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Rottmann, Markus

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Rottmann

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Markus

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Rottmann, Markus

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    Activation During Sinus Rhythm in Ventricles With Healed Infarction
    (Ovid Technologies (Wolters Kluwer Health), 2019-10) Rottmann, Markus; Kleber, Andre; Barkagan, Michael; Sroubek, Jakub; Leshem, Eran; Shapira-Daniels, Ayelet; Buxton, Alfred; Anter, Elad
    Background: In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit. Methods: In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit. Results: Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1m/sec differentiated inducible from non-inducible infarctions (p=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (AUC=0.84 [95% CI 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT. Conclusions: Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.