Europace Advance Access originally published online on November 15, 2007
Europace 2008 10(1):40-45; doi:10.1093/europace/eum238
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PACING
Investigation of pacing site-related changes in global restitution dynamics by non-contact mapping
1 Cardio Vascular, Medtronic Inc., 7601 Northland Drive, Brooklyn Park, MN 55428, USA; 2 Wessex Cardiac Centre, Southampton General Hospital, Mailpoint 46, Tremona Road, Southampton SO16 6YD, UK; 3 CRDM, Medtronic, Inc, 8200 Coral Sea Street NE, Mounds View, MN 55112, USA; 4 Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN 55455, USA; 5 Department of Physiology, University of Minnesota, Minneapolis, MN 55455, USA; 6 Department of Surgery, University of Minnesota, Minneapolis, MN 55455, USA
Manuscript submitted 27 July 2007. Accepted after revision 1 October 2007.
* Corresponding authors. Tel: +44 23 8079 6240; fax: +44 23 8079 8942.E-mail address: jmm{at}cardiology.co.uk
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Abstract |
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Aims: The determination of dynamic changes in ventricular repolarization may provide insight into arrhythmogenic mechanisms as a consequence of pacing site. This study investigated acute pacing site effects on global characteristics of electrical restitution using high resolution, non-contact mapping (NCM).
Methods and results: Activation-recovery intervals (ARIs) were determined from reconstructed left ventricular electrograms by the NCM system and were analysed during pacing from the right atrial appendage (RAA, intrinsic), right ventricular apex (RVA), and right ventricular septum (RVS) with extrasystoles delivered at intermediate and short coupling intervals in anesthetized swine (n = 5). Electrical restitution curves were determined by the S1–S2 pacing protocol. Activation-recovery interval restitution slopes were determined by the overlapping linear segments regression method. Global distribution of repolarization was defined as the coefficient of variation of the ARIs during restitution. The maximum ARI slopes yielded by RVA pacing were significantly greater than RAA pacing (0.44 vs. 0.32; P < 0.05) and RVS pacing (0.44 vs. 0.37; P = 0.05). There was no significant difference between RAA and RVS pacing (0.32 vs. 0.37). The global distribution of ARIs during restitution from RVA pacing was significantly greater than RAA pacing (12.0 vs. 8.1%; P < 0.05).
Conclusion: Right ventricular apex pacing is associated with impaired global repolarization patterns compared to RAA and RVS. These observations support the hypothesis that RVA pacing may be associated with increased risk of ventricular arrhythmias compared to RVS pacing.
Key Words: Pacing, Mapping, Dynamics, Arrhythmia, Electrical restitution
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Introduction |
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There is strong evidence that the choice of chronic pacing site impacts long-term ventricular function. Specifically, clinical research data have shown that chronic pacing at the right ventricular apex (RVA), the standard site, has been associated with the development of a number of harmful alterations to the heart, including1
–5 left ventricular (LV) electrical and mechanical dyssynchrony, chronic remodelling, LV dysfunction (systolic and diastolic), and the possible promotion of ventricular arrhythmias.3 Many of these maladies are the cause of non-physiologic electrical propagation through the heart, due to the site of activation, the RVA. Although these problems arise following chronic pacing, the non-physiologic conduction pattern (activation starting at the apex instead of following the normal conduction system activating both ventricles simultaneously) exists with acute pacing as well and alters the electrical properties of the heart as soon as initiated. The use of active fixation electrodes has allowed evaluation of several other pacing sites, and it is has been proposed that pacing the right ventricular septum (RVS) may yield haemodynamic benefit. It is postulated that electrical activation of the ventricles follows a more physiological pattern when paced from this site.6,7
Relevant to this postulation is the observation that destabilization of activation wavefronts has been shown to be influenced by the restitution properties of action potential duration (APD).8–10 The APD restitution curve portrays the relationship between local APD and the preceding diastolic interval. There is speculation that this relationship plays a role in the initiation of ventricular fibrillation (VF), i.e. the ‘restitution hypothesis’. Karma was an originator of this idea when he found that as the steepness of the restitution curve is increased, the cardiac tissue becomes more susceptible to alternans.11 The restitution hypothesis states that an APD restitution curve with a slope >1 may lead to repolarization alternans, wavebreak, and transition from ventricular tachycardia (VT) into VF.12 Thus, if this ‘restitution hypothesis’ holds true, we propose that pacing from the RVA rather than the right atrial appendage (RAA) or RVS may yield steeper slopes due to the subsequent impaired electrical depolarization and repolarization patterns elicited.
Controversies exist in the measurement of activation-recovery intervals (ARIs) in the positive T wave polarity.13,14 The use of ARIs reconstructed by non-contact mapping (NCM) to estimate local APDs has been previously validated with contact MAPs and contact unipoles,15,16 as has the use of NCM as a tool to investigate the spatial dispersion of APD restitution.17 In this study, high resolution NCM was employed to measure global ventricular repolarization, as well as to construct global and regional LV electrical restitution curves when acutely pacing from the RAA, RVS, and RVA. Although pacing was performed from the right side, left-sided electrical measurements were of interest to investigate possible differences between pacing sites on the electrical propagation and subsequent recovery of the left side of the heart. This information provides great insight to left-sided activation and repolarization, which are of utmost importance to overall heart function. Specifically, we tested the hypothesis that acute abnormal activation wavefronts alter restitution dynamics, and consider that this may be a potential mechanism of ventricular arrhythmogenesis.
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Surgical procedure
The following procedures were reviewed and approved by the University of Minnesota Institutional Animal Care and Use Committee, which ensures humane treatment of all animals as indicated by the ‘Guide for the Care and Use of Laboratory Animals (NIH)’.
Initial sedation was administered using 5–10 mg/kg telazol and 5–10 mg/kg thiopental intramuscularly in five healthy male Yorkshire swine (68 ± 10 kg). Thereafter, intravenous access via an ear vein was established for fluid (saline 0.9%) administration. The animals were then intubated and ventilated using a N2O/O2 mixture of 
60% N2O (air) and 40% O2 to maintain a PaCO2 of 40 ± 2 mm Hg. Isoflurane (>1 MAC) was administered to maintain anesthesia. Blood pressure was measured via the femoral access port, and a three-lead ECG (SpaceLabs Model 1020, SpaceLabs Inc., Chatsworth, CA) was used to monitor electrocardiograms continuously throughout the procedure. To maintain normal electrolyte balance and pH blood gas levels, blood gas analysis was performed throughout the procedure (Model 5700, Instrumentation Laboratory, Lexington, MA, USA). Millar pressure tip catheters (Millar Instruments Inc., Houston, TX, USA) were used to measure LV and right ventricular pressures; access was gained through the right carotid artery and the right jugular vein, respectively, using nine French (Fr) introducers.
Lead placement
In each animal, endocardial active fixation leads (Model 5076, Medtronic, Inc., Minneapolis, MN, USA) were implanted in each of the following sites under fluoroscopic guidance: the RAA, the RVA, and the RVS. The RAA pacing site was chosen for investigation as the ‘control’ site, as stimulation here represents the physiologic activation of the ventricle.
Non-contact mapping
Non-contact mapping of the LV was performed with the use of the EnSite® 3000 system (St. Jude Medical, St. Paul, MN, USA) and has been described previously.18,19 The system consisted of a 64-multielectrode array (MEA) which was used to measure endocardial electrical propagation patterns, and was mounted on a 7.5 mL inflatable balloon on a nine Fr catheter that was placed in the apex of the LV under fluoroscopic guidance via the left carotid artery. A heparin bolus of 300 IU/kg was injected prior to the deployment of the MEA catheter to prevent embolism from exiting the LV during the procedure.
A seven Fr roving electrophysiological (EP) catheter (Marinr MCxL, Medtronic, Inc., USA) was introduced into the LV through the right carotid artery and was used in conjunction with the MEA catheter to reconstruct the endocardial geometry of the LV using the NCM system’s EnGuide® tracking location technique. The system calculated the position of the roving EP catheter relative to the fixed, known position of the ring electrodes at either end of the MEA. A three-dimensional geometry of the ventricle was then determined. From this geometry, reconstructed unipolar electrograms (UEs) could be selectively displayed on the workstation screen by manual placement of a cursor on the endocardial geometry.
Construction of restitution curves
Constant pacing was performed at each of the three pacing sites at a baseline cycle length of 500 ms using a pulse width of 2 ms and stimulation strength of twice the diastolic threshold. The intrinsic heart rate of the swine was 100 bpm, therefore, in order to capture consistently, the cycle length of 500 ms (120 bpm) was chosen. After steady-state pacing had been established, an extra stimulus (S2) was introduced every 8-beat cycle, and the coupling interval varied by 10-20 ms with each cycle, depending on the ability of the heart to capture the impulse. The APD restitution curves were determined by plotting local ARIs at pre-specified sites against the respective preceding diastolic intervals.
Data analysis
NCM data were analysed using standard software with the Silicon Graphics workstation (version 4.0, Silicon Graphics Inc., Mountain View, CA, USA). Measurements were performed manually using electronic calipers from electrograms displayed on a colour monitor at 200 mm/s resolution.
Reconstructed UEs
Three different morphologies of UE T waves were defined: positive, negative, and biphasic. Activation-recovery intervals were measured by the alternative method to investigate the impact of pacing site on the global changes in restitution dynamics.15 The local ARI was measured between times of dV/dtmin of the QRS and: (i) dV/dtmax of the negative T wave; (ii) dV/dtmin of the positive T wave; and (iii) at the mean time between dV/dtmax and dV/dtmin for the biphasic T wave. For a T wave with double peak derivatives, the end of recovery was determined at the mean point of the two peaks. Diastolic interval was determined as the period from the end of ARI of the previous beat to dV/dtmin of the QRS complex of the beat of interest. A custom-designed template was used to display the paired UE and its first derivative (dV/dt). At each S1–S2 coupling interval, 12 sites were analysed from the LV geometry (Figure 1) in the manner described in previous similar studies and replicated here to allow consistency of data collection and interpretation.17 The local ARIs from each site were averaged over the entire ventricle in order to obtain the global response.
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Activation-recovery interval restitution slopes
The maximum slope for each restitution curve was fitted using the overlapping least-squares linear segments.20
Restitution slopes were analysed from 40 ms diastolic interval segments in steps of 10 ms, with the maximum slope used for the comparison with the other curves (Figure 2). Slopes were measured both regionally (at each of the 12 pre-specified segments of interest) and globally (average value of all regional slope values).
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Distribution of repolarization during restitution
The global distribution of repolarization during restitution was quantified using the standard deviation and the coefficient of variation (ratio of standard deviation and the mean, in percent). This analysis was performed at each of the 12 pre-specified sites in all ventricles.
Statistical analysis
Continuous data were presented as means ± SD when analysing the global distribution of repolarization. Data were presented as means ± 2*SEM when analysing maximum restitution slope to represent a 95% confidence interval. Activation-recovery interval restitution slope data were compared by one-way ANOVA and Wilcoxon matched, paired tests, paired by ventricular segment as well as pacing site. Activation-recovery interval distribution during restitution was compared by Wilcoxon and Mann–Whitney tests. A P-value 
0.05 was considered statistically significant.
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Results |
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Restitution curves were constructed using a basic drive cycle length of 500 ms from a total of 60 endocardial sites, 12 sites in each of the five LVs studied. At each of these sites, three curves were constructed, representing pacing from the RAA, RVA, and RVS. This resulted in a total of 180 restitution curves constructed for analysis.
The ARI restitution curves in each ventricle were variable in their shapes and slopes and could not be exponentially fitted with a simple exponential curve. This was true for pacing at each of the three pacing sites. Examples of global restitution curves from 12 sites determined simultaneously in the LV are given in Figure 3. The steep initial phase of the ARI restitution was found in the interval range between refractoriness and a diastolic interval of 100 ms.
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Activation-recovery interval restitution slopes
The maximum restitution slope was >1 in 14 (or 7%) of all sites examined. Only in two instances was a restitution slope >1 found during RAA pacing. There were six instances each when pacing from the RVA and RVS resulted in slopes >1. The mean maximum restitution slope when pacing from the RVA was significantly greater than when pacing from the RAA (0.44 ± 0.12 vs. 0.32 ± 0.08, P < 0.05), as well as from the RVS (0.44 ± 0.12 vs. 0.37 ± 0.13, P < 0.05). Yet, there was no significant difference in mean restitution slope between pacing at the RAA and RVS (P = ns).
Average activation-recovery interval and distribution during restitution
Pacing at the RAA elicited a mean ARI value of 252 ± 8 ms, whereas pacing at the RVA and RVS elicited values of 247 ± 12 and 247 ± 10 ms, respectively. The mean distribution of ARI (coefficient of variation) when pacing from the RAA was significantly less than when pacing from the RVA (3.2 ± 0.9 vs. 4.9 ± 0.7%, P = 0.05) (Figure 4); however, there was no significant difference in the mean distribution of ARI between pacing from the RAA and the RVS (4.1 ± 1.3%, P = ns) or between pacing from the RVA and at the RVS (P = ns).
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Distribution of global activation-recovery interval restitution slopes
When pacing from the RAA and RVS, the distribution of ARI slope values over the entire ventricle was fairly homogenous. However, when pacing from the RVA, ARI slope value distribution was much more spatially heterogeneous, with multiple areas of steep and shallow slopes (Figure 5). The restitution slopes were investigated regionally. Restitution curve steepness was analysed to determine whether it was dependent on the region of the ventricle from which the curve was generated. Using a qualitative analysis, the findings support regionalization of restitution slopes, especially in the case of the RVA pacing site in the posterior-basal quadrant.
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Discussion |
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Pacing from the ventricle has become a topic of major interest due to multiple studies, which have shown various detrimental effects of long-term RVA pacing.1
,4,5,21–24 Although we looked to investigate the impact that acute pacing from distinct sites has on the electrical properties of the heart, we anticipated that our findings would provide us additional insight as to why such detrimental issues came to be with time. We have systematically analysed global repolarization data from the swine LV employing high resolution NCM to investigate if pacing site influences the repolarization patterns of the heart. Abnormality of repolarization can be powerfully arrhythmogenic over time and may explain some of the increased mortality associated with long-term RVA pacing in some patient groups. Our major findings are (i) NCM can be used for the investigation and determination of restitution changes associated with pacing site; (ii) the mean maximum restitution slope when pacing from the RVA was significantly greater than when pacing from the RAA or RVS; (iii) the global distribution of repolarization associated with pacing at the RVA was significantly greater than when pacing at the RAA; and (iv) pacing from the RVA yielded a much more heterogeneous distribution of slope values over the ventricle than pacing from the RAA and RVS.
The ARI restitution curve has been previously described in human studies. In human right and left ventricles, the restitution curve assumes multi-phasic characteristics, with a steep initial phase, a supernormal phase, and subsequently, a plateau phase when approaching the steady-state diastolic intervals.15,17,25 Our results, using NCM to assess pacing site effects, are consistent with these studies.
Techniques for the assessment of global features of cardiac repolarization
Current techniques used for measuring global restitution in vivo are limited to three approaches: (i) conventional monophasic action potential (MAP) catheters; (ii) basket or sock arrays; and (iii) NCM.
Non-contact mapping has several advantages over the former techniques for the measurement of in vivo global restitution. It can instantaneously create high-resolution maps of the entire intact cardiac chamber under investigation. With each heartbeat, more than 3300 virtual electrograms are constructed across the entire endocardial surface, allowing for rapid acquisition of data. It is a procedure that has been validated with contact MAPs and contact unipoles for measurement of endocardial ventricular repolarization.15,19,26
Arrhythmogenic mechanisms related to repolarization
Many factors are believed to contribute dynamically induced wavebreak, such as cardiac memory and intracellular calcium cycling. However, some of the major contributions to the creation of this arrhythmogenic substrate lie within the properties of electrical restitution, and are borne witness to by APD restitution. The restitution hypothesis states that an APD restitution curve with a slope >1 may lead to repolarization alternans, wavebreak, and transition from VT into VF.12 This hypothesis stems from the idea that increased APD slope increases electrical instability, and that by flattening this slope, instability can be attenuated and VF can be ‘stabilized’ into VT. This hypothesis was first substantiated by Riccio et al. who found that drugs, which reduced the slope of the restitution relation prevented the induction of VF by rapid pacing and converted existing VF into VT.9 These results lent support to the hypothesis that a steeply sloped restitution relation is necessary for the development of ventricular arrhythmias. Garfinkel et al.27 had similar findings of a reduction in the steepness of the APD restitution curve with the use of bretylium, subsequently stabilizing wavebreak and converting VF into VT. Our data show that overall mean slopes are relatively low, compatible with the findings of Yuuki et al.10 Yet, when pacing from the RVA, ARI restitution slopes were found to be steeper on average than when pacing from the RAA and RVS.
Although our slope values were generally <1, one must be mindful of the fact that these experiments were performed on healthy hearts. It is possible that if RVA pacing elicits steeper restitution slopes than when pacing from the RAA and RVS in a healthy animal, then in an unhealthy heart with intrinsically steeper slopes, this may remain the case. In other words, RVA pacing may elicit slopes >1 earlier in the progression of cardiac disease than RAA or RVS pacing; however, this circumstance is merely speculative. We believe that other contributing factors such as the distribution of ARI or conduction velocity restitution in the global ventricle may play a more important role in arrhythmia susceptibility than slope value due to previous work performed in this area.17
Another possible arrhythmogenic substrate is heterogeneity of restitution. As an electrical impulse travels through and across the ventricular myocardium with various regions of steep and shallow slopes, electrical instability can develop and be reinforced as various heterogeneous reactions to an impulse pave the way for a re-entrant circuit. Once this circuit is initiated, because of the heterogeneity, it is difficult for stability to occur and therefore instability is maintained. This spatial heterogeneity of restitution kinetics may be responsible for the regional difference in induction of ventricular arrhythmias. Pak et al.28 found that specific regions of the heart had significantly steeper maximal restitution slopes than other regions. In the ‘steeply sloped’ regions the inducibility of sustained VT/VF was greater than in the regions with shallower slopes. In the work of Yuuki et al.,10 hearts with induced VF were compared to hearts without induced VF. The hearts with induced VF had a much higher regional heterogeneity in slope value distribution, in addition to higher slope values than the non-induced VF hearts. Nash et al.29 found that ARI restitution was spatially heterogenous, with regional organization of multiple discrete areas of steep and shallow slopes, even in patients at low risk of arrhythmias. These findings were observed both clinically and by way of a modelling study, proving that heterogeneity of restitution is a ‘potent arrhythmogenic substrate’ and influences the stability of re-entrant arrhythmias. The findings of the present study are consistent with those of Nash et al. and other previous studies.10,17 All of these observations suggest that magnitude of the restitution slopes 'in combination' with the pattern of their distribution may be important in determining arrhythmogeneity.
Finally, in the current study, pacing from the RVA elicited a greater distribution of repolarization changes during restitution than pacing from both the RAA and RVS. This parameter has not been investigated before in prior studies. We believe that this may represent an abnormal response of the global ventricular repolarization to heart rate changes and could be associated with an increased risk of arrhythmogenesis. However, further studies are required to elucidate this potential mechanism.
Study limitations
The present study investigated left-sided ventricular electrical restitution dynamics due to pacing at various right-sided sites. The lack of measurements on the right side of the heart could be considered a limitation. In creating the electrical restitution curves, short S1–S2 intervals were programmed. If these intervals became too short, arrhythmogenic activity occurred. If this was encountered, shorter intervals were not attempted, possibly underestimating slope value.
Non-contact mapping is a validated method of measuring local APDs, but like other approaches, has some limitations. These include the fact that the endocardial map is only viewed in the end-diastolic geometry and there is some uncertainty in the distance between the endocardial surface and the centre of the balloon catheter in a beating heart.
It should be noted again that there has been no assessment of arrhythmia susceptibility in this model and our comments on likely clinical relevance remain speculative.
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Conclusion |
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In this study, NCM was used to investigate the effect of pacing site on restitution dynamics. The results show that pacing site affects restitution dynamics, and RAA and RVS pacing elicit responses similar to each other, whereas RVA pacing elicits steeper slopes and greater spatial heterogeneity, which have been associated with increased arrhythmogenesis.8
,27–32 Because of these findings, along with the findings of others, we speculate that RVA pacing may be associated with an increased susceptibility to arrhythmias as a consequence of altered repolarization dynamics. Direct evidence of this relationship remains to be confirmed. |
Funding |
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This research was funded by the Biomedical Engineering Institute at the University of Minnesota and Medtronic, Inc.
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Acknowledgements |
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Much gratitude is owed to Monica Mahre for her support in manuscript editing.
Conflicts of Interest: Professor John M. Morgan has a research grant relationship with Medtronic, Inc. and is a Consulting Physician through Cardiac Rhythm Management Europe for Medtronic, Inc.
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