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      Vector Field Heterogeneity for the Assessment of Locally Disorganised Cardiac Electrical Propagation Wavefronts From High-Density Multielectrodes

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          Abstract

          High-density multielectrode catheters are becoming increasingly popular in cardiac electrophysiology for advanced characterisation of the cardiac tissue, due to their potential to identify impaired sites. These are often characterised by abnormal electrical conduction, which may cause locally disorganised propagation wavefronts. To quantify it, a novel heterogeneity parameter based on vector field analysis is proposed, utilising finite differences to measure direction changes between adjacent cliques. The proposed Vector Field Heterogeneity metric has been evaluated on a set of simulations with controlled levels of organisation in vector maps, and a variety of grid sizes. Furthermore, it has been tested on animal experimental models of isolated Langendorff-perfused rabbit hearts. The proposed parameter exhibited superior capturing ability of heterogeneous propagation wavefronts compared to the classical Spatial Inhomogeneity Index, and simulations proved that the metric effectively captures gradual increments in disorganisation in propagation patterns. Notably, it yielded robust and consistent outcomes for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} $\mathbf {4\times 4}$\end{document} grid sizes, underscoring its suitability for the latest generation of orientation-independent cardiac catheters.

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          Most cited references46

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          Promotion of atrial fibrillation by heart failure in dogs: atrial remodeling of a different sort.

          Studies of atrial fibrillation (AF) due to atrial tachycardia have provided insights into the remodeling mechanisms by which "AF begets AF" but have not elucidated the substrate that initially supports AF before remodeling occurs. We studied the effects of congestive heart failure (CHF), an entity strongly associated with clinical AF, on atrial electrophysiology in the dog and compared the results with those in dogs subjected to rapid atrial pacing (RAP; 400 bpm) with a controlled ventricular rate (AV block plus ventricular pacemaker at 80 bpm). CHF induced by 5 weeks of rapid ventricular pacing (220 to 240 bpm) increased the duration of AF induced by burst pacing (from 8+/-4 seconds in control dogs to 535+/-82 seconds; P<0.01), similar to the effect of 1 week of RAP (713+/-300 seconds). In contrast to RAP, CHF did not alter atrial refractory period, refractoriness heterogeneity, or conduction velocity at a cycle length of 360 ms; however, CHF dogs had a substantial increase in the heterogeneity of conduction during atrial pacing (heterogeneity index in CHF dogs, 2. 76+/-0.16 versus 1.46+/-0.10 for control and 1.51+/-0.06 for RAP dogs; P<0.01) owing to discrete regions of slow conduction. Histological examination revealed extensive interstitial fibrosis (connective tissue occupying 12.8+/-1.9% of the cross-sectional area) in CHF dogs compared with control (0.8+/-0.3%) and RAP (0. 9+/-0.2%) dogs. Experimental CHF strongly promotes the induction of sustained AF by causing interstitial fibrosis that interferes with local conduction. The substrates of AF in CHF are very different from those of atrial tachycardia-related AF, with important potential implications for understanding, treating, and preventing AF related to CHF.
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            Fibrosis and cardiac arrhythmias.

            In this review article about fibrosis and arrhythmias, we show that the amount of collagen, a normal element of the heart muscle, increases with age and in heart disease. The relation between fibrosis and electrophysiological parameters such as conduction, fractionation of electrograms, abnormal impulse initiation as well as arrhythmogenicity is discussed. Next to the amount of fibrosis, we offer data suggesting that collagen texture too plays a role in conduction slowing and arrhythmia vulnerability. Data are shown revealing that fibrosis can also be induced by reduced sodium channel and connexin43 expression. Finally contrast-enhanced magnetic resonance to detect fibrosis and ventricular tachycardia vulnerability in a noninvasive way as well as a reduction of fibrosis and arrhythmogenicity by inhibition of the renin-angiotensin-aldosterone system is discussed.
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              Increased vulnerability to atrial fibrillation in transgenic mice with selective atrial fibrosis caused by overexpression of TGF-beta1.

              Studies on patients and large animal models suggest the importance of atrial fibrosis in the development of atrial fibrillation (AF). To investigate whether increased fibrosis is sufficient to produce a substrate for AF, we have studied cardiac electrophysiology (EP) and inducibility of atrial arrhythmias in MHC-TGFcys33ser transgenic mice (Tx), which have increased fibrosis in the atrium but not in the ventricles. In anesthetized mice, wild-type (Wt) and Tx did not show significant differences in surface ECG parameters. With transesophageal atrial pacing, no significant differences were observed in EP parameters, except for a significant decrease in corrected sinus node recovery time in Tx mice. Burst pacing induced AF in 14 of 29 Tx mice, whereas AF was not induced in Wt littermates (P<0.01). In Langendorff perfused hearts, atrial conduction was studied using a 16-electrode array. Epicardial conduction velocity was significantly decreased in the Tx RA compared with the Wt RA. In the Tx LA, conduction velocity was not significantly different from Wt, but conduction was more heterogeneous. Action potential characteristics recorded with intracellular microelectrodes did not reveal differences between Wt and Tx mice in either atrium. Thus, in this transgenic mouse model, selective atrial fibrosis is sufficient to increase AF inducibility.
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                Author and article information

                Contributors
                Journal
                IEEE Open J Eng Med Biol
                IEEE Open J Eng Med Biol
                0076400
                OJEMB
                IOJEA7
                IEEE Open Journal of Engineering in Medicine and Biology
                IEEE
                2644-1276
                2024
                20 December 2023
                : 5
                : 32-44
                Affiliations
                [1] divisionITACA Institute, institutionUniversitat Politècnica de València, institutionringgold 16774; 46022 Valencia Spain
                [2] institutionUniversidad de Castilla-La Mancha, institutionringgold 97010; 16071 Cuenca Spain
                [3] divisionDepartamento de Fisiología, institutionUniversidad de València, institutionringgold 16781; 46010 Valencia Spain
                [4] institutionInstituto de Investigación INCLIVA, institutionringgold 526125; 46010 Valencia Spain
                [5] institutionCIBER E. Cardiovasculares; 28029 Madrid Spain
                [6] institutionCIBER E. Cardiovasculares; 28029 Madrid Spain
                [7] divisionDepartamento de Medicina, institutionUniversidad de València, institutionringgold 16781; 46010 Valencia Spain
                [8] institutionInstituto de Investigación INCLIVA, institutionringgold 526125; 46010 Valencia Spain
                [9] divisionServicio de Cardiología, institutionHospital Clínic Universitari de València, institutionringgold 16781; 46010 Valencia Spain
                [10] divisionITACA Institute, institutionUniversitat Politècnica de València, institutionringgold 16774; 46022 Valencia Spain
                [11] institutionCentro de Investigación Biomédica en Red Enfermedades Cardiovascular, institutionringgold 553232; 28029 Madrid Spain
                Article
                OJEMB-00077-2023
                10.1109/OJEMB.2023.3344349
                10914212
                38445238
                57764451-805a-488c-8e88-eb545c06b30f
                © 2023 The Authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License. For more information, see https://creativecommons.org/licenses/by-nc-nd/4.0/

                History
                : 28 July 2023
                : 22 October 2023
                : 28 November 2023
                : 28 November 2023
                : 23 February 2024
                Page count
                Figures: 11, Tables: 9, References: 46, Pages: 13
                Funding
                Funded by: institutionNational Research Program;
                Funded by: institutionMinisterio de Ciencia e Innovación, Spanish Government;
                Award ID: PID2019-109547RB-I00
                Award ID: PID2022-142514OB-I00
                Funded by: institutionInstituto de Salud Carlos II;
                Award ID: CIBERCV CB16/11/00486
                This work was supported in part by the National Research Program, Ministerio de Ciencia e Innovación, Spanish Government under Grants PID2019-109547RB-I00 and PID2022-142514OB-I00, and in part by Instituto de Salud Carlos II under Grant CIBERCV CB16/11/00486.
                Categories
                Article

                animal experimental models,cardiac signal processing,electrophysiology,high-density electrode catheters,vector field heterogeneity

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