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Left atrial microvascular endothelial dysfunction, myocardial inflammation and fibrosis after selective insular cortex ischemic stroke.
Int J Cardiol. 2019 10 01; 292:148-155.IJ

Abstract

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.

Authors+Show Affiliations

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.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.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.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.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.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31196685

Citation

Balint, Brittany, et al. "Left Atrial Microvascular Endothelial Dysfunction, Myocardial Inflammation and Fibrosis After Selective Insular Cortex Ischemic Stroke." International Journal of Cardiology, vol. 292, 2019, pp. 148-155.
Balint B, Jaremek V, Thorburn V, et al. Left atrial microvascular endothelial dysfunction, myocardial inflammation and fibrosis after selective insular cortex ischemic stroke. Int J Cardiol. 2019;292:148-155.
Balint, B., Jaremek, V., Thorburn, V., Whitehead, S. N., & Sposato, L. A. (2019). Left atrial microvascular endothelial dysfunction, myocardial inflammation and fibrosis after selective insular cortex ischemic stroke. International Journal of Cardiology, 292, 148-155. https://doi.org/10.1016/j.ijcard.2019.06.004
Balint B, et al. Left Atrial Microvascular Endothelial Dysfunction, Myocardial Inflammation and Fibrosis After Selective Insular Cortex Ischemic Stroke. Int J Cardiol. 2019 10 1;292:148-155. PubMed PMID: 31196685.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Left atrial microvascular endothelial dysfunction, myocardial inflammation and fibrosis after selective insular cortex ischemic stroke. AU - Balint,Brittany, AU - Jaremek,Victoria, AU - Thorburn,Victoria, AU - Whitehead,Shawn N, AU - Sposato,Luciano A, Y1 - 2019/06/02/ PY - 2019/04/18/received PY - 2019/05/15/revised PY - 2019/06/01/accepted PY - 2019/6/15/pubmed PY - 2020/6/13/medline PY - 2019/6/15/entrez KW - Arrhythmia KW - Coronary microvascular endothelial dysfunction KW - Myocardial fibrosis KW - Myocardial inflammation KW - Stroke SP - 148 EP - 155 JF - International journal of cardiology JO - Int. J. Cardiol. VL - 292 N2 - 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. SN - 1874-1754 UR - https://www.unboundmedicine.com/medline/citation/31196685/Left_atrial_microvascular_endothelial_dysfunction_myocardial_inflammation_and_fibrosis_after_selective_insular_cortex_ischemic_stroke_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0167-5273(19)32036-4 DB - PRIME DP - Unbound Medicine ER -