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OBJECTIVE: This study aims to assess the sensitivity of epicardial potential-based electrocardiographic imaging (ECGI) to the removal or interpolation of bad leads. Approach. We utilized experimental data from two distinct centers. Langendorff-perfused pig (n=2) and dog (n=2) hearts were suspended in a human torso-shaped tank and paced from the ventricles. Six different bad lead configurations were designed based on clinical experience. Five interpolation methods were applied to estimate the missing data. Zero-order Tikhonov regularization was used to solve the inverse problem for complete data, data with removed bad leads, and interpolated data. We assessed the quality of interpolated ECG signals and ECGI reconstructions using several metrics, comparing the performance of interpolation methods and the impact of bad lead removal versus interpolation on ECGI. Main results. The performance of ECG interpolation strongly correlated with ECGI reconstruction. The hybrid method exhibited the best performance among interpolation techniques, followed closely by the inverse-forward and Kriging methods. Bad leads located over high amplitude/high gradient areas on the torso significantly impacted ECGI reconstructions, even with minor interpolation errors. The choice between removing or interpolating bad leads depends on the location of missing leads and confidence in interpolation performance. If uncertainty exists, removing bad leads is the safer option, particularly when they are positioned in high amplitude/high gradient regions. In instances where interpolation is necessary, the inverse-forward and Kriging methods, which do not require training, are recommended. Significance. This study represents the first comprehensive evaluation of the advantages and drawbacks of interpolating versus removing bad leads in the context of ECGI, providing valuable insights into ECGI performance.
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BACKGROUND: The immediate impact of catheter ablation on left atrial mechanical function and the timeline for its recovery in patients undergoing ablation for atrial fibrillation (AF) remain uncertain. The mechanical function response to catheter ablation in patients with different AF types is poorly understood. METHODS: A total of 113 AF patients were included in this retrospective study. Each patient had three magnetic resonance imaging (MRI) studies in sinus rhythm: one pre-ablation, one immediate post-ablation (within 2 days after ablation), and one post-ablation follow-up MRI (≤ 3 months). We used feature tracking in the MRI cine images to determine peak longitudinal atrial strain (PLAS). We evaluated the change in strain from pre-ablation, immediately after ablation to post-ablation follow-up in a short-term study (< 50 days) and a 3-month study (3 months after ablation). RESULTS: The PLAS exhibited a notable reduction immediately after ablation, compared to both pre-ablation levels and those observed in follow-up studies conducted at short-term (11.1 ± 9.0 days) and 3-month (69.6 ± 39.6 days) intervals. However, there was no difference between follow-up and pre-ablation PLAS. The PLAS returned to 95% pre-ablation level within 10 days. Paroxysmal AF patients had significantly higher pre-ablation PLAS than persistent AF patients in pre-ablation MRIs. Both type AF patients had significantly lower immediate post-ablation PLAS compared with pre-ablation and post-ablation PLAS. CONCLUSION: The present study suggested a significant drop in PLAS immediately after ablation. Left atrial mechanical function recovered within 10 days after ablation. The drop in PLAS did not show a substantial difference between paroxysmal and persistent AF patients.
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Atrial fibrillation (AF) is the most common cardiac arrhythmia and is sustained by spontaneous focal excitations and re-entry. Spontaneous electrical firing in the pulmonary vein (PV) sleeves is implicated in AF generation. The aim of this simulation study was to identify the mechanisms determining the localisation of AF triggers in the PVs and their contribution to the genesis of AF. A novel biophysical model of the canine atria was used that integrates stochastic, spontaneous subcellular Ca2+ release events (SCRE) with regional electrophysiological heterogeneity in ionic properties and a detailed three-dimensional model of atrial anatomy, microarchitecture and patchy fibrosis. Simulations highlighted the importance of the smaller inward rectifier potassium current (IK1 ) in PV cells compared to the surrounding atria, which enabled SCRE more readily to result in delayed-afterdepolarisations that induced triggered activity. There was a leftward shift in the dependence of the probability of triggered activity on sarcoplasmic reticulum Ca2+ load. This feature was accentuated in 3D tissue compared to single cells (Δ half-maximal [Ca2+ ]SR = 58 µM vs. 22 µM). In 3D atria incorporating electrical heterogeneity, excitations preferentially emerged from the PV region. These triggered focal excitations resulted in transient re-entry in the left atrium. Addition of fibrotic patches promoted localised emergence of focal excitations and wavebreaks that had a more substantial impact on generating AF-like patterns than the PVs. Thus, a reduced IK1 , less negative resting membrane potential, and fibrosis-induced changes of the electrotonic load all contribute to the emergence of complex excitation patterns from spontaneous focal triggers. KEY POINTS: Focal excitations in the atria are most commonly associated with the pulmonary veins, but the mechanisms for this localisation are yet to be elucidated. We applied a multi-scale computational modelling approach to elucidate the mechanisms underlying such localisations. Myocytes in the pulmonary vein region of the atria have a less negative resting membrane potential and reduced time-independent potassium current; we demonstrate that both of these factors promote triggered activity in single cells and tissues. The less negative resting membrane potential also contributes to heterogeneous inactivation of the fast sodium current, which can enable re-entrant-like excitation patterns to emerge without traditional conduction block.
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Fibrilação Atrial , Veias Pulmonares , Animais , Cães , Fibrilação Atrial/etiologia , Cálcio , Átrios do Coração , Cálcio da Dieta , Potenciais de Ação , Fibrose , PotássioRESUMO
Central to the clinical adoption of patient-specific modeling strategies is demonstrating that simulation results are reliable and safe. Indeed, simulation frameworks must be robust to uncertainty in model input(s), and levels of confidence should accompany results. In this study, we applied a coupled uncertainty quantification-finite element (FE) framework to understand the impact of uncertainty in vascular material properties on variability in predicted stresses. Univariate probability distributions were fit to material parameters derived from layer-specific mechanical behavior testing of human coronary tissue. Parameters were assumed to be probabilistically independent, allowing for efficient parameter ensemble sampling. In an idealized coronary artery geometry, a forward FE model for each parameter ensemble was created to predict tissue stresses under physiologic loading. An emulator was constructed within the UncertainSCI software using polynomial chaos techniques, and statistics and sensitivities were directly computed. Results demonstrated that material parameter uncertainty propagates to variability in predicted stresses across the vessel wall, with the largest dispersions in stress within the adventitial layer. Variability in stress was most sensitive to uncertainties in the anisotropic component of the strain energy function. Moreover, unary and binary interactions within the adventitial layer were the main contributors to stress variance, and the leading factor in stress variability was uncertainty in the stress-like material parameter that describes the contribution of the embedded fibers to the overall artery stiffness. Results from a patient-specific coronary model confirmed many of these findings. Collectively, these data highlight the impact of material property variation on uncertainty in predicted artery stresses and present a pipeline to explore and characterize forward model uncertainty in computational biomechanics.
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Central to the clinical adoption of patient-specific modeling strategies is demonstrating that simulation results are reliable and safe. Indeed, simulation frameworks must be robust to uncertainty in model input(s), and levels of confidence should accompany results. In this study, we applied a coupled uncertainty quantification-finite element (FE) framework to understand the impact of uncertainty in vascular material properties on variability in predicted stresses. Univariate probability distributions were fit to material parameters derived from layer-specific mechanical behavior testing of human coronary tissue. Parameters were assumed to be probabilistically independent, allowing for efficient parameter ensemble sampling. In an idealized coronary artery geometry, a forward FE model for each parameter ensemble was created to predict tissue stresses under physiologic loading. An emulator was constructed within the UncertainSCI software using polynomial chaos techniques, and statistics and sensitivities were directly computed. Results demonstrated that material parameter uncertainty propagates to variability in predicted stresses across the vessel wall, with the largest dispersions in stress within the adventitial layer. Variability in stress was most sensitive to uncertainties in the anisotropic component of the strain energy function. Moreover, unary and binary interactions within the adventitial layer were the main contributors to stress variance, and the leading factor in stress variability was uncertainty in the stress-like material parameter that describes the contribution of the embedded fibers to the overall artery stiffness. Results from a patient-specific coronary model confirmed many of these findings. Collectively, these data highlight the impact of material property variation on uncertainty in predicted artery stresses and present a pipeline to explore and characterize forward model uncertainty in computational biomechanics.
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Vasos Coronários , Análise de Elementos Finitos , Estresse Mecânico , Humanos , Vasos Coronários/fisiologia , Incerteza , Fenômenos Biomecânicos , Modelos Cardiovasculares , Simulação por Computador , AnisotropiaRESUMO
Objective.Electrocardiographic imaging (ECGI) is a functional imaging modality that consists of two related problems, the forward problem of reconstructing body surface electrical signals given cardiac bioelectric activity, and the inverse problem of reconstructing cardiac bioelectric activity given measured body surface signals. ECGI relies on a model for how the heart generates bioelectric signals which is subject to variability in inputs. The study of how uncertainty in model inputs affects the model output is known as uncertainty quantification (UQ). This study establishes develops, and characterizes the application of UQ to ECGI.Approach.We establish two formulations for applying UQ to ECGI: a polynomial chaos expansion (PCE) based parametric UQ formulation (PCE-UQ formulation), and a novel UQ-aware inverse formulation which leverages our previously established 'joint-inverse' formulation (UQ joint-inverse formulation). We apply these to evaluate the effect of uncertainty in the heart position on the ECGI solutions across a range of ECGI datasets.Main results.We demonstrated the ability of our UQ-ECGI formulations to characterize the effect of parameter uncertainty on the ECGI inverse problem. We found that while the PCE-UQ inverse solution provided more complex outputs such as sensitivities and standard deviation, the UQ joint-inverse solution provided a more interpretable output in the form of a single ECGI solution. We find that between these two methods we are able to assess a wide range of effects that heart position variability has on the ECGI solution.Significance.This study, for the first time, characterizes in detail the application of UQ to the ECGI inverse problem. We demonstrated how UQ can provide insight into the behavior of ECGI using variability in cardiac position as a test case. This study lays the groundwork for future development of UQ-ECGI studies, as well as future development of ECGI formulations which are robust to input parameter variability.
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Artificial intelligence - machine learning (AI-ML) is a computational technique that has been demonstrated to be able to extract meaningful clinical information from diagnostic data that are not available using either human interpretation or more simple analysis methods. Recent developments have shown that AI-ML approaches applied to ECGs can accurately predict different patient characteristics and pathologies not detectable by expert physician readers. There is an extensive body of literature surrounding the use of AI-ML in other fields, which has given rise to an array of predefined open-source AI-ML architectures which can be translated to new problems in an "off-the-shelf" manner. Applying "off-the-shelf" AI-ML architectures to ECG-based datasets opens the door for rapid development and identification of previously unknown disease biomarkers. Despite the excellent opportunity, the ideal open-source AI-ML architecture for ECG related problems is not known. Furthermore, there has been limited investigation on how and when these AI-ML approaches fail and possible bias or disparities associated with particular network architectures. In this study, we aimed to: (1) determine if open-source, "off-the-shelf" AI-ML architectures could be trained to classify low LVEF from ECGs, (2) assess the accuracy of different AI-ML architectures compared to each other, and (3) to identify which, if any, patient characteristics are associated with poor AI-ML performance.
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Introduction: Premature ventricular contractions (PVCs) are one of the most commonly targeted pathologies for ECGI validation, often through ventricular stimulation to mimic the ectopic beat. However, it remains unclear if such stimulated beats faithfully reproduce spontaneously occurring PVCs, particularly in the case of the R-on-T phenomenon. The objective of this study was to determine the differences in ECGI accuracy when reconstructing spontaneous PVCs as compared to ventricular-stimulated beats and to explore the impact of pathophysiological perturbation on this reconstruction accuracy. Methods: Langendorff-perfused pig hearts (n = 3) were suspended in a human torso-shaped tank, and local hyperkalemia was induced through perfusion of a high-K+ solution (8 mM) into the LAD. Recordings were taken simultaneously from the heart and tank surfaces during ventricular pacing and during spontaneous PVCs (including R-on-T), both at baseline and high K+. Epicardial potentials were reconstructed from torso potentials using ECGI. Results: Spontaneously occurring PVCs were better reconstructed than stimulated beats at baseline in terms of electrogram morphology [correlation coefficient (CC) = 0.74 ± 0.05 vs. CC = 0.60 ± 0.10], potential maps (CC = 0.61 ± 0.06 vs. CC = 0.51 ± 0.12), and activation time maps (CC = 0.86 ± 0.07 vs. 0.76 ± 0.10), though there was no difference in the localization error (LE) of epicardial origin (LE = 14 ± 6 vs. 15 ± 11 mm). High K+ perfusion reduced the accuracy of ECGI reconstructions in terms of electrogram morphology (CC = 0.68 ± 0.10) and AT maps (CC = 0.70 ± 0.12 and 0.59 ± 0.23) for isolated PVCs and paced beats, respectively. LE trended worse, but the change was not significant (LE = 17 ± 9 and 20 ± 12 mm). Spontaneous PVCs were less well when the R-on-T phenomenon occurred and the activation wavefronts encountered a line of block. Conclusion: This study demonstrates the differences in ECGI accuracy between spontaneous PVCs and ventricular-paced beats. We also observed a reduction in this accuracy near regions of electrically inactive tissue. These results highlight the need for more physiologically realistic experimental models when evaluating the accuracy of ECGI methods. In particular, reconstruction accuracy needs to be further evaluated in the presence of R-on-T or isolated PVCs, particularly when encountering obstacles (functional or anatomical) which cause line of block and re-entry.
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The study of cardiac electrophysiology is built on experimental models that span all scales, from ion channels to whole-body preparations. Novel discoveries made at each scale have contributed to our fundamental understanding of human cardiac electrophysiology, which informs clinicians as they detect, diagnose, and treat complex cardiac pathologies. This expert review describes an engineering approach to developing experimental models that is applicable across scales. The review also outlines how we applied the approach to create a set of multiscale whole-body experimental models of cardiac electrophysiology, models that are driving new insights into the response of the myocardium to acute ischemia. Specifically, we propose that researchers must address three critical requirements to develop an effective experimental model: 1) how the experimental model replicates and maintains human physiological conditions, 2) how the interventions possible with the experimental model capture human pathophysiology, and 3) what signals need to be measured, at which levels of resolution and fidelity, and what are the resulting requirements of the measurement system and the access to the organs of interest. We will discuss these requirements in the context of two examples of whole-body experimental models, a closed chest in situ model of cardiac ischemia and an isolated-heart, torso-tank preparation, both of which we have developed over decades and used to gather valuable insights from hundreds of experiments.
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BACKGROUND: The role of fiber orientation on a global chamber level in sustaining atrial fibrillation (AF) is unknown. The goal of this study was to correlate the fiber direction derived from Diffusion Tensor Imaging (DTI) with AF inducibility. METHODS: Transgenic goats with cardiac-specific overexpression of constitutively active TGF-ß1 (n = 14) underwent AF inducibility testing by rapid pacing in the left atrium. We chose a minimum of 10 minutes of sustained AF as a cut-off for AF inducibility. Explanted hearts underwent DTI to determine the fiber direction. Using tractography data, we clustered, visualized, and quantified the fiber helix angles in 8 different regions of the left atrial wall using two reference vectors defined based on anatomical landmarks. RESULTS: Sustained AF was induced in 7 out of 14 goats. The mean helix fiber angles in 7 out of 8 selected regions were statistically different (P-Value < 0.05) in the AF inducible group. The average fractional anisotropy (FA) and the mean diffusivity (MD) were similar in the two groups with FA of 0.32±0.08 and MD of 8.54±1.72 mm2/s in the non-inducible group and FA of 0.31±0.05 (P-value = 0.90) and MD of 8.68±1.60 mm2/s (P-value = 0.88) in the inducible group. CONCLUSIONS: DTI based fiber direction shows significant variability across subjects with a significant difference between animals that are AF inducible versus animals that are not inducible. Fiber direction might be contributing to the initiation and sustaining of AF, and its role needs to be investigated further.
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Fibrilação Atrial , Animais , Fibrilação Atrial/diagnóstico por imagem , Imagem de Tensor de Difusão , Átrios do Coração/diagnóstico por imagem , Animais Geneticamente Modificados , CabrasRESUMO
BACKGROUND: Computational biomedical simulations frequently contain parameters that model physical features, material coefficients, and physiological effects, whose values are typically assumed known a priori. Understanding the effect of variability in those assumed values is currently a topic of great interest. A general-purpose software tool that quantifies how variation in these parameters affects model outputs is not broadly available in biomedicine. For this reason, we developed the 'UncertainSCI' uncertainty quantification software suite to facilitate analysis of uncertainty due to parametric variability. METHODS: We developed and distributed a new open-source Python-based software tool, UncertainSCI, which employs advanced parameter sampling techniques to build polynomial chaos (PC) emulators that can be used to predict model outputs for general parameter values. Uncertainty of model outputs is studied by modeling parameters as random variables, and model output statistics and sensitivities are then easily computed from the emulator. Our approaches utilize modern, near-optimal techniques for sampling and PC construction based on weighted Fekete points constructed by subsampling from a suitably randomized candidate set. RESULTS: Concentrating on two test cases-modeling bioelectric potentials in the heart and electric stimulation in the brain-we illustrate the use of UncertainSCI to estimate variability, statistics, and sensitivities associated with multiple parameters in these models. CONCLUSION: UncertainSCI is a powerful yet lightweight tool enabling sophisticated probing of parametric variability and uncertainty in biomedical simulations. Its non-intrusive pipeline allows users to leverage existing software libraries and suites to accurately ascertain parametric uncertainty in a variety of applications.
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Coração , Software , Incerteza , Simulação por Computador , BioengenhariaRESUMO
Computational models have made it possible to study the effect of fibrosis and scar on atrial fibrillation (AF) and plan future personalized treatments. Here, we study the effect of area available for fibrillatory waves to sustain AF. Then we use it to plan for AF ablation to improve procedural outcomes. CARPentry was used to create patient-specific models to determine the association between the size of residual contiguous areas available for AF wavefronts to propagate and sustain AF [fibrillatory area (FA)] after ablation with procedural outcomes. The FA was quantified in a novel manner accounting for gaps in ablation lines. We selected 30 persistent AF patients with known ablation outcomes. We divided the atrial surface into five areas based on ablation scar pattern and anatomical landmarks and calculated the FAs. We validated the models based on clinical outcomes and suggested future ablation lines that minimize the FAs and terminate rotor activities in simulations. We also simulated the effects of three common antiarrhythmic drugs. In the patient-specific models, the predicted arrhythmias matched the clinical outcomes in 25 of 30 patients (accuracy 83.33%). The average largest FA (FAmax) in the recurrence group was 8517 ± 1444 vs. 6772 ± 1531 mm2 in the no recurrence group (p < 0.004). The final FAs after adding the suggested ablation lines in the AF recurrence group reduced the average FAmax from 8517 ± 1444 to 6168 ± 1358 mm2 (p < 0.001) and stopped the sustained rotor activity. Simulations also correctly anticipated the effect of antiarrhythmic drugs in 5 out of 6 patients who used drug therapy post unsuccessful ablation (accuracy 83.33%). Sizes of FAs available for AF wavefronts to propagate are important determinants for ablation outcomes. FA size in combination with computational simulations can be used to direct ablation in persistent AF to minimize the critical mass required to sustain recurrent AF.
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Fibrilação Atrial , Ablação por Cateter , Humanos , Fibrilação Atrial/cirurgia , Antiarrítmicos/uso terapêutico , Cicatriz , Resultado do Tratamento , Átrios do CoraçãoRESUMO
Deep neural networks have shown promise in image reconstruction tasks, although often on the premise of large amounts of training data. In this paper, we present a new approach to exploit the geometry and physics underlying electrocardiographic imaging (ECGI) to learn efficiently with a relatively small dataset. We first introduce a non-Euclidean encoding-decoding network that allows us to describe the unknown and measurement variables over their respective geometrical domains. We then explicitly model the geometry-dependent physics in between the two domains via a bipartite graph over their graphical embeddings. We applied the resulting network to reconstruct electrical activity on the heart surface from body-surface potentials. In a series of generalization tasks with increasing difficulty, we demonstrated the improved ability of the network to generalize across geometrical changes underlying the data using less than 10% of training data and fewer variations of training geometry in comparison to its Euclidean alternatives. In both simulation and real-data experiments, we further demonstrated its ability to be quickly fine-tuned to new geometry using a modest amount of data.
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Coração , Redes Neurais de Computação , Simulação por Computador , Eletrocardiografia/métodos , Processamento de Imagem Assistida por Computador/métodosRESUMO
Predictive models and simulations of cardiac function require accurate representations of anatomy, often to the scale of local myocardial fiber structure. However, acquiring this information in a patient-specific manner is challenging. Moreover, the impact of physiological variability in fiber orientation on simulations of cardiac activation is poorly understood. To explore these effects, we implemented bi-ventricular activation simulations using rule-based fiber algorithms and robust uncertainty quantification techniques to generate detailed maps of model variability. Specifically, we utilized polynomial chaos expansion, enabling efficient exploration with reduced computational demand through an emulator function approximating the underlying forward model. Our study focused on examining the epicardial activation sequences of the heart in response to six stimuli locations and five metrics of activation. Our findings revealed that physiological variability in fiber orientation does not significantly affect the location of activation features, but it does impact the overall spread of activation. We observed low variability near the earliest activation sites, but high variability across the rest of the epicardial surface. We conclude that the level of accuracy of myocardial fiber orientation required for simulation depends on the specific goals of the model and the related research or clinical goals.
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Ventricular tachycardia (VT) is a life-threatening cardiac arrhythmia for which a common treatment pathway is electroanatomical mapping and ablation. Recent advances in both noninvasive ablation techniques and computational modeling have motivated the development of patient-specific computational models of VT. Such models are parameterized by a wide range of inputs, each of which is associated with an often unknown amount of error and uncertainty. Uncertainty quantification (UQ) is a technique to assess how variability in the inputs to a model affects its outputs. UQ has seen increased attention in computational cardiology as an avenue to further improve, understand, and develop patient-specific models. In this study we applied polynomial chaos-based UQ to explore the effect of varying the tissue conductivity of fibrotic border zones in a patient-specific model on the resulting VT simulation. We found that over a range of inputs, the model was most sensitive to fibrotic sheet direction, and uncertainty in fibrotic conductivity resulted in substantial variability in the VT reentry duration and cycle length. Overall, this study paves the way for future UQ applications to improve and understand VT models.
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The 12-lead electrocardiogram (ECG) is the most common front-line diagnosis tool for assessing cardiovascular health, yet traditional ECG analysis cannot detect many diseases. Machine learning (ML) techniques have emerged as a powerful set of techniques for producing automated and robust ECG analysis tools that can often predict diseases and conditions not detectable by traditional ECG analysis. Many contemporary ECG-ML studies have focused on utilizing the full 12-lead ECG; however, with the increased availability of single-lead ECG data from wearable devices, there is a clear motivation to explore the development of single-lead ECG-ML techniques. In this study we developed and applied a deep learning architecture for the detection of low left ventricular ejection fraction (LVEF), and compared the performance of this architecture when it was trained with individual leads of the 12-lead ECG to the performance when trained using the entire 12-lead ECG. We observed that single-lead-trained networks performed similarly to the full 12-lead-trained network. We also noted patterns of agreement and disagreement between network low LVEF predictions across the different lead-trained networks.
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Individual variability in parameter settings, due to either user selection or disease states, can impact accuracy when simulating the electrical behavior of the heart. Here, we aim to test the impact of inevitable uncertainty in conduction velocities (CVs) on the output of simulations of cardiac propagation, given three stimulus locations on the left ventricular (LV) free wall. To understand the role of physiological variability in CV in simulations of cardiac activation, we generated detailed maps of the variability in propagation simulations by implementing bi-ventricular activation simulations and quantified the effects by deploying robust uncertainty quantification techniques based on polynomial chaos expansion (PCE). PCE allows efficient stochastic exploration with reduced computational demand by utilizing an emulator for the underlying forward model. Our results suggest that CV within healthy physiological ranges plays a small role in the activation times across all stimulation locations. However, we noticed differences in variation coefficients depending on the stimulation site, i.e., LV endocardium, midmyocardium, and epicardium. We observed low levels of variation in activation times near the earliest activation sites, whereas there was higher variation toward the termination sites. These results suggest that CV variability can play a role when simulating healthy and diseased states.
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Patients with drug-refractory ventricular tachycardia (VT) often undergo implantation of a cardiac defibrillator (ICD). While life-saving, shock from an ICD can be traumatic. To combat the need for defibrillation, ICDs come equipped with low-energy pacing protocols. These anti-tachycardia pacing (ATP) methods are conventionally delivered from a lead inserted at the apex of the right ventricle (RV) with limited success. Recent studies have shown the promise of biventricular leads placed in the left ventricle (LV) for ATP delivery. This study tested the hypothesis that stimulating ATP from multiple biventricular locations will improve termination rates in a patient-specific computational model. VT was first induced in the model, followed by ATP delivery from 1-4 biventricular stimulus sites. We found that combining stimulation sites does not alter termination success so long as a critical stimulus site is included. Combining the RV stimulus site with any combination of LV sites did not affect ATP success except for one case. Including the RV site may allow biventricular ATP to be a robust approach across different scar distributions without affecting the efficacy of other stimulation sites. Combining sites may increase the likelihood of including a critical stimulus site when such information cannot be ascertained.
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Atypical atrial flutter is seen post-ablation in patients, and it can be challenging to map. These flutters are typically set up around areas of scar in the left atrium. MRI can reliably identify left atrial scar. We propose a personalized computational model using patient specific scar information, to generate a monodomain model. In the model conductivities are adjusted for different tissue regions and flutter was induced with a premature pacing protocol. The model was tested prospectively in patients undergoing atypical flutter ablation. The simulation-predicted flutters were visualized and presented to clinicians. Validation of the computational model was motivated by recording from electroanatomical mapping. These personalized models successfully predicted clinically observed atypical flutter circuits and at times even better than invasive maps leading to flutter termination at isthmus sites predicted by the model.
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Introduction: Myriad disorders cause right ventricular (RV) dilation and lead to tricuspid regurgitation (TR). Because the thin-walled, flexible RV is mechanically coupled to the pulmonary circulation and the left ventricular septum, it distorts with any disturbance in the cardiopulmonary system. TR, therefore, can result from pulmonary hypertension, left heart failure, or intrinsic RV dysfunction; but once it occurs, TR initiates a cycle of worsening RV volume overload, potentially progressing to right heart failure. Characteristic three-dimensional RV shape-changes from this process, and changes particular to individual TR causes, have not been defined in detail. Methods: Cardiac MRI was obtained in 6 healthy volunteers, 41 patients with ≥ moderate TR, and 31 control patients with cardiac disease without TR. The mean shape of each group was constructed using a three-dimensional statistical shape model via the particle-based shape modeling approach. Changes in shape were examined across pulmonary hypertension and congestive heart failure subgroups using principal component analysis (PCA). A logistic regression approach based on these PCA modes identified patients with TR using RV shape alone. Results: Mean RV shape in patients with TR exhibited free wall bulging, narrowing of the base, and blunting of the RV apex compared to controls (p < 0.05). Using four primary PCA modes, a logistic regression algorithm identified patients with TR correctly with 82% recall and 87% precision. In patients with pulmonary hypertension without TR, RV shape was narrower and more streamlined than in healthy volunteers. However, in RVs with TR and pulmonary hypertension, overall RV shape continued to demonstrate the free wall bulging characteristic of TR. In the subgroup of patients with congestive heart failure without TR, this intermediate state of RV muscular hypertrophy was not present. Conclusion: The multiple causes of TR examined in this study changed RV shape in similar ways. Logistic regression classification based on these shape changes reliably identified patients with TR regardless of etiology. Furthermore, pulmonary hypertension without TR had unique shape features, described here as the "well compensated" RV. These results suggest shape modeling as a promising tool for defining severity of RV disease and risk of decompensation, particularly in patients with pulmonary hypertension.