PACING
Determination of left ventricular volume changes by intracardiac conductance using a biventricular electrode configuration
1 Department of Cardiovascular Surgery, Semmelweis University, Budapest, Hungary; 2 Biotronik GmbH & Co. KG, Hartmannstrasse 65, Erlangen D-91052, Germany
Manuscript submitted 22 August 2005. Accepted after revision 18 April 2006.
* Corresponding author. Tel: +49 9131 8924 7600; fax: +49 9131 8924 7950. E-mail address: gerald.czygan{at}biotronik.com
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Abstract |
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Aims The feasibility of determining left ventricular (LV) volume changes by LV conductance measurements with an implantable device was investigated in an animal model.
Methods and results The haemodynamic state of six mongrel dogs was altered by overpacing with rates up to 140 bpm and by isoprenaline infusion with dosages up to 0.2 µg/kg/min. The LV conductance, aortic blood flow, and LV and aortic pressure were recorded. Conductance measurements were carried out using the two electrodes of a bipolar right ventricular pacing lead for current injection and two epicardial leads screwed into the mid-lateral LV wall for measuring the resulting voltage. Stroke conductance (SY) was correlated with the LV stroke volume (LVSV), which was computed from the aortic flow. The LVSV rose to 188±14% with increasing isoprenaline dosage. A strong correlation between the LV conductance SY and the LVSV was found (mean r=0.97). The LVSV decreased to 68±8% with an increasing pacing rate. Again, a strong correlation between SY and LVSV was found (mean r=0.89).
Conclusion This animal study confirms the feasibility of assessing changes in LVSV by determining the LV intracardiac conductance. This creates the possibility of continuous haemodynamic monitoring with implantable devices.
Key Words: Conductance, Haemodynamics, End-diastolic volume, Stroke volume, Sensor, Animal model
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Introduction |
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Monitoring the haemodynamic state of the circulatory system is important for the assessment of cardiovascular diseases. The determination of volume-, flow-, or pressure-related quantities gives fundamental insights into the performance of the cardiovascular system under normal and abnormal conditions. Impairment of cardiac performance may cause decompensation with severe symptoms. Efficient therapy management of congestive heart failure (CHF) requires close observation of the haemodynamic state. Recently, the benefits of cardiac resynchronization therapy (CRT) using implantable triple-chamber pacemakers with or without defibrillators (ICD) have been shown.1
–3 The optimization of device parameters and the observation of therapy progress require reliable monitoring methods. Along with clinical markers (such as the New York Heart Association (NYHA) classification or exercise capacity), and neuroendocrine indicators (such as brain natriuretic peptide or noradrenaline plasma levels), determination of left ventricular (LV) dimensions and volumes is used to predict clinical outcome and optimize therapy. Exercise capacity, peak oxygen consumption, right or LV pressure and their derivatives are used to observe the functional haemodynamic state.4–6
Haemodynamic parameters for monitoring CHF progression
Left ventricular ejection fraction (LVEF) is the most extensively used parameter for haemodynamic assessment of CHF patients, although its value is still the subject of debate.7 One disadvantage of LVEF is that it depends not only on the severity of CHF but also on the prevailing contractility as well as on pre- and afterload. Furthermore, if stroke volume (SV) is determined by the difference between end-diastolic and end-systolic volume, forward SV and mitral regurgitation are indistinguishable. Also the parameters derived from right ventricular (RV) and pulmonary capillary wedge pressure do not necessarily correlate with CHF progression, as classified by the NYHA Class or quality of life.8 As many therapies directly influence one or several of these haemodynamic parameters, their true therapeutic effect on CHF progression may be obscured. In this respect, LV end-diastolic volume (LVEDV) proved to be a reliable surrogate marker to determine the clinical outcome of CHF and the efficacy of therapies.4
Usually haemodynamic parameters are not determined during a follow-up visit to the hospital. Long-term monitoring of CHF progression markers with an implantable device has the advantage that the disease state can be continuously observed. Parameter variations can be compared with normal daily variability, so that true disease trends can be determined. Sudden changes in disease progression can be recognized immediately by the device or a remote monitoring centre, and the therapy can be adapted without delay, thus preventing hospitalizations.9,10
Long-term monitoring of LV volume parameters appears to be an attractive diagnostic option for the observation of CHF progression. The goal of this study was to investigate a method for monitoring LV volume parameters based on intracardiac conductance measurements. The conductance method has an advantage over other methods (e.g. RV pressure measurements10); it does not require special sensor leads and can be performed with standard pacemaker or ICD leads.
Intracardiac conductance measurements
Electrical conductance is characterized by the current flow through a substance and the voltage drop in this substance. Impedance is the reciprocal of conductance. Rushmer et al.11 were the first investigators to propose the determination of volume-related quantities of the left ventricle by the measurement of intracardiac electrical conductance or impedance, respectively. Baan et al.12,13 used an octapolar catheter to determine the absolute volume of the left ventricle. This method was used to record pressure–volume loops of the ventricle.14,15 As permanent placement of a catheter in the left ventricle is not safe for implantable device therapy, several investigators have adapted it to be used with right ventricular leads. Different applications have been proposed on the basis of this method,16 e.g. rate-adaptation based on SV,17,18 detection of the onset of ventricular fibrillation,19 or automatic discrimination of haemodynamically stable and unstable ventricular tachyarrhythmia.20,21
The determination of volume changes in the LV with standard pacing leads has not yet been investigated. The introduction of atriobiventricular implants for resynchronization therapy offers new possibilities for LV conductance measurements. Recent triple-chamber pacemakers or ICD devices use an additional LV lead either implanted in a lateral coronary vein introduced via the coronary sinus or placed epicardially to stimulate the LV. This lead can be used for conductance measurements. As the coronary veins are located close to the epicardium, it is expected that the conductance method delivers comparable results with both lead types.
Study objective
The objective of this animal study was to assess the feasibility of determining LV volume changes via LV conductance measurements with an implantable device. Changes in LV conductance during contraction (SY) and end-diastolic conductance (EDY) were determined. Invasive blood flow and pressure measurements were performed as a reliable and accurate reference on a beat-to-beat basis.
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An animal study was performed as the intended invasive haemodynamic reference measurements cannot be made in humans. Our laboratory meets the standards for good laboratory practice. The investigation conforms to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No. 85-23, revised 1996).
Animal preparation
The experiments were performed on six mongrel dogs (between 22 and 28 kg). The animals were anaesthetized with intravenous pentobarbital sodium (Nembutal, CEVA, initial dose 30 mg/kg). After tracheal intubation, the dogs were mechanically ventilated by a Cape CV2424 ventilator (Cape Co., Warwick, UK). One of the femoral arteries was cannulated for continuous arterial blood pressure monitoring (Electromedics XD003 probe, Electromedics Inc., Englewood, CO, USA). The carotid artery was prepared for the insertion of a pigtail catheter for LV pressure and contractility (dP/dtmax) measurements (Pigtail Catheter 4F, Cordis, Miami, FL, USA). A surface ECG was recorded (Madaus Schwarzer CU12, Munich, Germany and EPR1000plus, Biotronik, Germany) simultaneously with haemodynamic monitoring throughout the experiment. The chest was opened by a transsternal thoracotomy in the fifth intercostal space to access the heart. The ascending aorta was prepared for the placement of a flow probe (Transonic Flow Probe, Transonic Systems Inc., Ithaca, NY, USA). The atrioventricular (AV) node was radiofrequency (RF)-ablated (AbControl/A RF generator and AlCath Blue ablator catheter, both Biotronik) to keep the ventricular rhythm low for the pacing protocol. For one dog (dog 3), the injection of 0.5 mg metoprolol was necessary at the beginning of the measurements to depress junctional rhythm. The ventricular rate was <70 bpm after the ablation procedure in all animals except one (dog 3) whose intrinsic rate was 
110 bpm.
Lead placement and measurements
All electrodes were placed after the ablation of the AV node and remained in their position until the end of the protocol. Standard bipolar pacing leads were inserted into the right atrium (PX53-J, BP, Biotronik) and into the right ventricle (SLX65/11-BP). The RV lead was fixed in the apex with tines. The distance between the two electrodes was 31 mm. Two epicardial leads (ELC35-UP) were screwed into the LV epicardium for conductance measurements in a mid-lateral position and at a distance of 25 mm. The two LV electrodes were parallel to the RV electrodes.
The conductance signal was recorded with an externally connected Inos2CLS pacemaker (Biotronik). Biphasic current pulses with a constant amplitude of 600 µA and a pulse duration of 15 µs for each polarity were injected every 8 ms between the RV electrodes. The resulting voltage was measured between the two LV electrodes (Figure 1), and its time course was low-pass filtered at 40 Hz. This means that, in a strict sense, impedance was measured. The conductance Y was computed from the reciprocal impedance because it is expected to be proportional to volume.22 All conductance measurements were performed in a quadrapolar manner, i.e. different electrode pairs for current injection and voltage recording. This configuration yields better volume proportionality than tri-, bi-, or uni-polar configurations; the conductance signal for these latter configurations is dominated by local effects in the direct vicinity of the electrodes.22 The pacemaker was able to determine impedance signals with a programmable range in steps of factor 2 down to the smallest range of 3.33 
with sufficient resolution.
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Aortic flow was measured with a flow meter (T206, Transonic Systems), on the basis of the ultrasonic transit-time principle for all but the first dog (dog 1). This method is especially suited for animal research and has proved to be highly accurate and reliable.23
–25 The flow probe was fixed around the prepared ascending aorta. For dog 1, an electromagnetic flow probe was used, which was also fixed around the ascending aorta. Fluid-filled pigtail catheters were used for determining the blood pressure in the LV and the descending aorta. The conductance pacemaker was used for pacing. ECG, LV pressure, aortic pressure, aortic blood flow, conductance, pacing markers, and additionally intracardiac electrograms were recorded with a digital data acquisition system (PowerLab, ADInstruments, Castle Hill, NSW, Australia) during all investigations.
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In order to modulate the haemodynamic state, the pacing rate was modified by RV apical VVI overpacing. Upon changing the pacing rate, measurements were started after a steady state was reached at 30 s, as verified by the LV pressure signal, and lasted for 60–90 s.
After the pacing tests, the sympathomimetic drug isoprenaline was applied to alter the inotropic state. First, recordings for dosage zero were performed, and then the dosage was increased. When steady state was reached, conductance measurements were performed again lasting 60–90 s. Different numbers of dosage steps were possible for the animals. The pacing rate was kept constant above the intrinsic rhythm by RV VVI pacing during the drug intervention tests.
Data analysis
The continuous data were separated into single heart cycles. In order to extract SV information from the conductance signal, a ‘stroke conductance’ parameter SY was computed (Figure 2). For calculating SY, the difference between the extreme conductance values at end-diastole and end-systole was computed from EDY and end-systolic conductance (ESY). The EDY value was also recorded to evaluate it as a measure of LVEDV. End-diastolic conductance was the highest conductance value in a time window ranging from 50 ms before to 50 ms after the R-peak. The LVSV was calculated from the aortic flow signal. Aortic flow was integrated during the ejection phase of one heart cycle (the aortic flow represents the flow of blood out of the LV per unit time). The integral was then computed in a time interval that contains the complete ejection phase (Figure 2).
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In order to reduce signal variations caused by respiration and AV timing differences caused by VVI pacing, the conductance and flow signals were averaged over 2 (rate test) or 3 (drug test) respiratory cycles before computing the SY, EDY, and LVSV, respectively.
The SY and EDY values from the filtered signals were correlated with LVSV, and the correlation coefficient r of the linear regression was determined. To determine the accuracy of the conductance method for relative LVSV measurement, the width of the 95% confidence interval around the regression lines was computed, which quantifies the accuracy of predicting one variable by another.
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Figure 3 illustrates the recorded LV conductance signal of 250 consecutive cardiac cycles in one experiment. Signal variation was mainly caused by respiration.
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Pacing test
Haemodynamic variation was similar in all dogs during the pacing tests. With the pacing rate increasing, LVSV decreased for all animals, whereas LV contractility expressed by the maximum LV pressure gradient, LV dP/dtmax, increased slightly. Mean arterial pressure (MABP) showed only small changes.
Figure 4 shows the relationship between pacing rate and the different haemodynamic parameters. The results of the conductance measurements are shown in Figure 5, where data are normalized by setting SY and EDY at 1 for the lowest pacing rate achieved. SY showed the expected behaviour, decreasing with an increasing rate. Likewise EDY also behaved as expected, decreasing with decreasing LVSV.
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Drug test
Figure 6 shows the haemodynamic parameters during the drug test. Contractility increased with increasing drug dosage, as expected, except for dog 3. This animal showed a strong decrease in the haemodynamic parameters during the drug test. The reason was myocardial ischaemia induced by isoprenaline. ST-segment depression was visible in the ECG. Mean arterial pressure generally decreased for higher drug dosages. As isoprenaline has a vasodilator and positive inotropic effect, the balance between these two effects was detected whether the pressure increased or decreased. Except for dog 3, the LVSV increased by 70–100% in all animals.
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In Figure 7, the course of SY as a function of the drug dosage is shown. SY changed in the same direction as LVSV for all animals, including dog 3.
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During the drug tests, contractility significantly changed. Therefore, the relationship between LVSV and LVEDV was not expected to be linear, and LVSV cannot represent LVEDV, in comparison with the rate test. Also, no consistent relation between LVSV and EDY was found for the drug test, the correlation was not significant.
Correlation results for the rate and drug tests
The parameters SY and EDY, derived from the conductance signal, were correlated with LVSV. The relations SY vs. LVSV and EDY vs. LVSV are shown in Figure 8 in the left two panels for the rate tests, in the right panel for the drug test (SY only). The overall linear regression line including all animals is displayed. The correlation results for the rate and drug tests are displayed in Table 1. In contrast to the graphs, where the parameters were averaged for a complete pacing rate (Figure 5) or drug dosage sequence (Figure 7), the mean values of every two respiratory cycles, i.e., over 10 s for a respiratory rate of 12 c/min, were computed for regression analysis. The expected sign for the correlation coefficient r was positive for all correlations.
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Measurement accuracy
A strong correlation coefficient between SY and LVSV is required to use conductance as a measure of LVSV. In addition, the width of scatter of the data points around the regression line is of high importance. The width of the 95% confidence interval around the regression line was calculated for each individual and expressed as fraction of the LVSV value at the lowest rate or zero dosage, respectively (Table 2). The scatter was found to be sufficiently small for the application of monitoring LV volume.
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Haemodynamic observations
Both LVEDV and LVSV were expected to decrease during the pacing test with a rate increase at rest. Diastolic filling time shortens at higher heart rates, therefore reducing end-diastolic volume. The decreased LVEDV leads to a decreased LVSV due to the Frank–Starling mechanism. Furthermore, with an increased arterial blood pressure, the increased afterload may further reduce LVSV.
During the drug test, isoprenaline increases contractility and causes vasodilation, i.e., it reduces afterload. Both effects lead to a higher LVSV. The observed haemodynamic behaviour was consistent with physiological expectations. One dog (dog 3) became ischaemic during the drug test, which resulted in reduced pressures, reduced contractility, and reduced LVSV. For all other dogs, LVSV increased during drug intervention and decreased with overpacing. The dP/dtmax signal showed a mild increase during the pacing test and a strong increase during the drug test.
The LVEDV parameter was not measured directly in this study. For the pacing test, LVSV was used as an indirect measure of LVEDV, as they are related via the Frank–Starling principle. When contractility was unchanged, which was almost always the case for the rate test, LVEDV and LVSV were assumed to be proportional. Hence, EDY was correlated with LVSV.
The observed behaviour of the haemodynamic parameters during the tests performed may be different from the behaviour under atrial-synchronized conditions. However, the purpose of overpacing and drug application was to change the haemodynamic state, measuring reference haemodynamic parameters and conductance, in order to test their correlation under varying conditions. Owing to AV asynchrony in VVI pacing, i.e., a variable atrial contribution to ventricular filling, the haemodynamic and conductance signals showed beat-to-beat fluctuations. These signal variations were eliminated by averaging over several cardiac cycles.
Conductance measurements
The basis of the relationship between the conductance signal and ventricular volume are (a) the changing conductivity of the measurement region, i.e., the ratio of blood to myocardium and (b) the changing relative positions of the electrodes during contraction. The conductivity of blood is approximately 1.5 times as high as that of myocardial tissue at the measurement frequency used here.26,27 The current distribution and associated electric field are similar to the electric field of a dipole. The two LV epicardial electrodes measure the electric field strength at the position of the LV electrodes, which decreases with increasing distance between RV and LV electrodes. Therefore, the measured quadripolar conductance of the ventricle increases during diastole due to ventricular filling with the more conductive blood and the increased distance between the electrodes. The conductance decreases during systole and reaches its minimum at the end of the ejection phase.
The conductance method with standard pacing leads does not deliver absolute volume values. The conductance values depend on the positions and relative orientation of the implanted electrodes which are different for each individual, but were not changed during the study. Therefore, only relative values (i.e. volume changes) were determined.
Consistent regression slope signs of the correlations SY–LVSV and EDY–LVSV, high correlation coefficients, and small scatter around the regression lines were observed. For both tests, a strong correlation between LVSV and SY was found, as well as for the EDY–LVSV correlation. In the rate test, smaller correlation coefficients were found than in the drug test. This is partly caused by the smaller range in LVSV change that occurred in the rate test (factor 1.6) compared with the drug test (factor 1.9). The width of the 95% confidence interval was of comparable size in the two tests.
The accuracy found by the scatter analysis was 11–15% with averaging over two or three respiratory cycles. If the averaging time is increased, a correspondingly smaller scatter is expected. Hence, the method seems to be sensitive enough to detect LV dimensional changes with resynchronization therapy or to perform AV or VV interval optimization.
Along with LV conductance measurements, quadripolar RV measurements between the RV and right atrial leads and with a multipolar RV catheter, respectively, were performed using a small sample size. The RV conductance measurements showed inconsistent results among individuals. This is mainly caused by the irregular and flat shape of the RV in contrast to LV geometry, which has a simple symmetric (conical) shape. The RV conductance only reflects blood volume in that chamber section where the lead is located and does not represent the complete chamber volume. If conductance is determined between an RV and an atrial lead, the motion of the atrial lead may cause signal artefacts. Even if the RV conductance does not seem suitable for the assessment of small changes in SV, it still may be sufficient for detecting substantial decreases, e.g. from an unstable tachyarrhythmia.20
Study limitations
Our results were obtained from open chest measurements. Great differences are not expected if the measurement is performed in the closed chest, although the conductance signal amplitude might be smaller due to the thorax and lung tissue serving as an additional shunt conductor for the measurement current switched in parallel to the heart.
The volume of the human heart is 1.5–2 times larger than that of the dog's heart. This applies even more to the dilated heart with LVEDV values several times the normal value. This increased volume might also cause a smaller signal amplitude.
Heart disease may cause abnormal patterns of contraction related to abnormal electrical activation, for example, or to myocardial scars. These conditions could change the end-systolic geometrical shape of the left ventricle, therefore influencing the SY–LVSV correlation. However, these conditions are expected to have less influence on end-diastolic shape. Even though monitoring of LVEDV by EDY should be less affected, this issue requires further investigation.
The LV conductance measurements were performed with epicardial leads, whereas for human CRT implants intravenous leads are usually introduced via the coronary sinus. No differences are expected, if conductance is measured via a lead inside a coronary vein located on the myocardial surface. A transvenous lead may also be advantageous because the two electrodes are fixed on one lead body. However, this issue also needs to be investigated.
The study proves the general feasibility of determining LV volume changes with the LV conductance method in an acute setting using a canine model. We expect long-term measurements also to be feasible. Tissue ingrowth on the electrode may also influence the impedance signal during the first few weeks after implantation. The long-term behaviour still needs to be investigated.
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Conclusions |
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This animal study confirms the feasibility of monitoring LVSV changes by measuring intracardiac conductance in a biventricular electrode configuration. LVSV was determined by ultrasonic transit-time aortic flow measurement. On the basis of the Frank–Starling relation, a proportionality between conductance and LVEDV was found. The LV electrode implant position was chosen for CRT and was found to be suitable for this purpose.
This method provides the capability of long-term monitoring of LVEDV and LVSV, and hence LVEF using implantable devices. Changes in LVEDV, LVSV, and LVEF are important markers for the development and progression of heart failure. Continuous monitoring of these parameters may reveal the need for an earlier change in therapy, thus decreasing the rate of hospitalizations. Pharmaceutical and electrophysiological therapies may be optimized, especially if a complete record of these parameters is available to the physician in combination with remote patient monitoring systems.
Special sensor leads are not required for the conductance method. Standard bipolar RV leads and bipolar coronary sinus leads can be used, which are implanted in patients undergoing CRT with biventricular pacemakers or ICDs.
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The study was supported by Biotronik GmbH & Co. KG.
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