Bibliographies thématiques / Atrial fibrillation substrate

Littérature scientifique sur le sujet « Atrial fibrillation substrate »

Auteur : Grafiati
Publié le 11 mars 2023

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Articles de revues sur le sujet "Atrial fibrillation substrate"

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Arentz, Thomas, Björn Müller-Edenborn et Amir Jadidi. « Arrhythmogenic Atrial Substrate in Persistent Atrial Fibrillation ». JACC : Clinical Electrophysiology 4, no 1 (janvier 2018) : 97–98. http://dx.doi.org/10.1016/j.jacep.2017.11.009.

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Kottkamp, Hans. « On the Atrial Fibrillation Substrate ». Journal of the American College of Cardiology 74, no 10 (septembre 2019) : 1348–51. http://dx.doi.org/10.1016/j.jacc.2019.06.064.

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Roberts, Jason D., et Michael H. Gollob. « Atrial myopathy : A primary substrate for atrial fibrillation ». Heart Rhythm 19, no 3 (mars 2022) : 476–77. http://dx.doi.org/10.1016/j.hrthm.2021.12.011.

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Haïssaguerre, Michel, Matthew Wright, Mélèze Hocini et Pierre Jaïs. « The Substrate Maintaining Persistent Atrial Fibrillation ». Circulation : Arrhythmia and Electrophysiology 1, no 1 (avril 2008) : 2–5. http://dx.doi.org/10.1161/circep.108.764233.

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Calkins, Hugh. « The Dynamic Substrate for Atrial Fibrillation ». JACC : Clinical Electrophysiology 3, no 4 (avril 2017) : 403–4. http://dx.doi.org/10.1016/j.jacep.2016.12.003.

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Zghaib, Tarek, Ali Keramati, Jonathan Chrispin, Dong Huang, Muhammad A. Balouch, Luisa Ciuffo, Ronald D. Berger et al. « Multimodal Examination of Atrial Fibrillation Substrate ». JACC : Clinical Electrophysiology 4, no 1 (janvier 2018) : 59–68. http://dx.doi.org/10.1016/j.jacep.2017.10.010.

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Chimenti, Cristina, Matteo A. Russo, Angelo Carpi et Andrea Frustaci. « Histological substrate of human atrial fibrillation ». Biomedicine & ; Pharmacotherapy 64, no 3 (mars 2010) : 177–83. http://dx.doi.org/10.1016/j.biopha.2009.09.017.

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Kottkamp, Hans. « Atrial fibrillation substrate : The “unknown species”— From lone atrial fibrillation to fibrotic atrial cardiomyopathy ». Heart Rhythm 9, no 4 (avril 2012) : 481–82. http://dx.doi.org/10.1016/j.hrthm.2012.01.008.

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Medi, C., A. Teh, K. Roberts-Thomson, J. Morton, P. Kistler et J. Kalman. « Advanced Right Atrial Substrate Promotes Atrial Flutter over Atrial Fibrillation ». Heart, Lung and Circulation 21 (janvier 2012) : S99. http://dx.doi.org/10.1016/j.hlc.2012.05.250.

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Rivner, Harold, Raul D. Mitrani et Jeffrey J. Goldberger. « Atrial Myopathy Underlying Atrial Fibrillation ». Arrhythmia & ; Electrophysiology Review 9, no 2 (13 août 2020) : 61–70. http://dx.doi.org/10.15420/aer.2020.13.

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While AF most often occurs in the setting of atrial disease, current assessment and treatment of patients with AF does not focus on the extent of the atrial myopathy that serves as the substrate for this arrhythmia. Atrial myopathy, in particular atrial fibrosis, may initiate a vicious cycle in which atrial myopathy leads to AF, which in turn leads to a worsening myopathy. Various techniques, including ECG, plasma biomarkers, electroanatomical voltage mapping, echocardiography, and cardiac MRI, can help to identify and quantify aspects of the atrial myopathy. Current therapies, such as catheter ablation, do not directly address the underlying atrial myopathy. There is emerging research showing that by targeting this myopathy we can help decrease the occurrence and burden of AF.
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Thèses sur le sujet "Atrial fibrillation substrate"

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Scridon, Alina. « Atrial fibrillation : insights concerning the arrhythmogenic substrate ». Phd thesis, Université Claude Bernard - Lyon I, 2012. http://tel.archives-ouvertes.fr/tel-00933537.

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Atrial fibrillation is the most prevalent form of cardiac arrhythmia. Studies in animal modelshave provided important insights into arrhythmia mechanisms. However, to date, we do not dispose ofanimal models of spontaneous atrial arrhythmia.Thus, we aimed to develop a model of spontaneous atrial arrhythmia in rats and to assesspathophysiological mechanisms of these arrhythmias by using a multidisciplinary approach. We alsoaimed to assess the presence and the extent of inflammation and endothelial dysfunction, incriminatedin atrial fibrillation-related complications such as stroke, in atrial fibrillation patients.The animal study describes the first animal model of spontaneous atrial arrhythmias. We alsoprovide evidence that multiple mechanisms participate in arrhythmia occurrence in this model,particularly autonomic imbalance with relative vagal hyperactivity, left atrial endocardial fibrosis, anddecreased left atrial expression of the Pitx2 gene. In our clinical study, we found high levels ofvascular endothelial growth factor and von Willebrand factor in atrial fibrillation patients compared tosinus rhythm controls. These results suggest specific thromboembolic risk patterns according to theclinical form of arrhythmia and highlight a parallel evolution of atrial fibrillation and endothelialdysfunction. These results add new insights into the understanding of atrial arrhythmias. This new animalmodel could facilitate studies of pathophysiological mechanisms involved in atrial arrhythmias andallow assessment of efficacy and toxicity of therapeutic agents in a setting that faithfully reproducesthe clinical presentation of the arrhythmia
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Kojodjojo, Pipin. « Substrate and triggers of human atrial fibrillation ». Thesis, Institute of Cancer Research (University Of London), 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498071.

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Todd, Derick M. « Atrial fibrillation : a study of substrate and triggers ». Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29402.

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Mayyas, Fadia A. « Impact of Endothelin-1 System on Atrial Fibrillation Substrate ». Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1284647293.

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Benson, Bryce Eric. « Mapping the Substrate of Atrial Fibrillation : Tools and Techniques ». ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/634.

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Atrial fibrillation (AF) is the most common cardiac arrhythmia that affects an estimated 33.5 million people worldwide. Despite its prevalence and economic burden, treatments remain relatively ineffective. Interventional treatments using catheter ablation have shown more success in cure rates than pharmacologic methods for AF. However, success rates diminish drastically in patients with more advanced forms of the disease. The focus of this research is to develop a mapping strategy to improve the success of ablation. To achieve this goal, I used a computational model of excitation in order to simulate atrial fibrillation and evaluate mapping strategies that could guide ablation. I first propose a substrate guided mapping strategy to allow patient-specific treatment rather than a one size fits all approach. Ablation guided by this method reduced AF episode durations compared to baseline durations and an equal amount of random ablation in computational simulations. Because the accuracy of electrogram mapping is dependent upon catheter-tissue contact, I then provide a method to identify the distance between the electrode recording sites and the tissue surface using only the electrogram signal. The algorithm was validated both in silico and in vivo. Finally, I develop a classification algorithm for the identification of activation patterns using simultaneous, multi-site electrode recordings to aid in the development of an appropriate ablation strategy during AF. These findings provide a framework for future mapping and ablation studies in humans and assist in the development of individualized ablation strategies for patients with higher disease burden.
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Avogaro, Laura. « Investigation of the structural and molecular substrate of atrial fibrillation ». Doctoral thesis, Università degli studi di Trento, 2016. https://hdl.handle.net/11572/368493.

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Atrial fibrillation (AF) is the most common sustained arrhythmia worldwide and a frequent cause of hospitalization. Moreover, it represents one of the most frequent complication following cardiac surgery with an incidence of around 30% and an important predictor of patient morbidity. The exact pathophysiological mechanisms responsible for the onset and perpetuation of AF are not completely understood. However, clinical and experimental insights on the factors causing AF have suggested that atrial fibrillation is a multi-factorial phenomenon. Atrial fibrillation is characterized by a highly complex and irregular electrical activation of the atrial tissue, which is the manifestation of diverse abnormalities (electrical, structural, metabolic, neurohormonal, and/or molecular alterations) in diverse pathological conditions. In particular, it has been shown that fibrosis, a phenomenon in which extracellular matrix (ECM) components, mainly fibrillar collagen, accumulate between cardiomyocytes, leads to the inhomogeneous atrial electrical conduction typical of fibrillation. Recent studies have suggested that the deregulation of gene expression may act as a molecular mechanism of arrhythmogenesis. In particular, miRNAs, a new class of non-coding RNAs have rapidly emerged as one of the key players in the gene expression regulatory network, so variations in their expression levels may constitute a pathway for the arrhythmia-induced atrial remodeling. The present study aims to investigate the structural and molecular features of atrial tissue, with particular attention to fibrosis, which may be involved in the formation of a pro-arrhythmic substrate. By using both histological and advanced microscopy techniques, intramural fibrotic content and 3D collagen network properties were determined in atrial samples, collected during cardiac surgery in patients who developed or not AF. The quantitative analysis indicated a general decrease of collagen content from the outer (the epicardium) to the inner (the endocardium) myocardial wall, in the overall patient population. However, AF patients presented higher fibrotic values compared to sinus rhythm (SR) patients in the deeper myocardial layers, thus supporting the hypothesis that an accumulation of fibrotic tissue within the myocardial wall may represent an important structural contributor in the pathophysiology of AF. In addition to a quantitative assessment, collagen properties such as fibers orientation (degree and anisotropy) and scale dimension, were determined by non-linear optical microscopy techniques. The analysis revealed that in SR patients collagen network showed a fine architecture characterized by thin fibrils with changing angles and directions compared to AF, where fibers tended to pack-up in larger bundles of defined directions. A quantitative analysis of the 3D collagen network features, throughout the atrial wall, revealed that fibers orientation and scale dimension changed along tissue depth in both SR and AF patients, with larger values of orientation and fiber changes in AF tissues. These results highlight the spatial rearrangement and thickening of the 3D collagen network in AF patients, suggesting its possible role in the maintenance of the arrhythmia. Numerous evidence indicated that also an altered regulation of gene expression may play an important role in the mechanisms of atrial remodeling which underlie AF. In this perspective, the expression pattern of some miRNAs known to target different genes involved in diverse mechanisms that underlie AF was evaluated. A panel of miRNAs (miR-1, miR-133a/b, miR-30c, miR-29a/b, miR-208a/b, miR-328, miR-499, miR-590 and miR-21), principally involved in the formation of a pro-arrhythmic substrate, was selected after an accurate review of the literature and analyzed by RT-qPCR, in AF patients versus SR individuals. To accurately determine the levels of analyzed miRNAs, their expression data are usually normalized relatively to endogenous and/or exogenous reference genes. To date, no general agreement between different normalization strategies has been found, in particular in cardiac tissue, for the study of AF. For these reasons, a preliminary study aiming to establish the best endogenous reference genes for miRNAs data normalization was performed. Specifically, different well-established analysis tools such as NormFinder, GeNorm, BestKeeper and ∆Ct method, were applied on five commonly used endogenous reference transcripts such as 5S, U6, SNORD48, SNORD44 and miR-16. The suitable reference gene obtained, SNORD48, was applied for miRNAs data normalization. Our findings revealed that miRNAs expression levels were different in AF compared to SR patients. MiR-208a and miR-208b displayed statistically significant differences between the two populations. To investigate possible relationships between miRNAs expression levels and the fibrotic content a correlation measurement was also performed. Our analysis revealed that miR-21 and miR-208b were close to a significant correlation with fibrosis. In conclusion, this work introduced new techniques and implemented new methods of analysis for the study of the substrate of AF. In particular, the results obtained with this multiscale approach, from structural to molecular level, exacerbated the role of fibrosis as a critical contributor in the formation of a pro-arrhythmic substrate. Nonetheless, further studies are needed for a better understanding of the ways in which structural, molecular and also cellular remodeling may alter the impulse propagation in the myocardium.
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Qureshi, Norman. « The contact electrogram and its architectural determinants in persistent human atrial fibrillation : understanding the electroarchitecture of the arrhythmic substrate ». Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/56363.

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The understanding of the underlying mechanisms of the persistence of atrial fibrillation remains poor. Key to this is the relationship between structure - myocardial architecture, and function - electrical activity, and how these can be measured, interpreted and correlated clinically. We sought to address the hypothesis that the local electrogram morphology is determined by local atrial myocardial activation patterns, which are in turn determined by local atrial myocardial architecture. In addressing this hypothesis, we utilised improved techniques of atrial segmentation and detection of wall enhancements to more accurately delineate underlying de novo atrial myocardial fibrosis, with late-gadolinium enhanced cardiac magnetic resonance imaging (LGE- CMRI). Here, we demonstrated a predilection of native structural remodelling on the posterior left atrial wall. The electrophysiological changes underlying late-gadolinium enhancements were interrogated with high-density electroanatomic 3D mapping using a Kernel as a unit of measure, in the varying rhythms of AF, sinus and pacing, with drop in tissue voltages and conduction velocities in regions of fibrosis, but counter-intuitively, a higher extent of electrogram fractionation in healthy myocardium. We observed the rate and wavefront-activation dependency of voltage, emphasizing the importance of voltage maps being interpreted in the context of its rhythm. We have also described a novel technique of AF voltage mapping, with the metric of mean AF voltage sampled over 8 secs correlating well with LGE-CMRI defined fibrosis, and surprisingly better than that of sinus rhythm voltage suggesting that this metric may be more representative of the underlying atrial substrate. Lastly, reverse translational cell monolayer experiments in novel co-cultured neonatal ventricular rat myocytes and fibroblasts were carried out to corroborate clinical in vivo observations under the control of the basic science laboratory. These emphasized the contributions of the structural and functional changes to electrogram morphology (voltage and fractionation). The contact electrogram is the result of a complex dynamic functional electrophysiology, and its interactions with the underlying atrial myocardium. This increased understanding of structure and function (electroarchitecture) provides mechanistic insights essential if we are to progress beyond the current empiricism of catheter ablation strategies of persistent AF.
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Liuba, Ioan. « Focal atrial tachycardia : Insights concerning the arrhythmogenic substrate based on analysis of intracardiac electrograms and inflammatory markers ». Doctoral thesis, Linköping : Department of Medical and Health Sciences, Linköping University, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-20461.

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Tuan, Jiun Haur. « Electrophysiological substrates of atrial fibrillation : a frequency domain study of intra-cardiac electrograms ». Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/10105.

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The mechanisms responsible for maintenance of AF remain poorly understood. This thesis examines the frequency domain characteristics of AF in order to gain further insights into this arrhythmia. Through a series of studies involving patients undergoing catheter ablation for atrial fibrillation, intra-cardiac electrograms of AF were collected and analysed using Fast Fourier Transform to derive frequency domain parameters of dominant frequency (DF) and organization index (OI). It was found that intravenous flecainide reduced DF of AF, but only an associated increase in OI was predictive of successful return to sinus rhythm. In another study of patients having catheter ablation for persistent AF, a higher OI post-ablation was found to be associated with medium-term freedom of AF, suggesting that OI may be a useful guide to determine the extent of radiofrequency ablation needed. The effects of vagal blockade with atropine were also studied and compared with that of catheter ablation using a stepwise strategy of isolating the pulmonary veins, linear ablation and complex fractionated electrogram ablation, without deliberately targeting ganglionated plexi. This showed that atropine reduced DF and increased OI of AF electrograms, while decreasing mean RR intervals, standard deviation of RR intervals and 5th percentile of RR intervals. The directional changes of all the above parameters mirrored that of catheter ablation, suggesting that vagal blockade and catheter ablation not deliberately aimed at autonomic tissue can have similar effects on the frequency spectrum of AF, probably mediated through modulation of the autonomic tone. The relationship of regional DF and electrogram complexity as assessed by automated measurement of complex fractionated electrogram – mean (CFE-mean) were also compared, pre and post-ablation of the left atrium. There appeared to be only a modest correlation between the two and this was further weakened following ablation, suggesting that these are possibly separate substrate entities.
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Yusuf, Shamil. « Triggers and substrates in atrial fibrillation : an in-depth proteomic and metabolomic analysis ». Thesis, University of London, 2009. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518118.

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Chapitres de livres sur le sujet "Atrial fibrillation substrate"

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Ehrlich, Joachim R., Pierre Coutu, Yung-Hsin Yeh, Xiaoyan Qi et Stanley Nattel. « Cellular Electrophysiology and the Substrate for Atrial Fibrillation ». Dans Atrial Fibrillation, 37–56. Totowa, NJ : Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-163-5_4.

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Navaravong, Leenhapong, et Nassir F. Marrouche. « MRI definition of atrial substrate ». Dans Practical Guide to Catheter Ablation of Atrial Fibrillation, 101–8. Chichester, UK : John Wiley & Sons Ltd, 2015. http://dx.doi.org/10.1002/9781118658369.ch10.

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Capucci, A., M. Biffi et G. Boriani. « Lone Atrial Fibrillation : Which Anatomical and Electrophysiologic Substrate ? » Dans Cardiac Arrhythmias 1995, 199–202. Milano : Springer Milan, 1996. http://dx.doi.org/10.1007/978-88-470-2223-2_38.

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Bagliani, G., M. Adam, M. Villani, M. Pirrami, P. Franciosa, G. Carreras, R. Apolloni, M. G. Bendini, M. Ridarelli et A. S. Montenero. « Lone Atrial Fibrillation : What Is the Anatomical and the Electrophysiological Substrate ? » Dans Cardiac Arrhythmias 1999 - Vol.1, 50–57. Milano : Springer Milan, 2000. http://dx.doi.org/10.1007/978-88-470-2139-6_5.

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Aslanidi, Oleg V., Mark R. Boyett et Henggui Zhang. « Left to Right Atrial Electrophysiological Differences : Substrate for a Dominant Reentrant Source during Atrial Fibrillation ». Dans Functional Imaging and Modeling of the Heart, 154–61. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01932-6_17.

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Fan, Youqi, Benjamin J. Scherlag, Yu Liu, Heng Cai, Lilei Yu, Eric Hepler, Shailesh Male, Warren M. Jackman et Sunny S. Po. « Mapping of the Atrial Neural Network : Autonomic Mechanisms Underlying Complex Fractionated Atrial Electrograms and the Substrate for Atrial Fibrillation ». Dans Cardiac Mapping, 159–71. Oxford, UK : Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481585.ch17.

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Hernández, A., R. Alcaraz, F. Hornero et J. J. Rieta. « Relevance of the Atrial Substrate Remodeling during Follow-Up to Predict Preoperatively Atrial Fibrillation Cox-Maze Surgery Outcome ». Dans IFMBE Proceedings, 1005–8. Cham : Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-00846-2_249.

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Comtois, Philippe, Brett Burstein et Stanley Nattel. « Comparisons of Substrates Responsible for Atrial Versus Ventricular Fibrillation ». Dans Electrical Diseases of the Heart, 333–52. London : Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4881-4_20.

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Lin, Yenn-Jiang, Shih-Lin Chang, Li-Wei Lo et Shih-Ann Chen. « Mapping of the Atrial Electrogram in Sinus Rhythm and Different Atrial Fibrillation Substrates ». Dans Cardiac Mapping, 328–40. Oxford, UK : Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481585.ch28.

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López Armaretti, Marianela, Natalia Romina Balian et María Cristina Zurrú. « Atrial Cardiopathy and Cryptogenic Stroke ». Dans Cerebrovascular Diseases - Elucidating Key Principles [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103736.

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Cryptogenic stroke (CS) is defined as the presence of cerebral infarcts, the cause which has not been identified despite an appropriate diagnostic evaluation, and it accounts for approximately 30–40% of all ischemic strokes. There is a certain subgroup of CS with embolic characteristics on neuroimaging studies and no evidence of atrial fibrillation alternative or any alternative cause. Recent data suggest that disorders of the atrium, even without atrial fibrillation, could increase thromboembolic risk. The pathological atrial substrate, or atrial cardiopathy (AC), may be an important and underrecognized cause of cryptogenic strokes. This chapter will review the information on the rationale and data behind the concept of atrial cardiopathy, its pathophysiology, proposed biomarkers of atrial cardiopathy, and therapeutic implications.
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Actes de conférences sur le sujet "Atrial fibrillation substrate"

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Vraka, Aikaterini, Fernando Hornero, Joaquin Osca, Luca Faes, Raul Alcaraz et Jose J. Rieta. « Assisting Electrophysiological Substrate Quantification in Atrial Fibrillation Ablation ». Dans 2019 E-Health and Bioengineering Conference (EHB). IEEE, 2019. http://dx.doi.org/10.1109/ehb47216.2019.8969928.

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van Rosmalen, Frank, Laurent Pison, Tammo Delhaas, Harry Crijns, Stef Zeemering et Ulrich Schotten. « Local Atrial Conduction Velocity During Pacing as Indication of Atrial Fibrillation Substrate Complexity ». Dans 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.381.

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Aslanidi, O. V., R. Robinson, D. Cheverton, M. R. Boyett et Henggui Zhang. « Electrophysiological substrate for a dominant reentrant source during atrial fibrillation ». Dans 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5333573.

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Finotti, Emanuela, Edward J Ciaccio, Hasan Garan, Fernando Hornero, Raul Alcaraz et José J Rieta. « Study on the Stability of CFAEs to Characterize the Atrial Substrate in Atrial Fibrillation ». Dans 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.252.

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Mannion, J., SJ Lennon, J. Keaney, J. Galvin, J. O’Brien, G. Jauvert, E. Keelan, G. Szeplaki et U. Boles. « 2 Arrhythmogenic substrate stratification of posterior left atrial wall in atrial fibrillation versus sinus rhythm in persistent atrial fibrillation using automated voltage analysis ». Dans Irish Cardiac Society Annual Scientific Meeting & AGM (Virtual), October 7th – 9th 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-ics.2.

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Finotti, Emanuela, Edward J. Ciaccio, Hasan Garan, Fernando Hornero, Raul Alcaraz et Jose J. Rieta. « Assessing the Stability of Complex Fractionated Atrial Electrograms for the Characterization of Atrial Substrate in Atrial Fibrillation ». Dans 2020 International Conference on e-Health and Bioengineering (EHB). IEEE, 2020. http://dx.doi.org/10.1109/ehb50910.2020.9280211.

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Almeida, Tiago P., Xin Li, Bharat Sidhu, Arthur S. Bezerra, Mahmoud Ehnesh, Ibrahim Anton, Ibrahim A. Nasser et al. « Dominant Frequency and Organization Index for Substrate Identification of Persistent Atrial Fibrillation ». Dans 2021 Computing in Cardiology (CinC). IEEE, 2021. http://dx.doi.org/10.23919/cinc53138.2021.9662648.

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Aslanidi, O. V., M. A. Colman, Jichao Zhao, B. H. Smaill, S. H. Gilbert, J. C. Hancox, M. R. Boyett et Henggui Zhang. « Arrhythmogenic substrate for atrial fibrillation : Insights from an integrative computational model of pulmonary veins ». Dans 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6345906.

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Vraka, Aikaterini, Fernando Hornero, Aurelio Quesada, Luca Faes, Raul Alcaraz et José J Rieta. « Reliability of Local Activation Waves Features to Characterize Paroxysmal Atrial Fibrillation Substrate During Sinus Rhythm ». Dans 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.166.

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Ogbomo-Harmitt, "Shaheim, Ahmed Qureshi, Andrew P. King et Oleg Aslanidi". « Impact of Fibrosis Border Zone Characterisation on Fibrosis-Substrate Isolation Ablation Outcome for Atrial Fibrillation ». Dans 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.218.

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