EXPERIMENTAL STUDIES
Haemodynamic impact of the left ventricular pacing site during graded ischaemia in an open-chest pig model
INSERM U 441, University Bordeaux 2, CHU de Bordeaux, France
Manuscript submitted 15 September 2007. Accepted after revision 5 December 2007.
* Corresponding author: Hospital Haut Leveque Service Pr Clementy, Pessac, France. Tel: +33 5 57 65 65 65; fax: +33 5 57 65 65 43. E-mail address: bordacharp{at}hotmail.com
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Abstract |
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Aims: In post-operative setting after cardiac surgery, the choice of the optimal ventricular pacing site remains an issue, particularly in patients with ischaemic cardiomyopathy. We aimed to investigate the impact of the left ventricular (LV) pacing site in an animal model of incremental myocardial ischaemia.
Methods and results: Three epicardial LV pacing leads were implanted in 10 pigs [LV1 in the territory of the left anterior descending (LAD) artery, LV2 in the lateral border of this territory, LV3 in an anatomically opposed position]. A two-dimensional strain echocardiogram was performed at baseline and during two levels of incremental ischaemia, corresponding to 30 and 70% reduction of coronary flow in the LAD, during spontaneous sinus rhythm (SR) and during LV1, LV2, LV3, and multi-LV (LV1 + LV2 + LV3) pacing. At baseline (n = 10), LV + dP/dtmax was decreased (P < 0.01) during LV1, LV2, LV3, and multi-LV pacing compared with SR. At first level of ischaemia (n = 7; 3 animals died from ventricular fibrillation), LV1 pacing (ischaemic area) induced a significant decrease in LV + dP/dtmax compared with SR, LV2, LV3, and multi-LV pacing (P < 0.05). At second level of ischaemia (n = 6), LV1 pacing induced a significant decrease in LV + dP/dtmax associated with an increase in the extent of myocardium with echocardiographic post-systolic shortening compared with SR, LV2, LV3, or multi-LV pacing (P < 0.05). In contrast, multi-LV pacing induced a significant haemodynamic improvement compared with SR, LV1, LV2, and LV3 (P < 0.05).
Conclusions: Pacing within an ischaemic area has detrimental impact on acute global and regional LV function. More studies are needed to assess the impact of multi-LV pacing in chronic ischaemic conditions.
Key Words: Cardiac resynchronization therapy, Ischaemia, Animal
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Introduction |
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Advances in cardiac resynchronization therapy have led to an increased use of epicardial left ventricular (LV) pacing in the clinical setting of heart failure.1
–8 Temporary or permanent ventricular pacing is required in some patients with complete heart block and heart failure after cardiac surgery. In the post-operative setting, the choice of the optimal ventricular pacing site remains an issue, particularly in patients with ischaemic cardiomyopathy. Different factors, such as global and regional loading conditions, can interfere with myocardial energy requirements and with the extent of the ischaemic injury. In normal hearts, ventricular pacing produces regional ventricular asynchrony and induces major discrepancies between the amplitudes of the regional effective preload and segmental deformation.9,10 Therefore, the distance between the pacing site and the ischaemic area may be important in determining the pattern of regional deformation in ischaemically injured and non-injured myocardium. New echocardiographic techniques allowing analysis of LV strain are widely used in clinical practice to analyse the differences in amplitude and timing of segmental deformations.11–14 An acute haemodynamic and echocardiographic animal study was therefore undertaken to test the hypothesis that the location of the LV pacing site relative to the ischaemic area, as well as the number of pacing sites, may be major determinants of local deformation and global LV function in a porcine model of acute graded ischaemia.
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Methods |
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Animal preparation
The experimental protocols were handled in compliance with the Guiding Principles in the Use and Care of Animals published by the National institutes of Health (NIH Publication No. 85-23, Revised 1996).
Ten male York pigs, weighing between 40 and 45 kg and free of clinically evident disease, were used in this study. Pigs were sedated with an intramuscular injection of 20 mg/kg ketamine hydrochloride and anaesthetized with sodium pentobarbital (10 mg/kg). Slow intravenous infusion of saline maintained hydration throughout surgery, and anaesthesia was maintained using continuous intravenous infusion of ketamine (500 mg/h). The trachea was intubated through a midline cervical incision for connection to a respirator (Siemens Servo B, Berlin, Germany). Pigs were then ventilated using room air supplemented with oxygen. A 7F catheter was placed in the internal jugular vein for infusion of drugs and fluids. Arterial blood gases were monitored periodically (Radiometer, Copenhagen, Denmark), and ventilatory parameters were adjusted to maintain blood gases within physiological ranges. Animals were placed on a fluid filled heating pad to maintain rectal temperature between 37 and 38°C.
A 7F Millar cathetertip micromanometer (Millar Instruments Inc., Houston, USA) was introduced into the LV cavity via a carotid artery. The heart was exposed by a median sternotomy and lateral thoracotomy and suspended in a pericardial cradle. The left anterior descending (LAD) coronary artery was isolated distal to the first diagonal branch. A transonic flow probe (Transonic Systems Inc., Ithaca, USA) was positioned around the LAD for continuous measurement of coronary flow adjacent to a screw occluder.
Temporary myocardial pacing leads were attached to the upper surface of the right atrium and to the epicardium at three LV sites: one in the territory of the LAD artery (anterior wall, LV1), one at the border of this territory (lateral wall, LV2), and one in an anatomically opposed position (posterior wall, LV3) on the same short axis view, 1 cm below the base of the heart. The leads were connected to a four-channel external pulse stimulator (Medtronic, Inc., Minneapolis, USA) allowing setting of thresholds for each electrode separately and pacing of each of the electrodes separately or in combination.
Echocardiography
Standard echocardiography
Echocardiographic examinations were performed in all animals using a Vivid Seven digital ultrasound system (GE Medical Systems, Fairfield, USA). Three cardiac cycles were stored in cineloop format for offline analysis. Aortic ejection and aortic velocity-time integral (VTI) were assessed by pulse-wave Doppler imaging. The time to end-systole was measured as the time from the onset of QRS complex to the end of the aortic systolic ejection.
Strain measurements
Two-dimensional circumferential strain was measured as described previously by the use of a dedicated software package (EchoPac PC, GE).15,16 Two-dimensional strain is a novel non-Doppler-based method to evaluate systolic strain from standard bi-dimensional acquisitions (Figure 1). After tracing the endocardial contour on an end-diastolic frame, the software automatically tracks the contour on subsequent frames. Adequate tracking can be verified in real time and optimized, by adjusting the region of interest or manually correcting the contour. The software automatically divides the LV in six segments (anterior, antero-lateral, infero-lateral, inferior, infero-septal, antero-septal) and provides the curve of deformation during the cardiac cycle for these six LV segments. The reference frame for strain measurement is taken as the time of the pacing spike during ventricular pacing and the peak of QRS during atrial pacing. Transmural-averaged circumferential strain is calculated for each frame obtained during a cardiac cycle.
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Circumferential strain was assessed in a parasternal short-axis view at the level of the pacing leads. The amplitude of the strain was measured during end-systole (aortic valve closure). A segment was considered to exhibit post-systolic shortening if the end of the segmental shortening occurred after aortic valve closure.
Average values and standard deviations were calculated to assess potential beat-to-beat variations in strain measurement.
Experimental protocol
The pigs were allowed to stabilize for 20 min after surgical preparation to achieve a steady state before baseline acquisitions. Left ventricular pressure, aortic flow, and ECG signals were digitized at 200 Hz and stored on disk for offline analysis.
Echocardiographic and haemodynamic measurements were first performed at baseline in spontaneous sinus rhythm (SR) and during LV1, LV2, LV3, and multi-LV (LV1 + LV2 + LV3) pacing applied in random order. After studying two ventricular pacing sites, measurements were repeated during SR. Pacing was performed in VDD mode so that atrial sensing was used to govern ventricular pacing. The atrio-ventricular delay was programmed short (between 20 and 40 ms in the different animals) to ensure a complete ectopic ventricular capture and was not modified between the different pacing configurations. Measurements were performed on 5–10 cardiac cycles after 30 s of pacing at a particular site.
A 30% reduction in flow was then imposed with the screw occluder. The pigs were allowed to stabilize for 10 min to achieve a steady state, and all measurements were repeated in random order after 30 s in the different pacing configurations. A 70% reduction flow was then imposed with the screw occluder. The pigs were allowed to stabilize for 10 min to achieve a steady state before analysis of the different pacing configurations as described previously.
The animals were sacrificed by injection of an overdose of pentobarbital.
Statistical analysis
Continuous variables were compared by paired Wilcoxon–Mann–Whitney test. A value of P < 0.05 was considered statistically significant. Results are expressed as mean ± SEM. During each step of ischaemia (baseline, 30, or 70% reduction flow), for comparison of the effect of pacing from the various sites, each animal was used as its own control. During each step of ischaemia, to evaluate the significance of the effect of pacing site on haemodynamic variable and on segmental strain, one-way analysis of variance for repeated measurements was used on the number of animals alive. To evaluate the significance of the impact of ischaemia on the strain for one pacing configuration, only the pigs alive during the full protocol were used.
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Results |
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Baseline (n = 10)
The mean ventricular rate was 110 ± 7 bpm during SR with normal spontaneous impulse conduction without a significant difference between the different LV pacing configurations. Peak systolic LV pressure was significantly lower during LV1 pacing (92 ± 14 mmHg), LV2 pacing (94 ± 11 mmHg), LV3 pacing (90 ± 13 mmHg), and multi-LV pacing (94 ± 15 mmHg) compared with SR (108 ± 12 mmHg) (P < 0.05). We did not observe any significant difference in end-diastolic pressure and in end-diastolic echocardiographic volumes. The QRS duration was significantly longer during single-site LV pacing (LV1: 89 ± 5 ms, LV2: 91 ± 6 ms, LV3: 88 ± 5 ms) compared with SR (59 ± 5 ms; P < 0.01). Multi-LV pacing significantly reduced QRS duration compared with single-site LV pacing (P < 0.05) but QRS duration remained significantly longer than during SR (75 ± 4 vs. 59 ± 5 ms, P < 0.05). The maximum and minimum time derivatives of LV pressure (LV + dP/dtmax and LV – dP/dtmin) were significantly decreased during LV1, LV2, LV3, and multi-LV pacing compared with SR (P < 0.05). Echocardiographic aortic VTI was significantly decreased during LV1, LV2, LV3, and multi-LV compared with SR (P < 0.05) (Table 1). The different LV pacing configurations gave similar LV pressures, dP/dt, and aortic VTI.
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The mean echocardiographic frame rate during the different experiments and the different stages of the protocol was 72 ± 12 frames/s. During SR, we observed little difference in the amplitudes of end-systolic circumferential strain between the LV segments without any post-systolic shortening. In contrast, during LV1, LV2, and LV3 pacing, the time course and extent of shortening changed markedly from the pacing site to the most remote regions. The amplitudes of end-systolic circumferential strain were significantly decreased at the pacing site (anterior wall for LV1, lateral wall for LV2, and posterior wall for LV3) vs. SR (P < 0.05) and were significantly increased in LV segments remote from the pacing sites (posterior wall for LV1, septal wall for LV2, and anterior wall for LV3) (Figure 2). These remote segments exhibited significant pre-stretch and post-systolic shortening.
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During multi-LV pacing, these segmental differences were lower. The differences in amplitudes of segmental strain between multi-LV pacing and SR did not reach significance for any LV segments (Figure 3).
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First level of ischaemia (30% reduction flow) (n = 7)
Three pigs were excluded from the analysis due to lethal ventricular fibrillation. The mean heart rate was 112 ± 6 bpm in SR, a value comparable with what observed during LV pacing configurations. Peak systolic LV pressure was significantly lower during LV1 (87 ± 13 mmHg), LV2 (91 ± 14 mmHg), and LV3 (92 ± 15 mmHg) pacing compared with SR (103 ± 14 mmHg) (P < 0.05). The difference did not reach significance between multi-LV (95 ± 17 mmHg) and SR. The differences in QRS duration observed at baseline, during single-site, multisite ventricular pacing and SR were comparable with what observed in baseline conditions.
LV + dP/dtmax was significantly decreased during LV1, LV2, and LV3 pacing compared with SR (P < 0.05). LV + dP/dtmax was significantly higher during multisite LV than during LV1 pacing (P < 0.05). The difference in LV + dP/dtmax between SR and multi-LV did not reach significance. The echocardiographic aortic VTI was significantly decreased during LV1, LV2, and LV3 pacing compared with SR (P < 0.05) (Table1).
Thirty per cent reduction in coronary flow significantly decreased the amplitude of the end-systolic strain during SR in the anterior wall (ischaemic area) compared with baseline (–9.8 ± 3.4 vs. –12.3 ± 2.8; P < 0.05), whereas the amplitude of the strain was not significantly modified in the other segments. During LV1 pacing, the amplitude of the strain within the ischaemic area was not significantly different than in baseline conditions. In contrast, the amplitudes of the strain was significantly decreased in the inferior wall (–13.3 ± 2.7 vs. –11.6 ± 3.5; P < 0.05).
The amplitude of end-systolic strain measured during LV2, LV3, and multi-LV pacing was comparable with what measured in corresponding baseline conditions (Figure 3).
Second level of ischaemia (70% reduction flow) (n = 6)
One more pig succumbed due to lethal ventricular fibrillation during the second reduction of coronary flow. Measurements were therefore performed on six animals. The mean heart rate was 119 ± 5 bpm in SR without any significant difference between the different pacing configurations. Peak systolic LV pressure was significantly lower during LV1 (65 ± 12 mmHg) compared with LV2 (79 ± 9 mmHg), LV3 (81 ± 10 mmHg), multi-LV pacing (88 ± 10 mmHg), and SR (84 ± 11 mmHg) (P < 0.05). The QRS width in SR was significantly larger for this level of ischaemia than in baseline condition (88 ± 8 vs. 59 ± 5 ms; P < 0.05). Left ventricular pacing further increased QRS width to 117 ± 12 ms during LV1 pacing, a value significantly higher than what measured during LV2 (101 ± 10 ms) or LV3 (99 ± 11 ms) pacing. Multi-LV pacing lead to a QRS width value of (85 ± 9 ms), comparable with what observed in SR and significantly lower to what observed during single-site LV pacing (P < 0.05).
LV + dP/dtmax was significantly (P < 0.05) lower during LV1 compared with LV2, LV3, multi-LV pacing, and SR and was accompanied by a significant decrease in the echocardiographic aortic VTI (P < 0.05). Conversely, LV + dP/dtmax was significantly higher during multi-LV pacing compared with SR although the accompanying increase in echocardiographic aortic VTI did not reach significance (Table 1). Multi-LV pacing was the optimal pacing configuration (vs. SR or single-site LV pacing) in all six pigs.
The amplitude of the end-systolic strain during SR was significantly decreased in the anterior, antero-septal, and antero-lateral segments compared with baseline measurements, with significant post-systolic shortening.
LV1 pacing did not induce any further decrease in the amplitude of end-systolic strain in the anterior wall. However, the amplitude of end-systolic strain was significantly reduced in remote regions, with substantial post-systolic shortening in the studied six segments.
During multi-LV pacing, the amplitude of the end-systolic strain was significantly decreased in the anterior wall compared with baseline measurements obtained in the same pacing configuration. However, the extent of post-systolic shortening was decreased compared with SR or with single-site LV pacing since post-systolic shortening was observed in the anterior LV segment only (Figure 3).
The effects of LV2 and LV3 pacing inside and outside the ischaemic area were similar. The amplitude of end-systolic strain was decreased within the ischaemic area, and post-systolic shortening was observed in anterior, antero-septal, and antero-lateral segments.
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Discussion |
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The current animal experimental study, which evaluated the effects of ventricular pacing under acute ischaemic conditions, has yielded three principal findings. (i) During acute myocardial ischaemia, ventricular pacing within the ischaemic area has a deleterious effect on local and global mechanical functions. In addition, it induces a prolongation of LV electromechanical delays, with significant post-systolic shortening occurring both inside and outside the ischaemic area and a significant decrease in systolic shortening in non-ischaemic regions. (ii) There is no significant haemodynamic difference between pacing the functional border zone and pacing myocardium remote from the ischaemic area. (iii) During severe ischaemia, multi-LV pacing results in a significant haemodynamic improvement compared with single-site LV pacing and spontaneous ventricular activation. Increasing the number of pacing sites allows an improvement relative to the reduction of the extent of myocardium, with post-systolic shortening leading to a more effective contribution of the different LV segments to global LV function.
Baseline measurements
At baseline, atrio-synchronized ventricular pacing from the different LV sites was detrimental to mechanical function when compared with spontaneous ventricular activation. This difference could partially be explained by the short atrio-ventricular delays used in this study that may have altered the ventricular filling. The present study quantified the degree and extent of local segmental shortening during ventricular pacing. When moving from the early to the late activated regions, the pattern of contraction changed in parallel with the differences observed in effective local preload. Compared with multisite LV pacing, single-site epicardial pacing resulted in more interaction between early and late activated tissues and a more heterogeneous distribution of circumferential strain. The strains were highly decreased at the pacing site and significantly increased in regions remote from the pacing site, with increased regional pre-systolic stretch in those regions during single-site ventricular pacing. However, despite the marked differences in electrical activation, i.e. QRS width, and regional deformation, we did not note any significant difference in global LV contractility or stroke volume, i.e. aortic VTI, during single-site vs. multisite LV pacing. This may be explained by the important loss of effective contractile force at the pacing site, observed during single-site epicardial pacing, being compensated for by hyperfunctioning remote regions. Although our data did not demonstrate acute haemodynamic differences between single- and multi-LV pacing, we believe that the increased difference in regional deformation may lead to more detrimental long-term remodelling during single-site epicardial pacing.17
Pacing under ischaemic conditions
The present study was designed to obtain detailed insight into the effects of ventricular pacing on local and global myocardial functions under acute ischaemic conditions. Regional systolic function in the LV wall was assessed from an average of the transmural strain during graded LAD coronary artery stenosis. This was obtained by determining deformation of the LV wall at a high spatial resolution with the use of a two-dimensional strain echocardiographic technique. Our data provide evidence that, under acute ischaemic conditions, the sequence of contraction within the LV wall and the resultant severity of impairment of cardiac function depend on the number and location of pacing sites. Pacing the ischaemic area was detrimental and induced a prolongation of the different LV electromechanical delays, probably secondary to slow conduction around the pacing site. This was associated with a significantly increased mass of myocardium with decreased systolic shortening and increased post-systolic shortening and, consequently, a corresponding loss of effective ‘contractile mass’. A previous study has demonstrated that the presence of a postero-lateral scar was a predictive factor of non-response after cardiac resynchronization therapy in patients with heart failure.18 In this study, the LV lead was positioned in a high proportion of patients in a postero-lateral cardiac vein. It is likely that this was leading to stimulation inside ischaemic but still viable and excitable myocardium.
During acute reduction of coronary flow, there is a sharp and visual transition between ischaemic and non-ischaemic myocardium. It is well known that regional systolic function is impaired in the normally perfused myocardium immediately adjacent to an acutely ischaemic region. This functional border zone results more from mechanical interaction between ischaemic and non-ischaemic myocardium rather than from a transition of impaired contractility.19 The perfusion boundary is associated with correspondingly steep gradients in tissue ATP, creatine phosphate, and lactate. We did not demonstrate significant haemodynamic differences between pacing the functional border zone and pacing a region directly opposite to the ischaemic area. The echocardiographic analysis did not reveal differences in the mean duration of the different electromechanical delays, suggesting that the electrical activation and propagation did not differ significantly when pacing from these two regions. This indicates that the electrical propagation inside the functional border zone was probably preserved.
Finally, we have demonstrated that during severe ischaemic conditions leading to LV dysfunction, a significant haemodynamic improvement is obtained with multisite LV pacing compared with single-site LV pacing or spontaneous rhythm. At baseline, without the added insult of ischaemia, adding a second and third ventricular pacing site did not afford haemodynamic improvement. We hypothesize that in normal hearts, increasing the number of pacing sites increases the number of areas with impaired wall thickening and lack of effective deformation. In the presence of a large area of ischaemic myocardium, increasing the number of pacing sites may allow a reduction of activation time, thereby eliminating areas with severely delayed activation and the associated loss of contractile force. The echocardiographic analysis demonstrated that the extent of myocardium displaying post-systolic shortening was optimized with this pacing configuration even compared with spontaneous rhythm. Post-systolic shortening has been described in patients with ischaemic injury but also in patients with ventricular dyssynchrony. The myocardium with post-systolic shortening constitutes a potential contractile reserve, and the reduction of the mass of myocardium with post-systolic shortening is known as one of the mechanism responsible for the improvement described after cardiac resynchronization therapy.20
Clinical implications
The present study highlights the ability of echocardiography to reveal regional differences in myofibre shortening during abnormal electrical activation. The technique is safe, non-invasive, and directly applicable to patients. To design more effective and safe pacing therapies, it is of critical importance to understand the effects of epicardial pacing under ischaemic conditions. This animal study demonstrates that under conditions of acute myocardial ischaemia, the location of the optimal pacing site clearly depends on the location of the ischaemic area. During open-heart surgery, if implantation of epicardial pacing leads is required, the ischaemic area should be avoided. Similarly, during implantation of a multisite device, an ischaemic area should be avoided. Future technology will probably allow pacing from more than one or two ventricular sites. During severe ischaemia associated with LV dysfunction, increasing the number of pacing sites seems promising.
Limitations
There are some limitations in the design of the present acute study that limits the potential direct clinical implications. Indeed, the extrapolation of the data from the present study in pig hearts to patients with ischaemic heart disease should be done with care. Similarly, the potential clinical implications of this acute study are conditional and must be evocated very cautiously since the pigs did not show conventional criteria for resynchronization therapy such as dyssynchrony or severe chronic heart failure. Our findings may not be transferred to the typical patient receiving cardiac resynchronization therapy. Although the current study demonstrates a detrimental effect of local pacing during an ischaemic injury with regional dysfunction as observed in some patients with unstable angina, no data have demonstrated the effects of local pacing in a zone of irreversible injury (myocardial infarction). The acute improvement described with multi-LV pacing may be reached by additional oxygen consumption which might cause a deleterious long-term effect. The impact of the pacing site in patients with chronic ischaemia is more clinically relevant and needs to be further investigated. Two-dimensional strain echocardiography provides a transmural-averaged measurement of segmental strain. Future technology will probably provide separate analysis of the different transmural layers (endocardium, mid-wall, epicardium) and will probably be more appropriate to assess the alterations related to ischaemic conditions.
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