His–Purkinje system longitudinal dissociation: From bench to bedside. A case of output‐dependent fascicular capture

2021 ◽  
Vol 32 (4) ◽  
pp. 1174-1177
Author(s):  
Leonardo Marinaccio ◽  
Francesco Vetta ◽  
Barbara Ignatiuk ◽  
Daniele Giacopelli ◽  
Luigia A. Patrassi ◽  
...  



2018 ◽  
Vol 15 (5) ◽  
pp. 394-400
Author(s):  
Li Jie ◽  
Lu Weigang ◽  
Jing Jun ◽  
Wang Huaibao


2020 ◽  
Vol 5 (04) ◽  
pp. 368-372
Author(s):  
Seema Kale

AbstractVarying kinds of AV blocks can occur in the setting of myocardial ischaemia or due to degeneration of conduction system. Wenckebach AV block can present with typical Wenckebach periodicity or atypical periodicity. A variant of atypical Wenckebach periodicity may present like Mobitz II AV block. This is called Pseudo Mobitz II AV block. As we are aware that Mobitz II AV block is more dangerous and can suddenly convert into complete heart block, it is essential that we should try to differentiate between Mobitz and Pseudo Mobitz II blocks. Infact atypical Wenckebach cycles are quite common at both AV node and his Purkinje system.



2021 ◽  
Vol 3 (3) ◽  
pp. 517-522
Author(s):  
Pattara Rattanawong ◽  
Vatsal Ladia ◽  
Nareg Minaskeian ◽  
Dan Sorajja ◽  
Win-Kuang Shen ◽  
...  
Keyword(s):  


Author(s):  
Karli Gillette ◽  
Matthias A. F. Gsell ◽  
Julien Bouyssier ◽  
Anton J. Prassl ◽  
Aurel Neic ◽  
...  

AbstractPersonalized models of cardiac electrophysiology (EP) that match clinical observation with high fidelity, referred to as cardiac digital twins (CDTs), show promise as a tool for tailoring cardiac precision therapies. Building CDTs of cardiac EP relies on the ability of models to replicate the ventricular activation sequence under a broad range of conditions. Of pivotal importance is the His–Purkinje system (HPS) within the ventricles. Workflows for the generation and incorporation of HPS models are needed for use in cardiac digital twinning pipelines that aim to minimize the misfit between model predictions and clinical data such as the 12 lead electrocardiogram (ECG). We thus develop an automated two stage approach for HPS personalization. A fascicular-based model is first introduced that modulates the endocardial Purkinje network. Only emergent features of sites of earliest activation within the ventricular myocardium and a fast-conducting sub-endocardial layer are accounted for. It is then replaced by a topologically realistic Purkinje-based representation of the HPS. Feasibility of the approach is demonstrated. Equivalence between both HPS model representations is investigated by comparing activation patterns and 12 lead ECGs under both sinus rhythm and right-ventricular apical pacing. Predominant ECG morphology is preserved by both HPS models under sinus conditions, but elucidates differences during pacing.





1977 ◽  
Vol 40 (6) ◽  
pp. 957-964 ◽  
Author(s):  
C.Pratap Reddy ◽  
Anthony N. Damato ◽  
Masood Akhtar ◽  
Malkiat S. Dhatt ◽  
Joseph A.C. Gomes ◽  
...  
Keyword(s):  


1982 ◽  
Vol 49 (4) ◽  
pp. 982
Author(s):  
Chen Chia-maou ◽  
Robert J. Hariman ◽  
Anthony N. Datnato


1986 ◽  
pp. 141-150
Author(s):  
Masood Akhtar ◽  
Michael H. Lehmann ◽  
Stephen Denker ◽  
Rehan Mahmud


1978 ◽  
Vol 235 (1) ◽  
pp. H1-H17 ◽  
Author(s):  
A. L. Wit ◽  
P. F. Cranefield

Mechanisms that cause reentry were defined in rings of tissue cut from jellyfish as early as 1906 by Mayer. The concepts were developed by Mines and Garrey during the next 10 years. Lewis then tried to demonstrate that reentry caused atrial flutter. Lewis, Garrey, and later Moe also proposed that atrial fibrillation was caused by reentry. Rosenblueth provided additional experimental evidence that reentry could cause atrial arrhythmias after crushing the intercaval bridge of atrial muscle. Recent studies by Allessie using microelectrodes have provided detailed evidence for reentry in atrial tissue. Mines in 1913 also proposed that reentry could occur in the AV node. Scherf then introduced the concept of functional longitudinal dissociation as a cause of return extrasystoles and this was later shown to happen in the node by Moe and his colleagues. Reentry can also occur between atria and ventricles utilizing accessory connecting pathways. Schmitt and Erlanger in 1913 were the first to do experiments which indicated that reentry can also occur in the ventricles. Subsequently it was shown that reentry can occur in Purkinje fiber bundles. Reentry in ventricular muscle may also cause some of the arrhythmias that occur after myocardial infarction.



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