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(1)

Left Ventricular Mechanical

Dyssynchrony

(2)

Ventricular Mechanical

Dyssynchrony

• In Physiological conditions Cardiac Performance is co-determined by temporal and spatial mechanical dyssynchrony (Brutsaert JACC 1987)

• “It is conceivable that dyssynchrony represents a newly appreciated pathophysiological process that directly depresses Ventricular function” (Auricchio Circulation 2004)

• Mechanical Dyssynchrony is common in CHF, LBBB, LV Aneurysm and during Ischemia

• Influence of Mechanical Dyssynchrony on Cardiac Performance is not well documented

(3)

Characteristics LV Aneurysm

• LV post-infarction aneurysm is characterized by akinetic and/or dyskinetic LV wall motions.

• Non-uniformity of contraction and relaxation reduces mechanical efficiency of ventricular filling and ejection and contributes to diastolic and systolic dysfunction.

• LV aneurysm is associated with reduced EF due to LV dilatation to maintain stroke volume and with impaired LV relaxation.

(4)

LV Restoration Surgery

• Endo-ventricular patch plasty aneurysmectomy

(Dor Procedure) aims for LV reduction and

geometric remodeling to reduce akinesia,

dyskinesia and LV load to improve cardiac

performance

(5)

Study Objectives/Methods

• Intra-operative Evaluation of LV Contractile State and LV Mechanical Dyssynchrony in Patients

undergoing LV Restoration

• Contractile State was derived from LV Pressure-Volume Loops as determined by the conductance catheter technique (CD Leycom)

• Mechanical Dyssynchrony was determined by short-axis volume slices from the conductance catheter

(6)

An electro-magnetic field is applied between distal and proximal electrodes

Up to 7 electrode pairs

measure the conductance of intraventricular blood

segments perpendicular to the long heart axis

Segmental conductance changes reflects

time-varying segmental volume Total volume is calculated as the sum of segmental

volumes

(7)

Jul11011-all

5 segmental volume signals from apex (top) to base

Segmental volume combined with left

ventricular (LV) pressure give segmental P-V loops

Total volume signal combined with the LV pressure signal give the typical P-V loops (click at screen)

(8)

Ventricular Pressure-Volume Loops

• show the performance of the Heart in its role as a pump

• three load independent

indices of contractile state can be derived from P-V loops

• Systolic and Diastolic

disorders can be analyzed real-time

(9)

P-V Loops and Load Independent

Contractile State Indices

• 1) ESPVR= end-systolic

pressure volume

relationship, its slope =Ees

• 2) +dP/dt-EDV, the

Starling contractile state

• 3) PRSW= preload

recruitable stroke work

+dP/dt-EDV Ees PRSW= SW-EDV ESPVR

(10)

Calculated from segmental volume changes compared to total LV

volume changes

A segment is dyssynchronous when it is out of phase with total volume change

Expressed in % of time of total heart cycle or of systolic or

diastolic phase

Mechanical Dyssynchrony

Assessment

(11)

Patients Characteristics

• 9 patients with LV post-infarction aneurysm • Age 59-71 yrs

• NYHA class II-III

• Cardiac Index 1.6-2.5 L/min • Ejection Fraction 12-35% • CABG performed in 8pts

(12)
(13)
(14)

Hemodynamic Data P<.001 2.2±1 1.2±.6 Ees P<.01 72±22 42±22 PRSW P<.001 41±9 59±7 Tau P<.006 803±72 601±145 -dP/dt P<.03 1116±171 787±276 +dP/dt P<.03 13.8±3 9.4±3 EDP P<.001 78±18 123±35 EDV 48±12 46 ±12 SV P<.01 99±21 76±16 HR After LV Restor Before

(15)

Dyssynchrony Data

31±5** 23±6** 38±7 34±3 Total 25±13 17±6 24±7 21±11 Base1 22±5 14±5 20±9 15±7 Base2 22±10** 14±10** 36±10 27±7 Mid Seg 37±7* 25±10* 47±16 44±10 Apex2 49±7* 44±10* 64±14 62±15 Apex1 Diastole Systole Diastole Systole After LV Res Before *=P<.05, **=P<.01

(16)

0 1 2 3 4 20 70 120 ESV (ml/m2) E e s ( m m H g/ m l) R=-.763 n=18 p=.0002

(17)

0 1 2 3 4 10 20 30 40 SysDys % E e s ( m m H g/ m l) R= -0.725 n = 18 p = 0.00066 Schreuder et al JTCS 2005

(18)

Pressure- Volume Area concept

Suga et al,1982

(19)

0.0 0.2 0.4 0.6 0.8 0 10 20 30 40 SysDys B% E ne rE ff ic % R=.702 n=18 p=.0012 Schreuder et al JTCS 2005

(20)

0 1 2 3 -18 -13 -8 -3 2 ΔDiasDys (%) Δ E es ( m m H g/ m l) R=-.802 n=9 p=.009 Schreuder et al, JTCS 05

(21)

Summary LV Restoration

• LV Restoration Surgery improved immediately diastolic relaxation and Contractile State

• The decrease in LV mechanical dyssynchrony and increase in Contractile State markedly correlated

• LV mechanical dyssynchrony and Energy Efficiency inversely correlated

• LV volume reduction, reducing wall stress, and the grade of geometric remodeling determine the

(22)

Ventricular Mechanical

Dyssynchrony

• “It remains unknown whether dyssynchrony represents a

central pathophysiological process or is a marker of

progressing cardiac dysfunction in CHF”

Leclercq Circulation2004

• “It is conceivable that Dyssynchrony represents a newly

appreciated pathophysiological process that directly depresses ventricular function and ultimately leads to ventricular dilatation and CHF”

Auricchio Circulation 2004

• “It will be useful if additional methods can be developed that

identify dyssynchrony”

(23)

Acute Effects of IABP in a NYHA classIII patient, EF 23%, CABG

P-V loops in Clinical IABP Research

LV Volume LV Pressure Aortic Pressure Start IABP at 1:1

(24)

30 65 100 P ao ( m m H g ) Ees 0 20 40 60 80 100 250 300 2 1 P L V ( m m H g ) 230 290 350 1 2 Schreuder et al ATS 2005

(25)

s1 38 s2 45 s3 25 s4 24 s5 24 T V L V (m l) 33 Time (s) 6 0 Dys% 49 Dys% 42 21 22 16 28 Schreuder et al ATS 2005

(26)

-40 -30 -20 -10 0 -7 -6 -5 -4 -3 -2 -1 0 1 2 3 ΔSysDys(%) Δ E S V (m l) R=.67 n=15 p=.006 Schreuder et al ATS 2005

(27)

0 10 20 30 40 50 -7 -6 -5 -4 -3 -2 -1 0 1 ΔTDys(%) % Δ S V R=-.87 n=15 p=.00003 Schreuder et al ATS 2005

(28)

-8 -6 -4 -2 0 2 4 -60 -40 -20 0 %ΔEes Δ S y sD y s(% ) R=.68 n=15 p=.005 Schreuder et al ATS 2005

(29)

LV Mechanical Dyssynchrony

P<.05 36.4±4.8 38.6±5.5 Tot D Dys P<.01 29.7±5.4 32.3±5 Tot S Dys P<.05 24±8 27±8 Base D Dys P<.04 31.3±10 35.1±10 Mid D Dys P<.001 50±13 56.4±12 Apex S Dys On Off IABP

(30)

sep29018 LV Volume LV Pressure Aortic Pressure

Effects of very early IABP inflation at 1:4 in NYHA class II patient, EF 35%, undergoing LV aneurysmectomy

(31)

Too late IAB deflation at a 1:4 ratio in a NYHA class III patient, EF20%, undergoing LV aneurysmctomy+CABG

(32)

-60 -30 0 30 60 -5 -3 -1 1 3 5 ΔSysDys (%) % Δ S V r = -0.826 n = 24 p <0.00001 Relation between change in Stroke Volume (SV) and change in Systolic Dyssynchrony (Sys Dys) due to intra-beat changes in left ventricular afterload in heart failure patients.

(33)

Summary III

• SV changes due to intra-beat changes in afterload induced by early/late IAB inflation/deflation were best predicted by changes in SysDys

• LV performance during IABP is causally related to changes in LV afterload and its timing in the contraction and

relaxation phase, to contractile state, to preload and to concomitant changes in LV mechanical dyssynchrony.

• Brutsaert’s hypothesis that LV Dyssynchrony may act as a modulator of cardiac performance together with heart rate, contractile state, preload and afterload may therefore be applicable in heart failure patients.

(34)

Ventricular Mechanical Dyssynchrony

• “It remains unknown whether dyssynchrony represents a

central pathophysiological process or is a marker of progressing cardiac dysfunction in CHF”

Leclercq Circulation 2004

• “It is conceivable that Dyssynchrony represents a newly

appreciated pathophysiological process that directly depresses ventricular function and ultimately leads to ventricular dilatation and CHF” Auricchio Circulation 2004

• “It will be useful if addiotional methods can be developed

that identify dyssynchrony”

(35)
(36)
(37)

Beat-to-Beat Effects of RV Ventricular

Stimulation on LV Mechanical

Dyssynchrony and Performance

J Schreuder, A Michelucci, L Padaletti Careggi Hospital Florence, San Raffaele

(38)

Objective

To evaluate beat-to-beat hemodynamic effects of RV lead position in patients with normal EF undergoing an EP study.

End-point was evaluated according to the following variables:

•Mechanical dyssynchrony

•Systolic and diastolic performance •Loading conditions

(39)

Methods

Stimulation Selective sites:

AAI DDD-Apex

DDD-Free wall DDD-RVOT-S

Beat-to-Beat performance analysis from the LV Pressure-Volume plane and LV ventricular dyssynchrony analysis

(40)

140 20 60 100 105 115 125 S1 S2 S3 S4 S5 Vlv Plv ECG 140 20 60 100 105 115 125 Pl v ( m m Hg ) Vlv (ml) -1 0 -2 1 2 7 8 9 10 11 Time (s) A B

(41)

S1 S2 S3 S4 S5 Vlv Plv ECG -1 0 -2 1 2 Time (s) 10 11 9 12 13 120 0 40 80 Pl v ( m m Hg ) Vlv (ml) 115 85 95 105 120 0 40 80 115 85 95 105 A B

(42)

AAI RV-2s RV-9s RV-60s AAI-10s a b c d e SV ml 62 19 37 9aa 45 13aabb 45 13aa 64 18dd EF % 52 13 37 13aa 42 14aab 43 14aa 53 12dd LVEDV ml 126 54 118 56 120 54 118 50a 125 49d LVESV ml 61 40 65 43 63 41 61 38 62.6 38 +dP/dt mmHg/s 1645 319 1509 238 1603 243bb 1564 278 1648 313 -dP/dt mmHg/s 1738 300 1217 284aa 1411 307aabb 1516 344aacc 1690 333dd Tau ms 31 6 41 8aa 38 7aa 35.6 6.6aacc 33 6 DiaDysT % 20.9 7 26 4aa 23.3 7b 21.8 6.3a 19.6 7.2 SysDysB % 13 9 17 8aa 14 10b 14.4 9 14 8.5 DiaDysA % 21 7 26 7aa 23.3 8a 23.2 6a 21 7

(43)

ΔSysDysB% Δ EF% ΔDiaDys% Δ E F % ΔDiaDys% ΔSysDysB% R=.924 n=18 P<.0001 ΔSysDysB% r=-.925 n=18 p<.00001 r=-.907 n=18 p<.0001 r=-.862 n=18 p<.002 r=-.721 n=18 p<.001

(44)

ΔDiasDys% ΔDiasDys% ΔSV% ΔSV% Δ + d P /d t% r=-.698 n=18 p<.001 r=-.862 n=18 p<.0001 r=.862 n=18 p<.0001 r=.621 n=18 p<.005

(45)

Conclusions

• RV pacing acutely increased Systolic and Diastolic Dyssynchrony, decreased SV, and impaired

diastolic relaxation

• Recovery of Systolic Dyssynchrony was observed within a 10s time-span, suggesting intrinsic cardiac Dyssynchrony restoring properties

• Reciprocally LV or BiV pacing at best lead positioning (setting) should result in an acute Systolic Dyssynchrony decrease

(46)

Ventricular Mechanical

Dyssynchrony

• “It remains unknown whether dyssynchrony represents a

central pathophysiological process or is a marker of progressing cardiac dysfunction in CHF”

Leclercq Circulation2004

• “It is conceivable that Dyssynchrony represents a newly

appreciated pathophysiological process that directly depresses ventricular function and ultimately leads to ventricular dilatation and CHF”

Auricchio Circulation 2004

• “It will be useful if additional methods can be developed that

identify dyssynchrony”

(47)

Schreuder et al, Circ 1995

Synchronizing Effects of Cardiomyo-stimulation on Segmental Ventricular Volumes

(48)

Schreuder et al, Circ 1997

(49)

Schreuder et al, Circ 1997

(50)

2-17A 0 20 40 60 80 100 120 0 50 100 150 200 250 LV volume (ml) L V P re s s u re (m m H g )

PRE-SURGERY PRE-BYPASS POST-BYPASS

POST-SURGERY RE-CATH-1 RE-CATH-2

Schreuder et al JACC 2000

(51)

Pre - PLV Post - PLV Recatheterization A p e x B a se V to t S e g m e n ts 3-17B

(52)

50 60 70 80 90 100 0 1 2 3 4 Cardiac I ndex Sync (%)

(53)

Ventricular Mechanical

Dyssynchrony

• “It remains unknown whether dyssynchrony represents a

central pathophysiological process or is a marker of progressing cardiac dysfunction in CHF”

Leclercq Circulation2004

• “It is conceivable that Dyssynchrony represents a newly

appreciated pathophysiological process that directly depresses ventricular function and ultimately leads to ventricular dilatation and CHF”

Auricchio Circulation 2004

• “It will be useful if additional methods can be developed that

identify dyssynchrony”

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