Digital twins enable stratification of persistent atrial fibrillation patients for ablation diminishing unnecessary heart damage.

Pulmonary vein isolation (PVI), the standard-of-care for atrial fibrillation (AF), is effective even in some persistent AF (PsAF) patients despite atrial fibrosis proliferation, suggesting that PVI could not only be isolating triggers but diminishing arrhythmogenic substrates. Left atrial (LA) posterior wall isolation is the prevalent adjunctive strategy aiming to address PsAF arrhythmogenesis, however, its outcomes vary widely. To explore why current PsAF ablation treatments have limited success and under what circumstances each treatment is most effective, we utilized patient-specific heart digital twins of PsAF patients incorporating fibrosis distributions to virtually implement versions of PVI (individual ostial to wide antral) and posterior wall isolation.

Assessing the arrhythmogenic propensity of fibrotic substrate using digital twins to inform a mechanisms-based atrial fibrillation ablation strategy.

Atrial fibrillation (AF), the most common heart rhythm disorder, may cause stroke and heart failure. For patients with persistent AF with fibrosis proliferation, the standard AF treatment-pulmonary vein isolation-has poor outcomes, necessitating redo procedures, owing to insufficient understanding of what constitutes good targets in fibrotic substrates. Here we present a prospective clinical and personalized digital twin study that characterizes the arrhythmogenic properties of persistent AF substrates and uncovers locations possessing rotor-attracting capabilities.

Terminating ventricular tachyarrhythmias using far-field low-voltage stimuli: mechanisms and delivery protocols.

Background: Low-voltage termination of ventricular tachycardia (VT) and atrial fibrillation has shown promising results; however, the mechanisms and full range of applications remain unexplored.

Objectives: To elucidate the mechanisms for low-voltage cardioversion and defibrillation and to develop an optimal low-voltage defibrillation protocol.

Methods: We developed a detailed magnetic resonance imaging-based computational model of the rabbit right ventricular wall.

Integrative computational models of cardiac arrhythmias -- simulating the structurally realistic heart.

Simulation of cardiac electrical function, and specifically, simulation aimed at understanding the mechanisms of cardiac rhythm disorders, represents an example of a successful integrative multiscale modeling approach, uncovering emergent behavior at the successive scales in the hierarchy of structural complexity. The goal of this article is to present a review of the integrative multiscale models of realistic ventricular structure used in the quest to understand and treat ventricular arrhythmias. It concludes with the new advances in image-based modeling of the heart and the promise it holds for the development of individualized models of ventricular function in health and disease.

Mechanistic investigation into the arrhythmogenic role of transmural heterogeneities in regional ischaemia phase 1A.

Aims: Studies of arrhythmogenesis during ischemia have focused primarily on reentrant mechanisms manifested on the epicardial surface. The goal of this study was to use a physiologically-accurate model of acute regional ischemia phase 1A to determine the contribution of ischaemia-induced transmural electrophysiological heterogeneities to arrhythmogenesis following left anterior descending artery occlusion.

Methods And Results: A slice through a geometrical model of the rabbit ventricles was extracted and a model of regional ischaemia developed.

Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia.

Objectives: The purpose of this study is to characterize the changes in vulnerability to electric shocks during phase 1A of global ischemia in the rabbit ventricles and to determine the mechanisms responsible for these changes.

Background: Mechanisms responsible for the changes in cardiac vulnerability over the course of ischemia phase 1A remain poorly understood. The lack of understanding results from the rapid ischemic change in cardiac electrophysiologic properties, which renders experimental evaluation of vulnerability difficult.

Effect of acute global ischemia on the upper limit of vulnerability: a simulation study.

The goal of this modeling research is to provide mechanistic insight into the effect of altered membrane kinetics associated with 5-12 min of acute global ischemia on the upper limit of cardiac vulnerability (ULV) to electric shocks. We simulate electrical activity in a finite-element bidomain model of a 4-mm-thick slice through the canine ventricles that incorporates realistic geometry and fiber architecture. Global acute ischemia is represented by changes in membrane dynamics due to hyperkalemia, acidosis, and hypoxia.