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Acute effects of RV pacingon cardiac hemodynamicsand transvalvular impedance
M.Taborsky, M.Fedorco, T.Skala, E.Kocianova, D.Richter, D.Marek, J.Ostransky
Dept. of Internal Medicine - Cardiology, University Hospital, Olomouc, Czech Republic
Chronic right-ventricular apical pacing can affect the cardiac function
Electrical and mechanical desynchronization
Reduced myocardial performance with increased stress
Increased risk of AF and CHF
Open questions
Does right-ventricular pacing (RVP) also produce acute effects on cardiac hemodynamics ?
Can the RVP long-term consequences be predicted from the acute effects ?
What are the most sensitive indicators of pacing-induced hemodynamic troubles ?
Is the hemodynamic impact of RVP dependent on the pacing site ?
Can the risk be reduced by individual pacing site selection ?
Study design During dual-chamber implantation procedures for SSS or
AVB, the ventricular lead was sequentially positioned in RV apex and mid-septum.
Measurements: left-ventricular pressure and dP/dt; systolic and diastolic hemodynamic parameters assessed by
2D echocardiography and by echo and tissue Doppler; Transvalvular impedance (TVI).
Recording conditions: intrinsic activity; AAI pacing at 90 bpm; VDD and DDD pacing at 90 bpm with apical and septal
stimulation.
AEGM
VEGM
ECG I
LVP
dP/dt
TVI(Vring)
150 mmHg
2000 mmHg/s
50 Ohm
Set of tracings
QRS duration
0
5
10
15
20
25 50 75 100 125 150 175 200 225 250
ms
fre
qu
en
cy (
n)
IAVC
VDD in RVA
VDD in RVS
QRS duration
0
50
100
150
200
ms
IAVC
VDD in RVA
VDD in RVS
P < 0.001
Paired Student t-test (n=29)
The increase in QRS duration induced by ventricular pacing depends on the pacing site
Paired Student t-test (n=29)
QRS duration difference vs IAVC
0
5
10
15
20
-25 0 25 50 75 100 125 150
ms
fre
qu
en
cy (
n)
VDD in RVA
VDD in RVS
QRS duration difference vs IAVC
0
25
50
75
100
ms
VDD in RVA
VDD in RVS
P < 0.001
The increase in QRS duration induced by ventricular pacing depends on the pacing site
AEGM
VEGM
ECG II
LVP
2:1 AVBQRS 110 ms
VDD in RVAQRS 180 ms
VDD in RVSQRS 120 ms
RV septal stimulation improves QRS axis and duration with respect to apical pacing
IAVC VDD; 80 ms AV delay
ECG I
LVP
dP/dt
dP/dt max
0
500
1000
1500
2000
Apex Septum
Pacing site
mm
Hg
/s
IAVC
VDD
P < 0.002 P < 0.005
dP/dtmax is reduced by RV pacing at either site
dP/dt max % diff. (VDD vs IAVC)
-20
-10
0
10
-20 -10 0 10
apex
sep
tum
Septal pacingwas better
Apical pacingwas better
y = x
Was there individual preference for a specific pacing site?
ECG II
LVP
dP/dt
IAVC VDD; 80 ms AV delay
LVP decrese in 50 ms
-100
-75
-50
-25
0
Apex Septum
Pacing site
mm
Hg
IAVC
VDD
P < 0.02 P < 0.01
LVP decrease is affected
LVP sys
0
50
100
150
200
Apex Septum
Pacing site
mm
Hg
IAVC
VDD
n.s. n.s.
LVP dias
0
2.5
5
7.5
10
Apex Septum
Pacing site
mm
Hg
IAVC
VDD
P < 0.001 P < 0.002
LVP sysis not modifiedby VDD pacing
LVP diasis significantlyincreased
Rate increase to 90 bpm produced by:
AAI pacing
DDD pacing (80 ms AV delay) in RV apex
DDD pacing (80 ms AV delay) in mid-septum
Effects of cardiac rate on dP/dtmax and LVP sys
dP/dt max
-10
0
10
20
30
40
AAI DDD apex DDD septum
ch
an
ge
vs
sin
us
ra
te (
%)
P < 0.001
n.s.
P < 0.002
LVP sys
-30
-20
-10
0
10
AAI DDD apex DDD septum
ch
an
ge
vs
sin
us
ra
te (
mm
Hg
)
P < 0.05
n.s. n.s.
Effects of RV pacing on echocardiographicsystolic parameters
EF
0
20
40
60
80
IAVC VDD apex VDD septum
(%)
n.s. n.s.
Mitral annulus systolic velocity
0
4
8
12
IAVC VDD apex VDD septum
(cm
/s)
n.s. n.s.
E'
0
4
8
12
IAVC VDD apex VDDseptum
(cm
/s)
P < 0.02 n.s.
E
0
25
50
75
100
IAVC VDD apex VDDseptum
(cm
/s)
n.s.n.s.
DT
0
100
200
300
IAVC VDD apex VDDseptum
(ms
)
P < 0.02n.s.
E/E'
0
10
20
30
IAVC VDD apex VDDseptum
n.s.n.s.
Echocardiographic diastolic parameters
RV lead in mid septum
AAI60 bpm
DDD60 bpm
TVI
VEGM
AEGM
ECG II
LVP
60 Ohm
100 mmHg
TVI
In some cases, RV pacing induced virtually no change in TVI waveform
AEGM
VEGM
ECG I
TVI
Sinusrhythm
VDD
EDTVI 421 Ohm
ESTVI 460 Ohm
EDTVI 434 Ohm
ESTVI 461 Ohm
RV lead in mid septum
TVI
In some cases, RV pacing affected TVI amplitude
transition from AAI to VDD
AEGM
VEGM
I
TVI 60 Ohm
LVP
RV lead in apex
In other cases, RV pacing induced morphological changes in TVI
TVI with intrinsic activity
0
5
10
15
20
25
30
35
apex septum
fre
qu
en
cy (
n)
inappropriate
appropriate
TVI with intrinsic activity
0
5
10
15
20
25
30
Y/Y Y/N N/Y N/N
waveform OK in apex / septum
fre
qu
en
cy (
n) P = 0.371
McNemar's test
TVI was measured in both RV apex and septum in 32 patients.The success frequency was not significantly differentat the two recording sites.
TVI recording can be performed in RV septum as well as in apex
TVI modifications in VDD
0
20
40
60
80
100
OK ampl. <75% altered morphology
fre
qu
en
cy (
%)
Apex
Septum
The frequency of substantial morphological alterationswas much higher in RV apex than septum
Right ventricular pacing affects TVI properties
TVI in VDD
0
5
10
15
20
Y/Y Y/N N/Y N/N
waveform OK in apex / septum
fre
qu
en
cy (
n)
P = 0.008McNemar's test
TVI in VDD
0
5
10
15
20
Y/Y Y/N N/Y N/N
waveform OK in apex / septum
fre
qu
en
cy (
n)
P = 0.016McNemar's test
OK = no morphological alteration OK = no morphological alterationand amplitude 75%
With intrinsic rhythm, the TVI signal was appropriate at both RV apex and septum in 25 cases.
The frequency of cases featuring unaltered TVI waveform with VDD pacing was significantly higher in RV septum than apex.
OK = no morphological alteration OK = no morphological alterationand amplitude 75%
DDD was tested in 18 cases featuring appropriate TVI at both RV apex and septum with intrinsic rhythm.
The frequency of cases with unaltered TVI waveform in 90 bpm DDD was significantly higher in RV septum than apex.
TVI in DDD (90 bpm)
0
5
10
15
20
Y/Y Y/N N/Y N/N
waveform OK in apex / septum
fre
qu
en
cy (
n)
P = 0.041McNemar's test
TVI in DDD (90 bpm)
0
5
10
15
20
Y/Y Y/N N/Y N/N
waveform OK in apex / septum
fre
qu
en
cy (
n)
P = 0.046McNemar's test
CONCLUSIONS Right ventricular pacing applied in apex or mid-septum
acutely affected both systolic and diastolic function. The QRS duration was longer and the proportion of cases
featuring deep alterations in TVI waveform was higher with apical than septal pacing.
Left ventricular pressure and echocardiographic parameters were similarly affected by RV pacing applied at either site.
Septal stimulation might produce a shorter electrical interventricular delay and milder mechanical modifications in RV with respect to apical pacing, while LV hemodynamic indices dependent on the intraventricular synchronization seem to be less sensitive to the position of the pacing lead.
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