Visualization and functional characterization of the postinfarction arrhythmogenic substrate

Abstract

Much knowledge concerning the mechanisms and nature of the postinfarction arrhythmogenic substrate has been gathered in the past decades. The ever-expanding therapeutic options require more insight in the selection of postinfarction patients at risk for developing life-threatening arrhythmias as well as a better understanding of which therapy should be selected for an individual patient. Ideally, methods should be developed that 1) are non-invasive in nature 2) allow mapping during sinus rhythm 3) allow ablation during sinus rhythm. Aim of this thesis was to gain more knowledge on the genesis of postinfarction arrhythmias by utilizing combined electrophysiologic and computational techniques that allow visualization and functional characterization of the mechanisms underlying postinfarction ventricular arrhythmias. In chapter 2 the clinical value of body surface mapping to guide antiarrhythmic surgery is investigated. In chapter 3 the electrophysiological basis for failure of body surface mapping to identify the correct site of origin of postinfarction VT was analyzed by means of simultaneous multi-lead endocardial and body surface mapping of VT. In chapter 4 new ways are explored that allow mapping of the postinfarction arrhythmogenic substrate during sinus rhythm. In chapter 5 the use of signal averaged electrocardiography for detection of late potentials is extended to electrocardiographic monitoring of the entire body surface area. The purpose was twofold: 1) to investigate whether the sensitivity of signal averaged electrocardiography for detection of patients at risk can be increased and 2) to analyze the potential of spatially distributed late potentials at the body surface to anatomically delineate areas of slow conduction within the left ventricle. In chapter 6 disparity in repolarization is investigated. Invasively obtained, spatially dense endocardial electrophysiologic repolarization measurements are compared with non-invasive ECG and body surface map parameters that are believed to estimate disparity in repolarization. In chapter 7 the physical principles that form the basis of the computational techniques used for analysis of the postinfarction arrhythmogenic substrate in this thesis are explained. Finally, in chapter 8 clinical implications of the currently presented work are discussed and future directives for arrhythmia research are suggested.