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Using Vectorcardiography in Cardiac Resynchronization Therapy

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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.
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