Publications by authors named "Steffen Schuler"

Cardiovascular diseases account for 17 million deaths per year worldwide. Of these, 25% are categorized as sudden cardiac death, which can be related to ventricular tachycardia (VT). This type of arrhythmia can be caused by focal activation sources outside the sinus node.

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Purpose: Atrial fibrillation is one of the most frequent cardiac arrhythmias in the industrialized world and ablation therapy is the method of choice for many patients. However, ablation scars alter the electrophysiological activation and the mechanical behavior of the affected atria. Different ablation strategies with the aim to terminate atrial fibrillation and prevent its recurrence exist but their impact on the performance of the heart is often neglected.

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The ECG is one of the most commonly used non-invasive tools to gain insights into the electrical functioning of the heart. It has been crucial as a foundation in the creation and validation of models describing the underlying electrophysiological processes. However, so far, the contraction of the heart and its influences on the ECG have mainly been overlooked in models.

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Objective: To investigatecardiac activation maps estimated using electrocardiographic imaging and to find methods reducing line-of-block (LoB) artifacts, while preserving real LoBs.

Methods: Body surface potentials were computed for 137 simulated ventricular excitations. Subsequently, the inverse problem was solved to obtain extracellular potentials (EP) and transmembrane voltages (TMV).

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Ventricular coordinates are widely used as a versatile tool for various applications that benefit from a description of local position within the heart. However, the practical usefulness of ventricular coordinates is determined by their ability to meet application-specific requirements. For regression-based estimation of biventricular position, for example, a symmetric definition of coordinate directions in both ventricles is important.

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Large-scale electrophysiological simulations to obtain electrocardiograms (ECG) carry the potential to produce extensive datasets for training of machine learning classifiers to, e.g., discriminate between different cardiac pathologies.

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Background: Hypertrophic cardiomyopathy (HCM) is typically caused by mutations in sarcomeric genes leading to cardiomyocyte disarray, replacement fibrosis, impaired contractility, and elevated filling pressures. These varying tissue properties are associated with certain strain patterns that may allow to establish a diagnosis by means of non-invasive imaging without the necessity of harmful myocardial biopsies or contrast agent application. With a numerical study, we aim to answer: how the variability in each of these mechanisms contributes to altered mechanics of the left ventricle (LV) and if the deformation obtained in in-silico experiments is comparable to values reported from clinical measurements.

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The arrhythmogenesis of atrial fibrillation is associated with the presence of fibrotic atrial tissue. Not only fibrosis but also physiological anatomical variability of the atria and the thorax reflect in altered morphology of the P wave in the 12-lead electrocardiogram (ECG). Distinguishing between the effects on the P wave induced by local atrial substrate changes and those caused by healthy anatomical variations is important to gauge the potential of the 12-lead ECG as a non-invasive and cost-effective tool for the early detection of fibrotic atrial cardiomyopathy to stratify atrial fibrillation propensity.

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Background: Atrial fibrillation (AF) is the most common supraventricular arrhythmia, characterized by disorganized atrial electrical activity, maintained by localized arrhythmogenic atrial drivers. Pulmonary vein isolation (PVI) allows to exclude PV-related drivers. However, PVI is less effective in patients with additional extra-PV arrhythmogenic drivers.

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In both clinical and computational studies, different pacing protocols are used to induce arrhythmia and non-inducibility is often considered as the endpoint of treatment. The need for a standardized methodology is urgent since the choice of the protocol used to induce arrhythmia could lead to contrasting results, e.g.

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Presence of left atrial low voltage substrate in bipolar voltage mapping is associated with increased arrhythmia recurrences following pulmonary vein isolation for atrial fibrillation (AF). Besides local myocardial fibrosis, bipolar voltage amplitudes may be influenced by inter-electrode spacing and bipole-to-wavefront-angle. It is unclear to what extent these impact low voltage areas (LVA) in the clinical setting.

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Objective: Atrial flutter (AFl) is a common arrhythmia that can be categorized according to different self-sustained electrophysiological mechanisms. The non-invasive discrimination of such mechanisms would greatly benefit ablative methods for AFl therapy as the driving mechanisms would be described prior to the invasive procedure, helping to guide ablation. In the present work, we sought to implement recurrence quantification analysis (RQA) on 12-lead ECG signals from a computational framework to discriminate different electrophysiological mechanisms sustaining AFl.

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The solution of the inverse problem of electrocardiology allows the reconstruction of the spatial distribution of the electrical activity of the heart from the body surface electrocardiogram (electrocardiographic imaging, ECGI). ECGI using the equivalent dipole layer (EDL) model has shown to be accurate for cardiac activation times. However, validation of this method to determine repolarization times is lacking.

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Activation times (AT) describe the sequence of cardiac depolarization and represent one of the most important parameters for analysis of cardiac electrical activity. However, estimation of ATs can be challenging due to multiple sources of noise such as fractionation or baseline wander. If ATs are estimated from signals reconstructed using electrocardiographic imaging (ECGI), additional problems can arise from over-smoothing or due to ambiguities in the inverse problem.

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ECG imaging estimates the cardiac electrical activity from body surface potentials. As this involves solving a severly ill-posed problem, additional information is required to get a unique and stable solution. Recent progress is based on introducing more problem-specific information by exploiting the structure of cardiac excitation.

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Electrocardiographic Imaging (ECGI) requires robust ECG forward simulations to accurately calculate cardiac activity. However, many questions remain regarding ECG forward simulations, for instance: there are not common guidelines for the required cardiac source sampling. In this study we test equivalent double layer (EDL) forward simulations with differing cardiac source resolutions and different spatial interpolation techniques.

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Electrocardiographic imaging (ECGI) strongly relies on a priori assumptions and additional information to overcome ill-posedness. The major challenge of obtaining good reconstructions consists in finding ways to add information that effectively restricts the solution space without violating properties of the sought solution. In this work, we attempt to address this problem by constructing a spatio-temporal basis of body surface potentials (BSP) from simulations of many focal excitations.

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Radiofrequency ablation (RFA) therapy is the gold standard in interventional treatment of many cardiac arrhythmias. A major obstacle is nontransmural lesions, leading to recurrence of arrhythmias. Recent clinical studies have suggested intracardiac electrogram (EGM) criteria as a promising marker to evaluate lesion development.

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Intracardiac electrograms are the key in understanding, interpretation and treatment of cardiac arrhythmias. However, electrogram morphologies are strongly variable due to catheter position, orientation and contact. Simulations of intracardiac electrograms can improve comprehension and quantification of influencing parameters and therefore reduce misinterpretations.

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