Download Rate-responsive pacing regulated by cardiac haemodynamics

Europace (2005) 7, 234e241
Rate-responsive pacing regulated by cardiac
haemodynamics
Gianni Gasparini a,*, Antonio Curnis b,1, Michele Gulizia c,2,
Eraldo Occhetta d,3, Andrea Corrado a, Luca Bontempi b,
Giosuè Mascioli b, Giuseppina Maura Francese c, Miriam Bortnik d,
Andrea Magnani d, Franco Di Gregorio e,4, Alberto Barbetta e,
Antonio Raviele a
a
Unità Operativa di Cardiologia, Ospedale Umberto I, via Circonvallazione, 50,
30174 Mestre, Venezia, Italy
b
Unità Operativa di Cardiologia, Spedali Civili, P.le Ospedali Civili, 1,
25100 Brescia, Italy
c
Unità Operativa di Cardiologia, Ospedale S. Luigi - S. Currò, via Fleming, 24,
95100 Catania, Italy
d
Unità Operativa di Cardiologia, Ospedale Maggiore della Carità, Corso Mazzini, 18,
28100 Novara, Italy
e
Unità di Ricerca Clinica, Medico SpA, via Pitagora, 15, 35030 Rubano, Padova, Italy
Submitted 11 October 2004, and accepted after revision 21 February 2005
KEYWORDS
rate-responsive
pacing;
haemodynamic
sensors;
trans-valvular
impedance
Abstract Aims Trans-valvular impedance (TVI) recording has been proposed for
the assessment of cardiac haemodynamics, assuming an inverse relationship
between TVI and ventricular volume. We checked whether the TVI sensor can
drive the rate-responsive function of a cardiac pacemaker following changes in the
inotropic regulation of the heart.
Methods An external DDD-R pacemaker (Ext Sophòs by Medico, Padova, Italy)
equipped with the TVI detecting system was tested in 30 patients on the
implantation of conventional pacing leads for dual-chamber pacing. Pacing
* Corresponding author. Tel.: C39 041 2607201; fax: C39 041 2607235.
E-mail addresses: [email protected] (G. Gasparini), [email protected] (A. Curnis), [email protected] (M. Gulizia),
[email protected] (E. Occhetta), [email protected] (F. Di Gregorio).
1
Tel.: C39 030 3995552; fax: C39 030 3995821.
2
Tel.: C39 095 7594728; fax: C39 095 506773.
3
Tel.: C39 0321 3733413; fax: C39 0321 3733407.
4
Tel.: C39 049 8976755; fax.: C39 049 8976788.
1099-5129/$30 Ó 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.eupc.2005.02.115
Rate-responsive pacing
235
rate regulation was based on the relationship between the stroke volume and the
end-diastolic volume, inferred from TVI data. After sensor calibration in basal
conditions, beta-adrenergic stimulation was induced by i.v. administration of 2 mg/
ml/min isoprenaline (isoproterenol) (IPN). The actual cardiac rate, the TVI
waveform, the end-diastolic and systolic TVI in each cardiac cycle and the TVIindicated rate were stored in memory as a function of time and down-loaded at the
end of the session.
Results All patients with intrinsic atrial activity (28/30) showed a positive
chronotropic response to IPN, coupled with a significant increase in end-diastolic
TVI and a four-times larger increase in end-systolic TVI. The TVI inotropic index
mirrored the sinus rate time-course, with a linear correlation between the two
parameters (r2 O 0.7 in 25/28 cases). As a result, the TVI-indicated rate closely
reproduced the sinus rate.
Conclusions The study confirms the reliability of the haemodynamic information
derived from TVI and supports its application in the regulation of rate-responsive
pacing.
Ó 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights
reserved.
Introduction
Pacing rate adaptation to changing metabolic demand is an important factor in the electrical
therapy of cardiac bradyarrhythmias, improving
cardiac output regulation, exercise tolerance and
quality of life in patients with poor chronotropic
function or undergoing single-chamber ventricular
pacing [1e5]. Assessing the haemodynamic performance of the heart with an implanted pacemaker
would allow effective pacing rate control, relying
on the physiological correlation between the
inotropic and chronotropic cardiac function
[6e9]. Moreover, continuous haemodynamic monitoring in daily-life conditions could provide relevant diagnostic information, suitable for the
optimization of both the pacing configuration and
the patient’s pharmacological treatment [10e12].
Haemodynamic sensing is expected to address
at least one of the parameters characterizing the
pump function of the heart: i.e., blood pressure
and flow [13]. The chronic detection of right
ventricular pressure and dP/dt has been attempted by means of a piezoelectric sensor included in
the pacing lead [8,14,15], but this system was not
adapted for long term use. Other parameters
correlated with ventricular dP/dt, such as peak
endocardial acceleration (PEA) and the unipolar
ventricular impedance, are applied as indirect
contractility markers in commercially available
cardiac pacemakers [16e18].
Impedance measurement has also been proposed as a method to assess the stroke volume
(SV) and the ejection fraction (EF) with an implanted device, based on the assumption that the
electric impedance depends on the blood volume
contained in the cardiac chambers at any time
[19e21]. To minimize the impact of possible
additional factors on the impedance signal, special
recording configurations and careful data processing have been suggested [13]. In particular, transvalvular impedance (TVI) detection between an
atrial and a ventricular electrode has proved useful to improve the signal-to-noise ratio and the
stability of the recording system, producing an
impedance waveform which mirrors the timecourse of ventricular volume changes through the
cardiac cycle [22e25].
For experimental purposes, the TVI sensor has
been implemented in an external pacemaker,
which processes the impedance signal in order to
derive a contractility index from the relationship
between SV and preload, according to Starling’s
law [13,21]. Following the contractility index, the
pacing rate is automatically adapted to the inotropic status of the heart. The present study has
analyzed the rate dynamics indicated by the TVI
sensor under adrenergic challenge, to check
whether it was consistent with physiological
expectations and mimicked the sinus rate trend in
patients endowed with chronotropic competence.
Materials and methods
The tests were performed in 30 patients, affected
by sick sinus syndrome (33%), AV conduction disorders (50%) or both (17%), during the implantation
of a permanent dual-chamber pacing system according to the AHA/ACC guidelines. The study was
approved by the local Ethics Committees and
informed consent from patients was obtained.
236
Standard bipolar pacing leads from any manufacturer, positioned in the right atrial appendage and
the right ventricular apex, were temporarily connected to an external DDDR stimulator (Ext
Sophòs, Medico, Padova, Italy) featuring a rateresponsive function controlled by the TVI sensor
[26,27]. After TVI recording in basal conditions and
a short run of overdrive DDD pacing to transiently
increase the cardiac rate by 30 min1, beta-adrenergic stimulation was induced with 2 mg/ml/min
isoprenaline (IPN) administered i.v., stopping the drug
infusion when the cardiac rate exceeded 90 min1.
In addition to the surface ECG, arterial pressure
was continuously monitored by plethysmography
(Finometer, TPD Biomedical Instrumentations, Amsterdam, The Netherlands). Patients presenting
with ventricular or supraventricular tachyarrhythmias, coronary disease, dilated or hypertrophic
cardiomyopathies, severe valve diseases and any
possible contraindication to the administration of
a beta-agonist were excluded from the study.
The external pacemaker was connected to
a personal computer through an optically isolated
serial cable, to allow real-time display of the TVI
waveform, the pacemaker event markers, the TVIindicated rate (TVIR) and the actual cardiac rate,
throughout the test. TVI was measured by application of 64 Hz subthreshold current pulses of
125 ms duration and amplitude ranging from 15 to
45 mA. The tests were performed in one of the two
alternative TVI recording configurations: i.e., current injection and voltage recording between
atrial ring and ventricular tip or atrial ring and
ventricular ring electrodes, choosing the option
featuring the TVI maximum peak within the T wave
decay and the highest signal-to-noise ratio. The
TVI signal was recorded without high-pass filtering
so as to determine the absolute minimum and
maximum impedance in each cardiac cycle, which
were assumed to reflect the end-diastolic volume
(EDV) and the end-systolic volume (ESV), respectively. TVI values at rest were sampled in 128
consecutive cardiac cycles, before high-rate pacing and IPN administration. The mean peak-topeak amplitude at baseline, representing the
resting stroke volume (SV), was applied as a scale
unit to normalize any further modification in enddiastolic or end-systolic TVI and to infer corresponding changes in relative EDV and ESV. The
difference between EDV and ESV provided the
relative SV, which was further corrected to remove
the preload influence on the systolic performance,
derived from the linear relationship between SV
and EDV recorded at rest. Under test conditions,
any displacement from the reference line indicated a change in cardiac contractility induced by
G. Gasparini et al.
adrenergic modulation. The TVI inotropic index
(INX) was obtained from the equation:
INXZðpreload corrected SV resting SVÞ=
resting SV
and was applied to calculate the TVIR, according
to the relationship:
TVIRZBRCRR!INX!RG
where BR is the programmed basic rate, RR is the
cardiac rate at rest, and RG is a programmable
rate-gain, which allows individual tuning of the
rate-responsive system. INX and TVIR were updated every eight cardiac cycles based on the
corresponding average values of minimum diastolic
and maximum systolic TVI, in order to compensate
for possible artefacts due to respiration-induced
electrode movements. The average cardiac rate
(either intrinsic or paced) in the same eight cycles
was also calculated. The pacing rate applied by
the pacemaker followed the TVIR, allowing a maximum adaptation speed of 1 bpm per cardiac cycle.
All the above data were stored in the stimulator
memory as a function of time and down-loaded at
the end of the session.
Whenever possible, the INX values were compared with the sinus rate recorded at the same
time during IPN stimulation. The relative variation
in sinus rate (SNX) was defined as the difference
from 1 of the ratio between the current sinus
rate and the sinus rate at rest. Similarly, INX
represented the difference from 1 of the ratio
between the current SV and the resting SV,
corrected for possible preload changes. The relationship between INX and SNX was assessed by
linear regression analysis.
Data are presented as mean G standard deviation or as frequency distribution. The difference
between two means was evaluated by two-tailed
Student’s t test with a significance level of 0.05.
The goodness-of-fit of the linear regression between INX and SNX in each patient was expressed
by the coefficient of determination (squared
Pearson correlation coefficient: r2).
Results
The pacemaker was generally programmed in DDD
mode with a low basic rate (usually 40 min1) to
follow the intrinsic atrial rhythm. Spontaneous
atrial and ventricular activity was present in 13
patients, while atrial-driven ventricular pacing was
performed in 15 cases. Only in two cases was atrial
pacing applied from the beginning of the test. The
TVI was recorded with atrial and ventricular ring
Rate-responsive pacing
237
electrodes (AreVr) in 20 of 30 patients and with
atrial ring and ventricular tip electrodes (AreVt) in
the remainder. Average TVI values in telediastole
and telesystole are reported in Table 1. Although
the peak-to-peak amplitude of the TVI waveform
was higher in AreVt configuration, the relative
systolic increase was not significantly different
and the morphology of the signal was similar in
both TVI recording modalities. Representative
examples of the TVI signal derived in AreVt and
AreVr configurations are shown in Figs. 1 and 2,
respectively. In the presence of AV sequential
activity, the minimum TVI was recorded during
the atrial systole and the maximum peak occurred
during the decay phase of the T wave, at a time
consistent with the end of systolic ejection.
After TVI recording in basal conditions and
transient overdrive sequential pacing, IPN infusion
was started. All patients having intrinsic atrial
activity showed a positive chronotropic reaction
to the administration of the beta-agonist, with an
average sinus rate increase of 68 G 31% with
respect to the resting state. The chronotropic
effect was usually accompanied by a transient fall
in diastolic arterial pressure, while the systolic
pressure showed smaller changes, being either
slightly increased or decreased (Fig. 3) in different
patients. The initial TVI response to adrenergic
stimulation was a clear-cut increase in the maximum systolic peak, usually preceding any change
in the minimum diastolic value (Figs. 1 and 2). At
the time of maximal chronotropic activation, when
the cardiac rate usually exceeded 100 min1,
a statistically significant increase in maximum
systolic and minimum diastolic TVI was noticed in
100 and 82% of the cases, respectively. The effect
was larger on end-systolic than on end-diastolic
TVI. In contrast, if the cardiac rate was increased
by overdrive atrial pacing in the absence of
adrenergic stimulation, the end-diastolic TVI was
significantly increased in all the patients, while the
end-systolic TVI was never affected (Fig. 4).
When the rate-responsive function was enabled,
the pacemaker processed the TVI data in realtime, calculated INX and TVIR and modified the
pacing rate following the sensor indications. Since
the basic rate was programmed well below the
resting sinus rate, in most cases atrial pacing was
Table 1
inhibited throughout the test, allowing the comparison of INX and SNX trends. In the event of
overdrive atrial pacing, the rate-gain of the rateresponsive system was reduced to decrease TVIR
and restore the sinus rhythm. An example of the
time-course of INX and SNX under adrenergic
stimulation is shown in Fig. 5A. A linear relationship between the two variables was demonstrated
in 27 of 28 cases, with an average r2 of
0.81 G 0.13. The only exception was a patient
where INX started to rise together with the sinus
rate at the beginning of adrenergic stimulation,
but remained at a constant slightly elevated level
thereafter, in the presence of a marked and
progressively increasing chronotropic response.
The frequency distribution of r2 in the whole
patient group is shown in Fig. 6. The reliability of
INX as a predictor of SNX was neither dependent on
the TVI configuration nor on the modality of
ventricular activation (r2 averaged 0.81 G 0.12 in
the AreVr TVI subgroup; 0.81 G 0.14 in the AreVt
TVI subgroup; 0.82 G 0.07 in the subgroup with
intrinsic AV conduction; 0.80 G 0.16 in the subgroup undergoing atrial-driven ventricular pacing).
The linear regression of INX on SNX in each patient
provided the ideal rate-gain of the rate-responsive
system, corresponding to the reciprocal of the
regression slope. By applying the proper rate-gain
to INX and assuming a basic rate equal to the
resting sinus rate, the resulting TVIR trend closely
reproduced the sinus rate (Fig. 5B). At the time of
maximal chronotropic stimulation, the TVIR derived in each patient was equal to 96 G 14% of the
corresponding sinus rate. The absolute value of the
difference from 100 averaged 11 G 10%.
In the two patients undergoing atrial pacing from
the beginning of the test (basic rate Z 80 min1),
INX was increased during IPN administration up to
maximum values of 0.27 and 0.37, resulting in
a maximum pacing rate of 101 min1 (rate-gain Z 1)
and 95 min1 (rate-gain Z 0.5), respectively.
Discussion
Haemodynamic sensors have mostly been applied
in cardiostimulation to regulate the rate-responsive function according to the inotropic condition
Diastolic and systolic TVI values in AreVr and AreVt configuration
TVI recording
configuration
Minimum
peak (Ohm)
Maximum
peak (Ohm)
Peakepeak
excursion (Ohm)
Relative systolic
increase (%)
AreVr
AreVt
343 G 77
652 G 146
366 G 82
704 G 141
23 G 14
52 G 33
6.8 G 4.3
8.6 G 6.6
238
G. Gasparini et al.
300 ms
40
Figure 1 From top to bottom: surface ECG, TVI waveform, atrial (upward) and ventricular (downward) sensing
markers in basal conditions (left-hand panel) and during isoprenaline infusion (right-hand panel). Intrinsic AV
conduction in sinus rhythm. TVI was recorded in AreVt configuration. At baseline, the minimum diastolic and the
maximum systolic TVI averaged 484 and 523 Ohm, respectively. The TVI and the time scale are same for both the
panels: vertical bar Z 40 Ohm; horizontal bar Z 300 ms. The adrenergic stimulation induced a clear-cut increase in
systolic TVI.
of the heart. Currently available systems include
the PEA and the unipolar impedance sensor, which
can detect mechanical and electrical cardiac
parameters correlated with right ventricular dP/
dt [16e18]. Although positive clinical results have
generally been reported with both these sensors
[28e31], some controversial experience [32] as
well as practical and theoretical considerations
prompt further research in this field. Haemodynamic monitoring of cardiac function should be
better performed with conventional hardware
resources, while PEA recording requires a special
pacing lead equipped with a microaccelerometer
mounted at the tip [16,28]. In addition, both the
systems are sensitive to different manifestations
of the strength of cardiac contraction, which is
heavily dependent on the preload, according to
Starling’s law. Since preload changes are not
controlled by the autonomic nervous system and
can occur as a result of posture, skeletal muscle
activity and respiratory movements, a proper
definition of cardiac contractility in any functional
condition requires combined information on both
myocardial contraction strength and diastolic ventricular volume [13,21].
Relative changes in ventricular volume can be
inferred from electric impedance measurements,
using conventional pacing electrodes [19,20]. In
particular, impedance recording through the cardiac cycle in a trans-valvular configuration results
in a stable, periodic waveform, with minimum and
maximum peaks properly timed in correspondence
with the maximum and minimum ventricular
volume, respectively [22e25]. The TVI signal can
be recorded using a tip or a ring ventricular
electrode: therefore, close contact with the
Rate-responsive pacing
239
Figure 2 TVI waveform (upper tracing) and pacemaker event markers (lower tracing) in basal conditions (left-hand
panel) and during isoprenaline infusion (right-hand panel). VDD pacing: the smaller upward markers indicate atrial
sensing and the higher downward markers indicate ventricular stimulation. TVI was recorded in AreVr configuration.
At baseline, the minimum diastolic and the maximum systolic TVI averaged 334 and 351 Ohm, respectively. The TVI
and the time scale are same for both the panels: vertical bar Z 10 Ohm; horizontal bar Z 300 ms.
1.4
fraction of basal value
sinus rate
A direct validation of the real haemodynamic
meaning of TVI data was outside the aims of the
present study, requiring comparative echographic
assessment of ventricular volume under resting
and stress conditions, which is not practicable
during a pacemaker implantation procedure. However, the observed correlation between the TVI
inotropic index and the sinus rate trend under IPN
administration indirectly confirms the value of the
theoretical model, supporting the application of
140
120
edTVI
esTVI
relative variation (%)
ventricular wall is not required (Fig. 2). The
minimum diastolic TVI was previously shown to
increase with a change from supine to upright body
position [24], while the maximum systolic TVI was
demonstrated to increase with increasing cardiac
contractility [23e26]. All the above evidence
suggests that the TVI waveform is mainly modulated by the ventricular volume. Assuming an
inverse relationship between the two variables,
a haemodynamic model has been applied to
convert the TVI data in relative EDV, ESV, SV and
EF. Any change in diastolic or systolic TVI is
expressed as a fraction of the starting peak-topeak amplitude, representing an equal and opposite change in ventricular volume scaled as a fraction of the reference SV. The relationship between
SV and EDV specifies the cardiac inotropic state,
fully accounting for the preload influence on
systolic performance.
100
80
60
40
20
0
1.2
IPN
sys. P
-20
pacing
1
dias. P
0.8
0.6
0
50
100
150
200
time (s)
Figure 3 Time-course of sinus rate, diastolic arterial
pressure (dias. P) and systolic arterial pressure (sys. P)
during i.v. administration of 2 mg/ml/min isoprenaline
(IPN) in one patient.
IPN
Figure 4 Maximal effect of overdrive sequential
pacing at 30 min1 above the sinus rate (pacing), or
i.v. administration of 2 mg/ml/min isoprenaline (IPN), on
the end-diastolic TVI (white columns) and the endsystolic TVI (grey columns). The change with respect to
basal values is expressed as percent of the TVI peak-topeak excursion at rest. Both the procedures increased
end-diastolic TVI to a similar extent (the difference is
not statistically significant). In contrast, the end-systolic
TVI was significantly increased by IPN stimulation only,
remaining unchanged under overdrive pacing.
240
G. Gasparini et al.
1
SNX
INX
relative score
0.8
0.6
0.4
0.2
IPN
0
-0.2
0
100
200
A
300
400
500
time (cycles)
120
bpm
100
80
IPN
60
40
sinus rate
TVIR
20
0
100
200
B
300
400
500
time (cycles)
Figure 5 A: time-course of relative changes in sinus
rate (SNX: thicker line) and TVI inotropic index (INX:
lighter line) during adrenergic stimulation (IPN). The
linear regression of INX on SNX in this patient showed
r2 Z 0.87, with slope of 0.94. B: time-course of the sinus
rate (thicker line) and the TVI-indicated rate (lighter
line) in the same example.
TVI as an advanced tool for haemodynamic regulation of rate-responsive pacing. IPN is expected to
induce acute positive chronotropic and inotropic
effects with a similar time-course. Indeed, all
tested patients showed a significant increase in
INX - SNX correlation
number of cases
12
10
8
6
sinus rate, coupled with a reduction in diastolic
arterial pressure, which was likely due to the wellknown vasodilating action of the beta-agonist. At
the same time, the systolic pressure was less
affected, suggesting that the fall in vascular resistance might have been compensated by an
increase in systolic flow. Consistently, the TVI
sensor detected an increase in SV, resulting from
a large reduction in the ESV with respect to a much
smaller reduction in EDV. The former can be
explained by the increase in myocardial contractility induced by adrenergic stimulation; the latter
can be due to the increased cardiac rate, with
corresponding shortening of the diastolic filling
time. A statistically significant decrease in EDV was
also obtained when the cardiac rate was enhanced
by overdrive sequential pacing. In the same condition, ESV was unaffected and the SV was consequently reduced. However, any change in SV
totally due to a change in preload does not modify
the INX and therefore has no effect on the TVIR.
The data processing system prevents a direct
positive or negative feedback of the pacing rate
on the TVIR, which is only influenced by the up and
down regulation of myocardial contractility mediated by the adrenergic input to the heart.
Although TVI is intended as a monitor of right
heart haemodynamic activity, its main indications
can be extended to the left side as well, where
corresponding preload and SV modification are
expected to occur in common physiological and
pathological conditions [21]. The ability to discriminate the haemodynamic expression of cardiac
contractility from the preload effects is an important advance in haemodynamic sensor technology,
which is expected to improve pacing rate regulation in all circumstances entailing a modification in
venous return. Furthermore, the prospect of obtaining diagnostic information on the trend of
diastolic ventricular filling, as well as on the
ejected blood volume, in changing daily-life conditions by an implanted device, makes TVI an
appealing new tool in the medical care of pacemaker patients.
4
2
References
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
r2
Figure 6 Linear regression analysis of the relationship
between inotropic index (INX) and relative sinus rate
change (SNX). Frequency distribution of the coefficient
of determination (r2) obtained in each patient. Horizontal axis values indicate the bin range upper limit. A good
correlation was demonstrated in 27 of 28 cases.
[1] Kristensson BE, Arnman K, Rydén L. The haemodynamic
importance of atrioventricular synchrony and rate increase
at rest and during exercise. Eur Heart J 1985;6:773e8.
[2] Lindemans FW, Rankin IR, Murtaugh R, Chevalier PA.
Clinical experience with an activity sensing pacemaker.
Pacing Clin Electrophysiol 1986;9:978e86.
[3] Rognoni G, Bolognese L, Aina F, Occhetta E, Magnani A,
Rossi P. Respiratory dependent atrial pacing management
Rate-responsive pacing
[4]
[5]
[6]
[7]
[8]
[9]
[10]
[11]
[12]
[13]
[14]
[15]
[16]
[17]
of sinus node disease. Pacing Clin Electrophysiol 1988;11:
1853e9.
Rosenqvist M, Arén C, Kristensson BE, Nordlander R,
Schüller H. Atrial rate-responsive pacing in sinus node
disease. Eur Heart J 1990;11:537e42.
Hedman A, Hjemdahl P, Nordlander R, Åström H. Effects of
mental and physical stress on central haemodynamics and
cardiac sympathetic nerve activity during QT interval
sensing rate responsive and fixed rate ventricular inhibited
pacing. Eur Heart J 1990;11:903e15.
Chirife R. Physiological principles of a new method for rate
responsive pacing using the pre-ejection interval. Pacing
Clin Electrophysiol 1988;11:1545e54.
Schaldach M. Automatic adjustment of pacing parameters
based on intracardiac impedance measurements. Pacing
Clin Electrophysiol 1990;13:1702e10.
Bennett T, Sharma A, Sutton R, Camm AJ, Erickson M,
Beck R. Development of a rate adaptive pacemaker
based on the maximum rate-of-rise of right ventricular
pressure (RV dP/dtmax). Pacing Clin Electrophysiol 1992;15:
219e34.
Pichlmaier AM, Braile D, Ebner E, et al. Autonomic nervous
system controlled closed loop cardiac pacing. Pacing Clin
Electrophysiol 1992;15:1787e91.
Padeletti L, Porciani MC, Ritter P, et al. Atrioventricular
interval optimization in the right atrial appendage and
interatrial septum pacing: a comparison between echo and
peak endocardial acceleration measurements. Pacing Clin
Electrophysiol 2000;23:1618e22.
Bordachar P, Garrigue S, Reuter S, et al. Hemodynamic
assessment of right, left, and biventricular pacing by peak
endocardial acceleration and echocardiography in patients
with end-stage heart failure. Pacing Clin Electrophysiol
2000;23:1726e30.
Occhetta E, Magnani A, Bortnik M, Francalacci G, Di
Gregorio F, Vassanelli C. Hemodynamic sensors: their
impact in clinical practice. In: Raviele A, editor. Cardiac
arrhythmias 2003. Milan: Springer-Verlag Italia; 2003. p.
713e8.
Chirife R. Hemodynamic assessment with implantable
pacemakers. How feasible and reliable is it? In:
Raviele A, editor. Cardiac arrhythmias 2003. Milan:
Springer-Verlag Italia; 2003. p. 705e12.
Heynen H, Sharma A, Sutton R, et al. Clinical experience
with VVIR pacing based on right ventricular dP/dt. Eur J
Cardiac Pacing Electrophysiol 1991;1:138e46.
Kay GN, Philippon F, Bubien RS, Plumb VJ. Rate modulated
pacing based on right ventricular dP/dt: quantitative
analysis of chronotropic response. Pacing Clin Electrophysiol 1994;17:1344e54.
Rickards AF, Bombardini T, Corbucci G, Plicchi G, the
Multicenter PEA Study Group. An implantable intracardiac
accelerometer for monitoring myocardial contractility.
Pacing Clin Electrophysiol 1996;19:2066e71.
Osswald S, Cron T, Gradel C, et al. Closed-loop stimulation
using intracardiac impedance as a sensor principle:
correlation of right ventricular dP/dt max and intracardiac
impedance during dobutamine stress test. Pacing Clin
Electrophysiol 2000;23:1502e8.
241
[18] Plicchi G, Marcelli E, Parlapiano M, Bombardini T. PEA I and
PEA II based implantable haemodynamic monitor: pre
clinical studies in sheep. Europace 2002;4:49e54.
[19] Chirife R. Acquisition of hemodynamic data and sensor
signals for rate control from standard pacing electrodes.
Pacing Clin Electrophysiol 1991;14:1563e5.
[20] Chirife R, Ortega DF, Salazar A. Feasibility of measuring
relative right ventricular volumes and ejection fraction
with implantable rhythm control devices. Pacing Clin
Electrophysiol 1993;16:1673e83.
[21] Chirife R, Tentori MC, Mazzetti H, Dasso D. Hemodynamic
sensors: are they all the same? In: Raviele A, editor.
Cardiac arrhythmias 2001. Milan: Springer-Verlag Italia;
2001. p. 566e75.
[22] Di Gregorio F, Morra A, Finesso M, Bongiorni MG. Transvalvular impedance (TVI) recording under electrical and
pharmacological cardiac stimulation. Pacing Clin Electrophysiol 1996;19:1689e93.
[23] Gasparini M, Curnis A, Mantica M, et al. Hemodynamic
sensors: what clinical value do they have in heart failure?
In: Raviele A, editor. Cardiac arrhythmias 2001. Milan:
Springer-Verlag Italia; 2001. p. 576e85.
[24] Bongiorni MG, Soldati E, Arena G, Di Gregorio F,
Barbetta A, Mariani M. Hemodynamic sensors: what clinical
value do they have in chronotropic incompetence? In:
Raviele A, editor. Cardiac arrhythmias 2001. Milan:
Springer-Verlag Italia; 2001. p. 595e601.
[25] Di Gregorio F, Curnis A, Pettini A, et al. Trans-valvular
impedance (TVI) in the hemodynamic regulation of cardiac
pacing. In: Mitro P, Pella D, Rybár R, Valocik G, editors.
Cardiovascular diseases 2002. Bologna: Monduzzi Editore;
2002. p. 53e7.
[26] Gasparini G, Curnis A, Gulizia M, et al. Can hemodynamic
sensors ensure physiological rate control? In: Raviele A,
editor. Cardiac arrhythmias 2003. Milan: Springer-Verlag
Italia; 2003. p. 725e31.
[27] Bongiorni MG, Soldati E, Arena G, et al. Transvalvular
impedance: does it allow automatic capture detection? In:
Raviele A, editor. Cardiac arrhythmias 2003. Milan:
Springer-Verlag Italia; 2003. p. 733e9.
[28] Langenfeld H, Krein A, Kirstein M, Binner L. Peak
endocardial acceleration based clinical testing of the
‘‘BEST’’ DDDR pacemaker. Pacing Clin Electrophysiol
1998;21:2187e91.
[29] Clémenty J, Kobeissi A, Garrigue S, Jaı̈s P, Le Metayer P,
Haı̈ssaguerre M. Validation by serial standardized testing of
a new rate-responsive pacemaker sensor based on variations in myocardial contractility. Europace 2001;3:124e31.
[30] Griesbach L, Gestrich B, Wojciechowski D, et al. Clinical
performance of automatic closed-loop stimulation systems. Pacing Clin Electrophysiol 2003;26:1432e7.
[31] Santini M, Ricci R, Pignalberi C, et al. Effect of autonomic
stressors on rate control in pacemakers using ventricular
impedance signal. Pacing Clin Electrophysiol 2004;27:
24e32.
[32] Cron TA, Hilti P, Schächinger H, et al. Rate response of
a closed-loop stimulation pacing system to changing
preload and afterload conditions. Pacing Clin Electrophysiol 2003;26:1504e10.