Europace (2005) 7, 234e241
Rate-responsive pacing regulated by cardiac haemodynamics
a
Unita` Operativa di Cardiologia, Ospedale Umberto I, via Circonvallazione, 50, 30174 Mestre, Venezia, Italy b Unita` Operativa di Cardiologia, Spedali Civili, P.le Ospedali Civili, 1, 25100 Brescia, Italy c Unita` Operativa di Cardiologia, Ospedale S. Luigi - S. Curro`, via Fleming, 24, 95100 Catania, Italy d Unita` Operativa di Cardiologia, Ospedale Maggiore della Carita`, Corso Mazzini, 18, 28100 Novara, Italy e Unita` 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 Sopho `s 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
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Gianni Gasparini a,*, Antonio Curnis b,1, Michele Gulizia c,2, Eraldo Occhetta d,3, Andrea Corrado a, Luca Bontempi b, ` Mascioli b, Giuseppina Maura Francese c, Miriam Bortnik d, Giosue Andrea Magnani d, Franco Di Gregorio e,4, Alberto Barbetta e, Antonio Raviele a
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.
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.
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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
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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 Sopho `s, 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
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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
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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
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300 ms 40
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
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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.
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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.
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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.
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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
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 4 2
References
0 0.1
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0.3
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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, Ryde ´n 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
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bpm
100
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.
Rate-responsive pacing
[4]
[5]
[6]
[7]
[8]
[10]
[11]
[12]
[13]
[14]
[15]
[16]
[17]
[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, Ryba ´r 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] Cle ´menty J, Kobeissi A, Garrigue S, Jaı¨s P, Le Metayer P, Haı¨ssaguerre 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, Scha ¨chinger H, et al. Rate response of a closed-loop stimulation pacing system to changing preload and afterload conditions. Pacing Clin Electrophysiol 2003;26:1504e10.
Downloaded from http://europace.oxfordjournals.org/ by guest on May 17, 2013
[9]
of sinus node disease. Pacing Clin Electrophysiol 1988;11: 1853e9. Rosenqvist M, Are ´n C, Kristensson BE, Nordlander R, Schu ¨ller H. Atrial rate-responsive pacing in sinus node disease. Eur Heart J 1990;11:537e42. ˚stro Hedman A, Hjemdahl P, Nordlander R, A ¨m 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.
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