Ventricular fibrillation: combined myocardial substrate and Purkinje ablation

Taggart, Peter; Nash, Martyn P.; Lambiase, Pier D.

doi:10.1093/eurheartj/ehab912

Cited by 5 publications

(4 citation statements)

References 23 publications

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“…There are some limitations to our clinical VF data. Firstly, ECGI has not been validated for VF and may not fully capture the complexity of epicardial wavefronts in VF [ 46 ]. Additionally, as the subjects were undergoing defibrillation testing, our analysis was limited to the first few seconds of VF.…”

Section: Discussionmentioning

confidence: 99%

Information theory-based direct causality measure to assess cardiac fibrillation dynamics

Shi,

Sau,

et al. 2023

J. R. Soc. Interface.

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Understanding the mechanism sustaining cardiac fibrillation can facilitate the personalization of treatment. Granger causality analysis can be used to determine the existence of a hierarchical fibrillation mechanism that is more amenable to ablation treatment in cardiac time-series data. Conventional Granger causality based on linear predictability may fail if the assumption is not met or given sparsely sampled, high-dimensional data. More recently developed information theory-based causality measures could potentially provide a more accurate estimate of the nonlinear coupling. However, despite their successful application to linear and nonlinear physical systems, their use is not known in the clinical field. Partial mutual information from mixed embedding (PMIME) was implemented to identify the direct coupling of cardiac electrophysiology signals. We show that PMIME requires less data and is more robust to extrinsic confounding factors. The algorithms were then extended for efficient characterization of fibrillation organization and hierarchy using clinical high-dimensional data. We show that PMIME network measures correlate well with the spatio-temporal organization of fibrillation and demonstrated that hierarchical type of fibrillation and drivers could be identified in a subset of ventricular fibrillation patients, such that regions of high hierarchy are associated with high dominant frequency.

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Section: Discussionmentioning

confidence: 99%

Information theory-based direct causality measure to assess cardiac fibrillation dynamics

Shi,

Sau,

et al. 2023

J. R. Soc. Interface.

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“…Theoretical reconstructions remain useful in predicting physiological end effects ( Alrabghi et al, 2023 ; Hancox et al, 2023 ). Ultimate translatability of such results still requires direct human clinical electrophysiological studies with recently innovated electrocardiographic ( Van Der Werf and Lambiase, 2021 ) and electrical mapping capacities ( Taggart et al, 2022 ).…”

Section: A Hierarchy Of Mechanisms For Ion Channel Modificationmentioning

confidence: 99%

Cardiac arrhythmogenesis: roles of ion channels and their functional modification

Lei,

Salvage,

Jackson

et al. 2024

Front. Physiol.

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Cardiac arrhythmias cause significant morbidity and mortality and pose a major public health problem. They arise from disruptions in the normally orderly propagation of cardiac electrophysiological activation and recovery through successive cardiomyocytes in the heart. They reflect abnormalities in automaticity, initiation, conduction, or recovery in cardiomyocyte excitation. The latter properties are dependent on surface membrane electrophysiological mechanisms underlying the cardiac action potential. Their disruption results from spatial or temporal instabilities and heterogeneities in the generation and propagation of cellular excitation. These arise from abnormal function in their underlying surface membrane, ion channels, and transporters, as well as the interactions between them. The latter, in turn, form common regulatory targets for the hierarchical network of diverse signaling mechanisms reviewed here. In addition to direct molecular-level pharmacological or physiological actions on these surface membrane biomolecules, accessory, adhesion, signal transduction, and cytoskeletal anchoring proteins modify both their properties and localization. At the cellular level of excitation–contraction coupling processes, Ca2+ homeostatic and phosphorylation processes affect channel activity and membrane excitability directly or through intermediate signaling. Systems-level autonomic cellular signaling exerts both acute channel and longer-term actions on channel expression. Further upstream intermediaries from metabolic changes modulate the channels both themselves and through modifying Ca2+ homeostasis. Finally, longer-term organ-level inflammatory and structural changes, such as fibrotic and hypertrophic remodeling, similarly can influence all these physiological processes with potential pro-arrhythmic consequences. These normal physiological processes may target either individual or groups of ionic channel species and alter with particular pathological conditions. They are also potentially alterable by direct pharmacological action, or effects on longer-term targets modifying protein or cofactor structure, expression, or localization. Their participating specific biomolecules, often clarified in experimental genetically modified models, thus constitute potential therapeutic targets. The insights clarified by the physiological and pharmacological framework outlined here provide a basis for a recent modernized drug classification. Together, they offer a translational framework for current drug understanding. This would facilitate future mechanistically directed therapeutic advances, for which a number of examples are considered here. The latter are potentially useful for treating cardiac, in particular arrhythmic, disease.

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“…Advances in mapping electrical activity in whole human hearts hold enormous promise for a greater understanding of arrhythmias in a clinical setting [ 115 ]. Recent work highlights the importance of rotors and wavelets of electrical activity in ventricular fibrillation [ 116 , 117 ] and considers the involvement of the Purkinje fibre network [ 118 , 119 ].…”

Section: The Role Of the Sarcoplasmic Reticulum In The Generation Of ...mentioning

confidence: 99%

Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal Ca²⁺

Terrar

2023

Phil. Trans. R. Soc. B

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Rhythms of electrical activity in all regions of the heart can be influenced by a variety of intracellular membrane bound organelles. This is true both for normal pacemaker activity and for abnormal rhythms including those caused by early and delayed afterdepolarizations under pathological conditions. The influence of the sarcoplasmic reticulum (SR) on cardiac electrical activity is widely recognized, but other intracellular organelles including lysosomes and mitochondria also contribute. Intracellular organelles can provide a timing mechanism (such as an SR clock driven by cyclic uptake and release of Ca 2+ , with an important influence of intraluminal Ca 2+ ), and/or can act as a Ca 2+ store involved in signalling mechanisms. Ca 2+ plays many diverse roles including carrying electric current, driving electrogenic sodium–calcium exchange (NCX) particularly when Ca 2+ is extruded across the surface membrane causing depolarization, and activation of enzymes which target organelles and surface membrane proteins. Heart function is also influenced by Ca 2+ mobilizing agents (cADP-ribose, nicotinic acid adenine dinucleotide phosphate and inositol trisphosphate) acting on intracellular organelles. Lysosomal Ca 2+ release exerts its effects via calcium/calmodulin-dependent protein kinase II to promote SR Ca 2+ uptake, and contributes to arrhythmias resulting from excessive beta-adrenoceptor stimulation. A separate arrhythmogenic mechanism involves lysosomes, mitochondria and SR. Interacting intracellular organelles, therefore, have profound effects on heart rhythms and NCX plays a central role. This article is part of the theme issue ‘The heartbeat: its molecular basis and physiological mechanisms’.

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Ventricular fibrillation: combined myocardial substrate and Purkinje ablation

Cited by 5 publications

References 23 publications

Information theory-based direct causality measure to assess cardiac fibrillation dynamics

Information theory-based direct causality measure to assess cardiac fibrillation dynamics

Cardiac arrhythmogenesis: roles of ion channels and their functional modification

Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal Ca²⁺

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Ventricular fibrillation: combined myocardial substrate and Purkinje ablation

Cited by 5 publications

References 23 publications

Information theory-based direct causality measure to assess cardiac fibrillation dynamics

Information theory-based direct causality measure to assess cardiac fibrillation dynamics

Cardiac arrhythmogenesis: roles of ion channels and their functional modification

Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal Ca2+

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Product

Resources

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Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal Ca²⁺