of Ln LVP Vs time)
Normal <40 ms
Relaxation is complete by 3.5 tau
Larger value of tau-more impaired relaxation

14. A simpler method to determine tau-
ᵼ= IVRT/ln( syst.pressure)-ln( LA pressure).
tau is preload independent but afterload dependent.
limitation- the isovolumic LV pressure decay is not a simple exponential decay.
Actually LV pressure falls faster during the latter part of isovolumic relaxation.

15. NON INVASIVE ASSESMENT OF RELAXATION.
By means of doppler echo.
The transmitral flow velocity vs time profile is affected by impaired relaxation in a variable manner.
a)relaxation impaired but LA pressures not elevated : slower LV pressure decay and higher LV minimum pressure assoc with impaired relaxation will ↓ the early diastolic LA-LV pressure gradient.

16. E/A ratio.
Healthy young individuals , most diastolic filling occurs in early diastole.
E/A ratio is > 1.
In impaired relaxation, early diastolic filling ↓es progressively, and a vigorous atrial contraction (‘ atrial kick occurs”)

17. Doppler profile of impaired relaxation.
E vel- will be reduced.
Duration of early diastolic filling will be prolonged- E dec time.
Reduced LA emptying during early diastole ↑es atrial preload, and the velocity of filling with atrial contraction (Avel)↑es while the E/A ratio decreases.

19. DT is prolonged in impaired relaxation.
Deceleration time
DT is prolonged in impaired relaxation.
Longer time required for equilibration of LA and LV pressures.
Normal value is 193+_ 23 msecs.
However when prolonged this index fails to distinguish b/w normal and pseudonormal ratio.

20. PULMONARY VENOUS PATTERN.
-provides a window towards assesment of diastolic function.
-normally consists of 3 waveforms,
a)systolic forward flow,b) diastolic forward flow c) atrial flow reversal.
Systolic forward flow is due to
1) atrial relaxation.
2) mitral annulus descent towards cardiac apex with vent systole.
3) Biphasic in 37% individuals.

21. Biphasicity-
a) s1 is due to atrial relaxation→ lowers LA pressure→pulm venous return into LA →↑ LA volume.
b) second peak s2 in mid to late systole is provided by an additional increase in LA volume as the mitral annulus descends towards card. Apex in vent systole.
Pulm venous systolic forward flow is closely related to LA pressure.
When LA pressure is elevated systolic filling from pulm veins is reduced.

22. Diastolic forward flow-
occurs in diastole when there is an open conduit b/w the pulm veins,LA ,open mitral valve and the LV.
reflects LV filling.
normally diastolic flow is slightly less than systolic forward flow velocity.

23. Atrial flow reversal-
- refers to the retrograde flow back into the pulm veins, secondary to atrial contraction.
- with atria contraction, blood is not only ejected into LV but also backward into pulm. Veins.
-the magnitude and duration of atrial flow reversal is determined by transmitral and atriovenous pressure gradients, which are influenced by LA syst. Fn, LA and LV compliance.

26. Pseudonormalisation.
Transition from impaired relaxation to restrictive physiology.
Transmitral inflow may resemble a normal profile.
Result of decreased LV compliance alongwith a moderate increase in LA pressure.
Higher driving pressure across the mitral valve.
If there is also a ↓ in the compliance of the ventricle, ventricular pressure rises rapidly in early diastole and the previously lengthened dec. time is shortened.

27. USE OF THE VALSALVA MANEUVER
How does it help in unmasking diastolic dysfunction?
-reduces the elevated LA pressure on performing the maneuver.
-suspend breathing at the end of normal inspiration and then to strain down without breathing at expiration.
- An adequate valsalva maneuver is defined as a 10% redn in maximal E velocity from the baseline.

28. TRANSMITRAL DOPPLER FLOW PATTERNS
NORMAL E/A RATIO OF PSEUDONORMALISATION.
UNMASKING OF DIASTOLIC DYSFUNCTION USING THE VALSALVA MANEUVER.
ADVANCED DIASTOLIC DYSFUNCTION.

29. Use of pulmonary venous flow profile.
Pts with a pseudonormal filling pattern have an elevated LVEDP which can be identified by
a)increase in flow reversal into the pulm. Veins with atrial contraction and/or
b) shortening of duration of the mitral A wave compared with pulmonary venous AR duration with atrial contraction.
Disadvantages-
difficulty in obtaining a pulm venous profile.

30. ILLUSTRATION-SYMPTOM FREE SUBJECT WITH NORMAL 2D ECHO.
Mitral inflow doppler show s E velocity .8m/sec. and A velocity of .6 m/sec.
DT was normal at 200 msec..
Difficult to differentiate b/w normal and pseudonormal here.
Pulm venous doppler-
Predominant systolic forward flow-.6m/sec.
Diastolic forward flow is .4 m/sec.
Pulm venous atrial flow reversal velocity is < .4 m/sec and duration is lesser than duration of A wave.

31. Use of color M-mode prop velocity
This modality allows acquisition of information about velocity, time and space along the entire line of the M- mode cursor.
Accurately assess the transmitral propagation flow velocity from the mitral annulus across the cavity of the LV.
Appears to be preload independent- hence may be useful in identification of pts with pseudonormal inflow.
Normal prop . Velocity m/s.
Abnormal relaxation results in significant slowing of this velocity.
Pseudonormalisation can be identified when flow propagation velocity is < .50 m/s.

32. Method of obtaining Color M- mode flow propagation velocity
4 chamber view.
M-mode cursor placed as parallel as possible to flow direction.
Temporally performed in early diastole,coincident with the E wave.
-shift the color baseline to a new nyquist limit, an aliasing border ( blue to red)-
Then a tangent is drawn from the mitral valve to a point 4 cm distal., representing the early diastolic flow propagation velocity.

33. Restrictive physiology
Relaxation is still impaired in these individuals but it is now masked by a marked ↑ in LA pressure.
Crossover b/w LA and LV pressure is not delayed.
Mitral valve opening occurs earlier than normal.
↑ed LA pressure increases transmitral gradient, in early diastole - ↑ peak E wave.
Early opening of mitral valve – shortening of IVRT.
Rapid equalisation of pressures and hence dec. time is shortened.
Because of high LVEDP-little or no filling occurs with atrial contraction- blunted A wave.
Thus E/A ratio is > 2.

34. The pulm. venous trace in restrictive filling.
Increase in diastolic forward flow(D) wave and a ↓ in systolic forward flow( S) wave.
Due to
a) rapid vent. Filling in diastole due to elevated LA pressure and ↓ LV compliance.
b)it follows that there must be ↑ filling of the atrium via pulm veins in diastole.
c)with most of the atrial filling in diastole , there is a decrease in syst. Filling.

35. ↑ed flow reversal into pulm veins during atrial contraction( AR velocity).
Duration of flow reversal is longer than that of the mitral A wave.
This phenomenon can be explained by ↑ed LVEDP.

37. Diastolic MR and TR may be present in pts with restrictive physiology.
Indicative of markedly elevated vent.diastolic pressure that>> LA pressure→reversal of flow through diastole.
Restrictive filling is associated with greater filling pressures , more symptoms and a worsened prognosis.

38. Doppler tissue imaging in diast. Fn assessment.
Tissue doppler imaging records systolic and diastolic velocities in the myocardium and the corners of the mitral annulus.
For the purpose of diastolic function assesment, the tissue doppler mitral annulus velocity is of prime importance.

39. Method Apical 4 chamber view.
Sample volume placed on the annulus near mitral valve insertion.
Both septal and medial sites should be recorded.
Because of high signal amplitude, spectral gain should be lowered.
High sweep speed b/w cm/sec.

40. Most useful measurement is peak annular velocity in early diastole-e’.
E’ velocity depends primarily on LV relaxation.
When diastolic function is abnormal e’ is relatively independent of preload.
However when diastolic function is normal, e’ ↑es with higher filling pressure.
Usually combined with E to obtain the familiar E/e’ ratio.

41. E’ should be measured from both septal and lateral locations.
Most pts lateral e’ will be higher than septal e’s and thus E/e’ will be lower if the lateral position is used for e’.
Septal e’< 8 cm/s and/or lateral e’ < 10cm/s suggest diastolic dysfunction.

42. E/e’ ratio.
E velocity obtained from the transmitral flow pattern and e’ from TDI of the lateral mitral annulus.
Rough hemodynamic correlation.
Correlation is better in pts with depressed EF but reasonable in pts with normal EF.
E/e’< 8- normal filling pressures.
E/e’ > 15- correlates with a PCWP > 12 mmHg.
Many pts fall in the intermediate zone where the E/e’ ratio is >8 and <15 ,such pts cannot be determined to have diast dysfunction by this method alone.

44. Difficulties.
Not reliable in pts with prosthetic mitral valves, annular rings and significant annular calcification.
Or In regional wall motion abnormalities.

45. LV diastolic stiffness.
Stiffness or elastance is defined as the relationship between the change in stress and the resulting strain.
Elastance of the LV varies over the cardiac cycle (time-varying elastance.
End-systolic and end-diastolic elastance are defined by the changes in systolic or diastolic pressure associated with a change in ESV or EDV.

46. EDPVR

47. EDPVR-end diastolic pressure vol. relationship
Why EDPVR?-evaluates the passive diastolic ventricular properties unlike tau which is for active vent. relaxation.
Only way to truly demonstrate that HFnlEF pts have abnormalities of passive diastolic properties is to demonstrate an upward shift of the pressure vol.curve.
Also by characterising EDPVR it is possible to demonstrate that not only is the LVEDP elevated ,but the ventricles have ↓ capacitance( ↓ filling volume at any given filling pressure).

48. In the absence of an upward shift LVEDP may be increased simply because of ↑ preload vol., without any change in diastolic properties.
STIFFNESS-( beta)
Slope of the pressure vol. relationship
Depends on filling pressures.
Increase in vent. Pressures leads to increase in calculated stiffness.

49. STIFFNESS ASSESSMENT BY DOPPLER ECHO.
If there is doppler evidence of increased filling pressures, and LV dimension or volume is normal, then ↑ stiffness is inferred.
Furthermore, if the deceleration time of the early diastolic transmitral flow velocity profile is short, despite evidence of impaired relaxation (reduced e’), rapid equalization of LV and LA pressures during early diastolic filling and increased LV diastolic stiffness are inferred.

50. ATRIAL DYSFUNCTION IN DIASTOLIC HEART FAILURE.
Mean LA pressure- the resistance to filling that pulm venous system faces.
Early on in diast.Hf the LA systolic fn compensates for reduced filling→ atrial failure ensues.
Hemodynamic trace of LA pressure waveform- large v waves( in the absence of MR)→reflects ↓LA compliance.
↓ LA compliance may play a role in dev. Of Pulm HT in HFnlEF.
↓LA syst fn necessitates higher LA mean pressures for augmenting early diastolic filling.

51. LEFT ATRIAL VOLUME
An increase in LA size is the morphological expression of chronic diastolic dysfunction.
Chamber vol. should be obtained from 4-c and 2-c views.
LA area should be measured at end systole, when volume is largest.
Minnesota based popn study( n=2042) characterised LAVindexed –
23+-6 ml/ m2( normal).
25+-8ml/m2(grade 1 diastolic dysn).
31+_8 ml/ m2( grd 2 diast. Dysfn).
ml/ m2( grd ¾ diast. Dysfn.)

53. EMERGING CONCEPTS OF DIASTOLIC DYSFUNCTION
Not isolated from systole. tan et al
In HFnlEF there are combined systolic and diastolic abnormalities-involving ventr. Twist and deformn( strain) which lead to↓ vent, suction,delayed untwisting and impaired early diast. Filling- operative in exercise when diastole shortens.

55. In diastolic HF-↑ in LV diastolic pressure→↑ in LA pressure and pulm venous pressure- signs and symptoms of pulm venous congestion.
Postcapillary pulm HTN may precipitate Right heart failure.
LV stroke vol. and card. Output may decline due to ↓ EDV ( preload).
Chronic elevation of pulm venous pressure may be assoc. with ↑ PVR.

56. SUMMARY

58. REFERENCES 1) Braunwald’s heart disease- 9th edition.
2)Fiegenbaum’s echocardiography-7th edition.
3)Echocardiography-the normal examination and measurements-Bonita Anderson.
4) Manual of cardiovascular medicine-4th edition.- Griffin.
5) Diastolic dysfunction and left atrial volume- a population based study.Pritchett,Mahoney et al- JACC. 2005;45(1):87-92.
6)Diastolic heart failure –review,Mandinov et al. Cardiovascular Research 45 (2000) 813–825.
7) Current Perspectives on Cardiac Function in Patients With Diastolic Heart Failure- Wang and Nagueh, Circulation. 2009;119:
8)The deconvolution of diastole-Marwick, Editorial comment.JACC. Vol. 54, No. 1, 2009.
9) Heart failure with a normal ejection fraction-is it really a disorder of diastolic function.?Burkhoff et al-Circulation 2003;107:
10)Cardiac hemodynamic evaluation-a manual of cardiac catheterization and echocardiography

59. Thank you!