Activation During Sinus Rhythm in Ventricles With Healed Infarction: Differentiation Between Arrhythmogenic and Nonarrhythmogenic Scar.
Animals
Body Surface Potential Mapping
/ methods
Cicatrix
/ physiopathology
Disease Models, Animal
Endocardium
/ physiopathology
Heart Conduction System
/ physiopathology
Heart Rate
/ physiology
Heart Ventricles
/ diagnostic imaging
Myocardial Infarction
/ complications
Swine
Tachycardia, Ventricular
/ diagnosis
adipose tissue
balloon occlusion
collagen
infarction
ventricular tachycardia
Journal
Circulation. Arrhythmia and electrophysiology
ISSN: 1941-3084
Titre abrégé: Circ Arrhythm Electrophysiol
Pays: United States
ID NLM: 101474365
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
entrez:
11
10
2019
pubmed:
11
10
2019
medline:
12
5
2020
Statut:
ppublish
Résumé
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. 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. 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 ≤0.1 m/s differentiated inducible from noninducible infarctions ( 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.
Sections du résumé
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 ≤0.1 m/s differentiated inducible from noninducible infarctions (
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.
Identifiants
pubmed: 31597477
doi: 10.1161/CIRCEP.119.007879
pmc: PMC6814309
mid: NIHMS1540370
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e007879Subventions
Organisme : NHLBI NIH HHS
ID : T32 HL007374
Pays : United States
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