Using Vectorcardiography In
Cardiac Resynchronization
Therapy
By L.Lindeboom
BMTE 10.19
Report Internship
Catharina Hospital Eindhoven Eindhoven University of Technology
Supervisors
Dr. Ir. M. van ‘t Veer Dr. B.M. van Gelder Dr. Ir. M.C.M. Rutten Prof. Dr. N.H.J. Pijls
1 Abstract
(English) The conductive system of the heart may be affected by a heart disease due to direct damage of the Purkinje bundle branches or by a changed geometry in a dilated heart. As a result the electrical activation impulse will no longer travel across the preferred pathway and a loss of ventricular synchrony, prolonged ventricular depolarization and a corresponding drop in the cardiac output is observed. During cardiac resynchronization therapy (CRT) a biventricular pacemaker is implanted, which is used to resynchronise the contraction between different parts of the myocardium. Optimize pacing lead placement and CRT device programming, is important to maximize the benefit for the selected patients. The use of vectorcardiography (VCG) for CRT optimization is investigated.
In current clinical practice a 12-lead electrocardiogram (ECG) is used to measure the electric cardiac activity of a patient. Each cell in the heart can be represented as an electrical dipole with differing direction during a heartbeat. A collection of all cellular dipoles will result in a single dipole, the cardiac electrical vector. Spatial visualization of the intrinsically three- dimensional phenomena, using VCG, might allow for an improved interpretation of the electric cardiac activity as compared to the one dimensional projections of a scalar ECG.
The VCG loops of one healthy subject and two subjects with a left bundle branch block (LBBB) and two subjects with a right bundle branch block (RBBB) are qualitatively described. It is shown that different electrical activation patterns will indeed result in different VCG’s and that the VCG loops give an intuitive insight into the conductive pathways. Differences in VCG loops after right ventricular and left ventricular pacing and the influence of lead placement are analyzed.
(Dutch - Samenvatting) Door directe of indirecte schade aan het elektrische geleidingssysteem van het hart, bereikt de elektrische prikkel verschillende delen van het hart niet gelijktijdig, waardoor de samentrekking van het hart niet synchroon zal plaatsvinden. Door het implanteren van een biventriculaire pacemaker wordt getracht het hartspierweefsel op verschillende plaatsen, met verschillende tijdsintervallen, elektrisch te stimuleren om het samentrekken van het hart te resynchroniseren. Het gebruik van vectorcardiografie (VCG) bij het zoeken naar de optimale plaatsing en de optimale tijdsinstellingen van de pacemaker, wordt onderzocht.
Elke cel in het hart kan worden gezien als een kleine elektrische dipool, verschillend van grootte en richting gedurende een hartcyclus. Door het optellen van alle dipolen ontstaat de elektrische hartvector. Met gebruik van het standaard 12-afleidingen electrocardiogram (ECG), is het mogelijk om de elektrische hartvector uit te rekenen en weer te geven in een vectorcardiogram, waarbij de twaalf figuren van het ECG worden gereduceerd tot één figuur voor het VCG.
De VCG’s van één gezond testpersoon, van twee testpersonen met een linkerbundeltakblok en van twee testpersonen met een rechterbundeltakblok worden kwalitatief beschreven en vergeleken. De invloed van rechter- en linkerventrikel pacing wordt tevens beschreven. De VCG’s lijken een goed inzicht te geven in de geleiding van de elektrische prikkel over het hart.
2 Contents
1. Introduction 5
1.1 Background 5 1.2 Cardiac Resynchronization Therapy 6 1.3 Electrocardiography 6 1.4 Description of Vectorcardiogram 7 1.4.1 Healthy subject 7 1.4.2 LBBB 9 1.4.3 RBBB 9 1.4.4 Pacing 10 1.5 Project goal 11
2. Materials and Methods 12
2.1 Patient population and data acquisition 12 2.2 Signal analysis 12 2.2.1 Filtering of the ECG signal 12 2.2.2 Calculation of the VCG 12 2.2.3 Definition of an average heartbeat 13 2.2.4 Differentiation of the depolarization wave 13 2.3 Qualitative measures of the VCG 15 2.4 Quantitative measures of the VCG 15 2.4.1 Mean electrical axis 15 2.4.2 VCG loop area 16 2.4.3 Duration of depolarization 16
3. Results 17
3.1 Measurements 17 3.2 Healthy subject, LBBB subjects and RBBB subjects 17 3.2.1 Healthy subject 17 3.2.2 Bundle branch blocks 18 3.2.3 Overall observations 20 3.3 RV and LV pacing 20 3.3.1 RV pacing 20 3.3.2 LV pacing 21 3.3.3 Overall observations 22
4. Discussion and Conclusions 23
4.1 Healthy VCG 23 4.2 VCG of LBBB intrinsic and with pacing 23 4.3 VCG of RBBB intrinsic and with pacing 23
3 4.4 Pacing lead position 23 4.5 Normalization of the VCG 24 4.6 VCG in CRT 24 4.7 Quantification of the VCG 25 4.8 Repolarization 25 4.9 Summary of conclusions 25
5. Future Directions 27
6. References 28
Appendix A – ECG’s 29 Appendix B – 3D Representations of VCG loops 36 Appendix C – 2D Representations of VCG loops 43
4 1. Introduction
1.1 Background
Heart failure, defined as the inability of the heart to supply sufficient blood flow to the organs in the body, is an important cause of hospitalization in patients older than 65 years. Due to the impairment of the cardiac output, patients suffer from breathlessness and fatigue. Initial causes for heart failure include hypertension, valvular heart disease, cardiomyopathy, and ischemic heart disease, often accompanied by dilatation of the ventricles of the heart and alterations in the electrical activation patterns [1] .
The heart is endowed with a system for the generation and conduction of electrical impulses to cause rhythmical and synchronic contractions of the heart muscle (see figure 1). Initially the rhythmical electrical impulses are generated in the sinus node (or S-A node) and travel via the atria towards the atrioventricular node (A-V node).
Special Purkinje fibers lead the impulses from the A-V node through the A-V bundle into the ventricles. These fibers divide into a left and a right bundle branch. Each branch spreads downward towards the apex of the heart, progressively dividing into smaller branches. The ends of the Purkinje fibers penetrate about one third of the muscle mass. Because the speed of transmission of the impulse in these Purkinje fibers is about 5 times higher than transmission through the heart muscle Figure 1 The cardiac rhytmical excitation system itself, the conduction system causes the (Adapted from Textbook of Medical Physiology Eleventh electrical impulse to arrive at almost all Edition, Guyton and Hall, Chapter 10) segments of the ventricles within a narrow time span resulting in a synchronous contraction. This is required for an effective pumping by the two ventricular chambers of the heart [2].
In a number of patients suffering from heart failure the conduction system might be affected due to direct damage of the conductive system by myocardial ischemia or by the changed geometry in the dilated heart. In these cases the bundle braches of the Purkinje system become diseased or damaged and will stop to conduct the electrical impulses. Since the electrical impulse can no longer travel across the preferred pathway, it will move through the muscle fibers, which slows the electrical conduction and which changes the directional propagation of the impulse. The impulse will arrive at different segments of the heart with an increased time interval. A differentiation between a left of a right bundle branch block (LBBB and RBBB respectively) is made. As a result of the BBB, there is a loss of ventricular synchrony, ventricular depolarization is prolonged and a corresponding drop in the cardiac output is observed.
5 1.2 Cardiac Resynchronization Therapy
Cardiac resynchronization therapy (CRT) aims to reduce the symptoms of breathlessness and fatigue in patients suffering from heart failure, with delayed and dyssynchronous left ventricular contraction as a result, by restoration of a more physiological sequence in cardiac activation. Resynchronisation is achieved by the implantation of a biventricular pacemaker or biventricular ICD (implantable cardioverter defibrillator) which enables activation of the myocardium at different locations and with different time delays (see figure 2). The goal of CRT is to activate both ventricles simultaneously to restore the synchrony between the ventricles [1] .
To predict the optimal lead placement Figure 2 Graphical representation of the heart in a section and the optimal time interval between perpendicular to the septum of the heart. The red dots indicate the the pacing electrodes currently regions for possible lead positions. echocardiography and measurements of pressure build-up are used. Echocardiography is used to identify mechanical dyssynchrony with the use of tissue Doppler imaging (TDI), which measures the systolic and diastolic velocity in different segments of the myocardium. A notable regional variation in velocities is a typical appearance in patients with dyssychronous ventricle contraction. This method requires experience in echocardiography and is very time consuming and rather operant dependent [3] .
A more objective and reproducible method is to measure the amount of pressure increase per unit of time (or dP/dt) in the left ventricle, which evaluates the pumping effectiveness of the heart. An optimal lead placement and an optimal timing interval between the pacing electrodes for the biventricular pacemaker are found with a maximal value in dP/dt [4] .
Several randomized controlled trials and numerous observational studies have demonstrated improvements in exercise capacity and quality of life after CRT procedures in patients suffering from heart failure. Despite these advances approximately 25% of patients who meet current criteria for implantation of a CRT device do not show objective evidence of clinical benefit (the ‘non-responders’) [3]. Implantation of a CRT device is expensive, time consuming and involves invasive medical surgery. It is important to optimize pacing lead placement and device programming to maximize the benefit for the selected patients. Alternative methods for optimization are investigated.
1.3 Electrocardiography
In current clinical practice a standard 12-lead electrocardiogram (ECG) is used to measure the electric cardiac activity of a patient. The change in the electrical activation of the heart caused by a LBBB and a RBBB are recognized as different waves in the different
6 electrocardiographic leads. Besides these intrinsic conduction disorders, different activation patterns as a result of different pacing lead positions in CRT will also result in different ECG’s. In a standard 12-lead ECG a projection of the electric cardiac vector is drawn along standardized leads. The connections for the standard ECG are shown in figure 3.
The electric cardiac vector is a superposition of the numerous electrical dipoles that exist during the depolarization of the cardiac muscle at each point in time. This is further explained in paragraph 1.4.
The voltage which is recorded in a normal ECG depends on the placement of the electrodes on the body surface of a patient, the amount of excited cardiac muscle and the body composition of the patient. Because of resistance of the tissue between the heart and the skin, the measured signal will decrease with an increasing distance from the heart muscle. Figure 3 Arrangement of electrodes for a standard Because the separate leads in the ECG give a projection 12-lead ECG of the cardiac electrical vector along one single direction (Adapted from Textbook of Medical Physiology spatial information is difficult to interpret from 12 Eleventh Edition, Guyton and Hall, Chapter 11) different images. Thereby, redundant information is presented in a 12-lead ECG. Spatial visualization of the intrinsically three-dimensional phenomenon in a single image might allow for an improved interpretation of the electric cardiac activity as compared to the one-dimensional projections of a scalar ECG.
In 1956 Frank developed a method with which he was able to obtain a 3D representation of the electrical activity of the heart, represented by a right-left axis (X), a head-to-feet (cranial to caudal) axis (Y) and a front-back (anterior to posterior) axis (Z) [5]. Frank used seven electrodes to calculate the X, Y and Z potentials. The electrode placement and the X, Y and Z directions are shown in figure 4. From the scalar X, Y and Z coordinates it is possible to obtain the instantaneous cardiac vector, whose path in space builds the vectorcardiographic loop or a vectorcardiogram.
1.4 Description of the Vectorcardiogram
1.4.1 Healthy subject
Figure 4 Frank vectorcardiographic lead Figure 5 shows the depolarization of the heart for a healthy system. Seven electrodes used are denoted subject, together with the expected ECG and VCG. The figure with A, C, E, I, M, H and F. shows the result of the depolarization on the cardiac vector in the frontal plane as indicated by the red axes in figure 5A.
7 Figure 5 Schematic drawing of different time steps of the cardiac electrical impulse pathway during depolarization for a healthy subject in the frontal plane as indicated by the red arrows in panel A. The expected VCG and ECG (shown under the heart respectively) are plotted for successive time steps in panel B-F. While the impulse travels over the heart, the resultant vector changes in direction and magnitude. Tracking the direction and magnitude of the resultant vector in time results in the VCG loop. The ECG only gives the magnitude of the vector. The small loop indicated with “p” within the larger VCG loop represents the electrical activity of the atria. (Adapted from 'Presentation and Analysis of Vector Electrocardiograms', Anna Redz, March 1998)
As the impulse travels from the A-V node into the ventricles through the Purkinje system, the impulse arrives in the left bundle branch slightly before the right bundle branch. Depolarization starts from the left side of the septum. Initially the cardiac vector is pointing from left to right, which is visible in a vector pointing to the right in the VCG (figure 5B). Then the vector changes direction as the depolarization wave expands towards the apex and the LV and RV (figure 5C). Because the left ventricle consists of more muscle mass, it will take slightly longer to completely depolarize this ventricle. The vector in the VCG is a resultant vector from multiple existing dipoles over the heart, with the larger potential differences appearing in the left ventricle. Hence, the resultant vector in the VCG will therefore mainly be directed to the left (figure 5D and 5E ). Furthermore the loop will mainly be directed caudal as can be seen by the vector pointing towards the apex (figure 5C and 5D). When the heart is completely depolarized, no dipoles will exist and the loop is closed.
In the horizontal plane (defined by the x- and z-axis, see figure 4) the left ventricle is positioned behind the right ventricle. Because larger potential differences appear in the left ventricle the main direction of the loop in 3D will be posterior.
8 1.4.2 LBBB
Figure 6 Schematic overview of depolarization with LBBB in the frontal plane, as indicated by the red arrows in A. The right ventricle will depolarize before the left ventricle. The impulse will travel via the apex of the heart towards the left ventricle resulting in a mainly cranial oriented VCG (C and D)
Figure 6 gives a schematic overview of the depolarization for a subject with a LBBB in the frontal plane, as indicated with the red arrows in figure 6A . The depolarization of the right ventricle will be normal and the impulse will travel from the right ventricle to the left ventricle via the apex. The vector starts pointing caudal (see figure 6B) changing in a vector with the main direction being cranial ( figure 6C and 6D). The last part of the VCG loop will be directed more to the left because the depolarization follows the left ventricular free wall (figure 6D).
Looking in the horizontal plane, the VCG will mainly be pointing posterior towards the left ventricle, because the right ventricle depolarization is ahead of the left ventricular depolarization.
1.4.3 RBBB
Figure 7 Schematic overview of depolarization with RBBB in the frontal plane, as indicated by the red arrows in A. Depolarization of the left ventricle will be ahead of depolarization of the left ventricle. The impulse will travels via the apex of the heart towards the right ventricle resulting in a mainly cranial direction (C en D). 9 In figure 7 a schematic overview of the depolarization in the frontal plane for a subject with RBBB is given. The red arrows in figure 7A indicate the frontal plane. The impulse will travel from the left ventricle to the right ventricle via the apex. One would expect again a mainly cranial direction of the loop (figure 7C and 7D). The vector will point to the right during the beginning of depolarization (figure 7B) and will swing to the left as depolarization in the left ventricle takes place. When the depolarization in the left ventricle is completed, the vector will turn to the right side again (figure 7D)
The horizontal plane will indicate that the cardiac vector points anterior in this case, because the left ventricle will be depolarized before of the right ventricle.
1.4.4 Pacing
Figure 8 Pacing in the horizontal plane (B and C) and in the frontal plane (E). The green arrows in A indicate the horizontal plane. The red arrows in D indicate the frontal plane. Lead placement will influence the direction of the cardiac electrical vector as is shown with the red arrows in B,C and E.
A change in electrical activation will not only occur in case of bundle branch blocks, but the use of a pacemaker will also influence the electrical impulse propagation over the heart. The changes in the impulse conduction will be visible in the VCG as well.
Generally speaking it is possible to pace the left or the right ventricle (LV or RV). The main difference in the VCG between LV and RV will be observed in the horizontal plane, as is shown in figure 8B. When pacing the right ventricle, the vector will be directed posterior . Pacing the left ventricle will lead to a vector directed anterior .
To indicate vector directions on the right-left and the cranial-caudal axes, the exact placement of the lead will influence this direction. The position of the leads with respect to the X-axis will influence the right-left direction. A lead positioned to the right, will generally cause the vector to be directed to the left and vice versa (figure 8C).
When positioning the lead towards the apex of the heart this will lead to a vector in cranial direction, while a pace position towards the basis of the heart will give a more caudal directed vector (figure 8E).
10 It is important to notice that RV pacing for a LBBB subject will most likely not change the directions of the vector drastically. The same characteristics will be visible because the pacing will cause the right ventricle to depolarize ahead of the left ventricle, as is the case with a LBBB. The same holds for LV pacing of a RBBB subject.
1.5 Project goal
The goal of this project is to qualitatively describe vectorcardiograms for patients suffering from heart failure accompanied with conduction disorders that require CRT. The pathologic VCG’s will be compared to a normal VCG. Influence of lead placement will be investigated by analysis of vectorcardiograms after right and left ventricular pacing.
11 2. Materials and Methods
2.1 Patient population and data acquisition
Standard 12-lead ECGs were recorded for patients with a LBBB, a RBBB, and for healthy individuals. The differentiation between patients with a LBBB and a RBBB was made according to the standard criteria on the 12-lead ECG. A bundle branch block can be diagnosed when the duration of the QRS complex on the ECG exceeds 120 milliseconds. A right bundle branch block typically causes prolongation of the last part of the QRS complex, and may shift the heart's electrical axis slightly to the right. Left bundle branch block widens the entire QRS complex, and in most cases shifts the heart's electrical axis to the left [2] .
All patients with a LBBB and patients with a RBBB required CRT. For these latter groups the intrinsic rhythm was measured, before the pacemaker was activated. The pacemaker was then used for RV and LV pacing and the ECG was recorded again. For the healthy individuals only the intrinsic rhythm was recorded.
During the implantation of the CRT device the 12-lead ECG was recorded for a period of 5 seconds for each setting (intrinsic, RV pacing, and LV pacing). Data was exported and analyzed offline. The data sampling rate was 977 points per second and the measured voltages were in mV. All procedures were performed in the Catharina Hospital in Eindhoven.
2.2 Signal analysis
2.2.1 Filtering of the ECG signal
Pacemaker spikes and baseline wander in the ECG signal were removed by a Butterworth filter. Frequencies above 30 Hz and frequency below 0.25 Hz were eliminated. The lowpass filter had less than 3 dB of ripple in the passband, defined from 0 to 30 Hz, and at least 50 dB of attenuation in the stopband, which was defined from 60 Hz to 489 Hz (the Nyquist frequency). The response of the highpass filter was set to less than 3 dB of ripple in the passband, defined from 0.95 Hz to the Nyquist frequency at 489 Hz, and at least 50 dB of attenuation in the stopband from 0 Hz to 0.25 Hz.
2.2.2 Calculation of the VCG
As described in paragraph 1.3, Frank used a special electrocardiographic lead system, consisting of seven electrodes, to derive the X, Y and Z leads [5]. To minimize clinical interference the standard recorded 12-lead ECG was used to calculate the Frank X, Y and Z leads, instead of changing to a Frank lead system.
To calculate the X, Y and Z leads from a standard 12-lead ECG the inverse Dower matrix was used [6]. This method operates by calculating the VCG as a fixed linear combination of ECG signals as depicted below.