Abstract-The sequences of activation and recovery of the heart have physiological and clinical relevance. We report on progress made over the last years in the method that images these timings based on an equivalent double layer on the myocardial surface serving as the equivalent source of cardiac activity, with local transmembrane potentials (TMP) acting as their strength. The TMP wave forms were described analytically by timing parameters, found by minimizing the difference between observed body surface potentials and those based on the source description. The parameter estimation procedure involved is non-linear, and consequently requires the specification of initial estimates of its solution. Those of the timing of depolarization were based on the fastest route algorithm, taking into account properties of anisotropic propagation inside the myocardium. Those of recovery were based on electrotonic effects. Body surface potentials and individual geometry were recorded on: a healthy subject, a WPW patient and a Brugada patient during an Ajmaline provocation test. In all three cases, the inversely estimated timing agreed entirely with available physiological knowledge. The improvements to the inverse procedure made are attributed to our use of initial estimates based on the general electrophysiology of propagation. The quality of the results and the required computation time permit the application of this inverse procedure in a clinical setting.

Electrocardiographic imaging (ECGI) reconstructs the electrical activity of the heart from a dense array of body-surface electrocardiograms and a patient-specific heart-torso geometry. Depending on how it is formulated, ECGI allows the reconstruction of the activation and recovery sequence of the heart, the origin of premature beats or tachycardia, the anchors/hotspots of re-entrant arrhythmias and other electrophysiological quantities of interest. Importantly, these quantities are directly and non-invasively reconstructed in a digitized model of the patient’s three-dimensional heart, which has led to clinical interest in ECGI’s ability to personalize diagnosis and guide therapy. Despite considerable development over the last decades, validation of ECGI is challenging. Firstly, results depend considerably on implementation choices, which are necessary to deal with ECGI’s ill-posed character. Secondly, it is challenging to obtain (invasive) ground truth data of high quality. In this review, we discuss the current status of ECGI validation as well as the major challenges remaining for complete adoption of ECGI in clinical practice. Specifically, showing clinical benefit is essential for the adoption of ECGI. Such benefit may lie in patient outcome improvement, workflow improvement, or cost reduction. Future studies should focus on these aspects to achieve broad adoption of ECGI, but only after the technical challenges have been solved for that specific application/pathology. We propose ‘best’ practices for technical validation and highlight collaborative efforts recently organized in this field. Continued interaction between engineers, basic scientists, and physicians remains essential to find a hybrid between technical achievements, pathological mechanisms insights, and clinical benefit, to evolve this powerful technique toward a useful role in clinical practice.

We present results from a study in which endocardial and epicardial activation sequences, both for ventricular stimulated and for atrioventricular-conducted activation, were reconstructed from (pseudo) body surface potentials. The study consists of 2 parts. In part I, transmural activation mapping was © 2016 American Heart Association, Inc. Original Article Circ Arrhythm ElectrophysiolBackground-Noninvasive imaging of cardiac activation before ablation of the arrhythmogenic substrate can reduce electrophysiological procedure duration and help choosing between an endocardial or epicardial approach. A noninvasive imaging technique was evaluated that estimates both endocardial and epicardial activation from body surface potential maps. We performed a study in isolated and in situ pig hearts, estimating activation from body surface potential maps during sinus rhythm and localizing endocardial and epicardial stimulation sites. Methods and Results-From 3 Langendorff-perfused pig hearts, 180 intramural unipolar electrograms were recorded during sinus rhythm and ectopic activation, together with pseudo-body surface potential map ECGs in 2 of them. From 4 other anesthetized pigs, 64-lead body surface potential maps were recorded during sinus rhythm and ventricular stimulation from 27 endocardial and epicardial sites. The ventricular activation pattern was computed from the recorded QRS complexes. For both Langendorff-perfused hearts, the calculated epicardial and endocardial activation patterns showed good qualitative correspondence to the patterns obtained with needle electrodes. Absolute timing difference for sinus rhythm was 10±5 and 11±8 ms respectively, and for ectopic activation 6±5 and 7±6 ms, respectively. Calculated activation for the in situ hearts in sinus rhythm was similar to patterns recorded in Langendorff-perfused hearts. During stimulation, the distance between the stimulation site and calculated site of earliest activation was 18 (15-27) mm, and 23 of 27 stimulation sites were correctly mapped to either endocardium or epicardium. performed in Langendorff-perfused, isolated pig hearts, while recording pseudo body surface maps (BSMs) from the boundary of a fluid-filled container with integrated electrodes in which the heart was suspended. In part II, BSMs and catheter electrograms were recorded simultaneously in intact pigs. The data from part I were used to adapt our inverse method to porcine electrophysiology and to evaluate it using a simple, homogeneous volume conductor (ie, the fluid-filled container), with transmural activation mapping as a reference. However, BSMs are measured on the surface of the torso, which is irregularly shaped, and contains organs with low conductivity (eg, lungs) and blood with high conductivity. This will affect the current distribution within the thorax and, thereby, the potentials generated at the body surface. Therefore, experiments in intact adult pigs were used to show the ability of our noninvasive mapping technique to reliably determine ventricular activation and dis...

New strict LBBB criteria increase the specificity of complete LBBB diagnosis in the presence of LV hypertrophy/dilatation and incomplete LBBB, which is critical for selecting CRT patients.

Computational modeling in electrocardiography often requires the examination of cardiac forward and inverse problems in order to non-invasively analyze physiological events that are otherwise inaccessible or unethical to explore. The study of these models can be performed in the open-source SCIRun problem solving environment developed at the Center for Integrative Biomedical Computing (CIBC). A new toolkit within SCIRun provides researchers with essential frameworks for constructing and manipulating electrocardiographic forward and inverse models in a highly efficient and interactive way. The toolkit contains sample networks, tutorials and documentation which direct users through SCIRun-specific approaches in the assembly and execution of these specific problems.

This feasibility study of a novel myocardial activation-based ECGI using only the standard 12-lead ECG shows promise to localize the origin of PVC. This ECGI method yields activation estimates of isochrones on both ventricles from which the PVC origin location is derived. This method has the capability to localize the PVC from any part of the ventricular endocardium, intra-myocardium or epicardium.

A method is described to determine the effect on the ECG of a reduced propagation velocity within an ischemic zone. The method was designed to change the activation sequence throughout the ventricles interactively, i.e. with a response time in the order of a second. The timing of ventricular ischemic activation was computed by using the fastest route algorithm, based on locally reduced values of the propagation velocities derived from a standard, normal activation sequence. The effect of these local reductions of the velocities on the total activation sequence, as well as the changes in the electrocardiogram that these produce, are presented.

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