Left atrial microvascular endothelial dysfunction, myocardial inflammation and fibrosis after selective insular cortex ischemic stroke.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 10 2019
Historique:
received: 18 04 2019
revised: 15 05 2019
accepted: 01 06 2019
pubmed: 15 6 2019
medline: 13 6 2020
entrez: 15 6 2019
Statut: ppublish

Résumé

Insular cortex (IC) ischemic strokes are associated with increased risk of cardiac arrhythmias. We have previously hypothesized that the anatomical substrate for post-stroke neurogenic arrhythmias comprises stroke-induced left atrium (LA) coronary microvascular endothelial dysfunction (CMED), and myocardial inflammatory infiltration (MII) leading to myocardial fibrosis. We investigated whether selectively induced IC ischemic stroke in rats results in histopathological changes in the LA. Insular ischemic stroke was induced in 6-month old male Wistar rats via unilateral stereotaxic injection of endothelin-1 into the left or right IC. The control group consisted of rats injected with saline. We histologically examined the LA 28 days after stroke for CMED, MII, and fibrosis. We performed linear regression analyses to assess correlation between the 3 histopathological outcomes. We compared these findings in the distal LA and the LA-pulmonary vein border (LA-PV border), a region of rich autonomic innervation. Right and left IC stroke led to CMED, MII, and fibrosis in the LA. MII was significantly correlated with CMED and fibrosis. The LA-PV border had significantly greater MII and fibrosis than the distal LA. There were no differences in coronary microvascular and myocardial changes between left and right IC strokes. Left and right insular ischemic strokes resulted in CMED, MII, and fibrosis, the pathological hallmark of arrhythmogenic LA tissue. Since these changes were greater within the LA-PV border than in the distal LA tissue, the role of preganglionic fibers at the ganglionated plexi as part of neurogenic arrhythmogenesis warrants further investigation.

Sections du résumé

BACKGROUND
Insular cortex (IC) ischemic strokes are associated with increased risk of cardiac arrhythmias. We have previously hypothesized that the anatomical substrate for post-stroke neurogenic arrhythmias comprises stroke-induced left atrium (LA) coronary microvascular endothelial dysfunction (CMED), and myocardial inflammatory infiltration (MII) leading to myocardial fibrosis. We investigated whether selectively induced IC ischemic stroke in rats results in histopathological changes in the LA.
METHODS
Insular ischemic stroke was induced in 6-month old male Wistar rats via unilateral stereotaxic injection of endothelin-1 into the left or right IC. The control group consisted of rats injected with saline. We histologically examined the LA 28 days after stroke for CMED, MII, and fibrosis. We performed linear regression analyses to assess correlation between the 3 histopathological outcomes. We compared these findings in the distal LA and the LA-pulmonary vein border (LA-PV border), a region of rich autonomic innervation.
RESULTS
Right and left IC stroke led to CMED, MII, and fibrosis in the LA. MII was significantly correlated with CMED and fibrosis. The LA-PV border had significantly greater MII and fibrosis than the distal LA. There were no differences in coronary microvascular and myocardial changes between left and right IC strokes.
CONCLUSIONS
Left and right insular ischemic strokes resulted in CMED, MII, and fibrosis, the pathological hallmark of arrhythmogenic LA tissue. Since these changes were greater within the LA-PV border than in the distal LA tissue, the role of preganglionic fibers at the ganglionated plexi as part of neurogenic arrhythmogenesis warrants further investigation.

Identifiants

pubmed: 31196685
pii: S0167-5273(19)32036-4
doi: 10.1016/j.ijcard.2019.06.004
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

148-155

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Brittany Balint (B)

Vulnerable Brain Laboratory, Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University. 339 Windermere Rd, London, ON N6A 5A5, Canada; Heart & Brain Laboratory, Western University, 339 Windermere Rd, London, ON, N6G 5A5, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada.

Victoria Jaremek (V)

Vulnerable Brain Laboratory, Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University. 339 Windermere Rd, London, ON N6A 5A5, Canada; Heart & Brain Laboratory, Western University, 339 Windermere Rd, London, ON, N6G 5A5, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada.

Victoria Thorburn (V)

Vulnerable Brain Laboratory, Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University. 339 Windermere Rd, London, ON N6A 5A5, Canada; Heart & Brain Laboratory, Western University, 339 Windermere Rd, London, ON, N6G 5A5, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada.

Shawn N Whitehead (SN)

Vulnerable Brain Laboratory, Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University. 339 Windermere Rd, London, ON N6A 5A5, Canada; Heart & Brain Laboratory, Western University, 339 Windermere Rd, London, ON, N6G 5A5, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada.

Luciano A Sposato (LA)

Heart & Brain Laboratory, Western University, 339 Windermere Rd, London, ON, N6G 5A5, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada; Department of Clinical Neurological Sciences, London Health Sciences Centre, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada; Department of Epidemiology & Biostatistics, Schulich School of Medicine & Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada; Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond St. N., London, ON N6A 5B7, Canada; Lawson Research Institute, 750 Base Line Rd E, London, ON N6C 2R5, Canada. Electronic address: Luciano.Sposato@LHSC.on.ca.

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Classifications MeSH