Sudden cardiac deaths have higher proportion of left stellate ganglionitis.
Cardiac arrhythmia
Cardiovascular disease
Inflammation
Stellate ganglion
Sudden cardiac death
Sympathetic nervous system
Journal
Forensic science, medicine, and pathology
ISSN: 1556-2891
Titre abrégé: Forensic Sci Med Pathol
Pays: United States
ID NLM: 101236111
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
accepted:
18
02
2022
pubmed:
30
3
2022
medline:
18
5
2022
entrez:
29
3
2022
Statut:
ppublish
Résumé
One of the hypothesized mechanisms of sudden cardiac death in humans is an arrhythmia precipitated by increased sympathetic outflow to a compromised heart. The stellate ganglia provide the main sympathetic innervation to the heart, where the left stellate ganglion appears to play a role in arrhythmogenesis. Case reports of sudden cardiac death have described left stellate ganglion inflammation but no larger studies have been performed. Thus, we have specifically assessed whether the left stellate ganglion was inflamed in those dying from sudden cardiac death versus other causes of death. Thirty-one left stellate ganglia were resected from cadavers diagnosed with sudden cardiac deaths and compared with 18 ganglia from cadavers diagnosed with non-sudden cardiac deaths. Ganglia were stained with hematoxylin and eosin and lymphocytic aggregates compared. The proportion of left stellate ganglion inflammation (77%) was significantly higher in deaths from sudden cardiac deaths than non-sudden cardiac deaths (33%). This study provides information on a previously recognized, but understudied, structure that may help understand sudden cardiac death. We found high prevalence of stellate ganglion inflammation and propose that this may trigger sympathetic storms.
Identifiants
pubmed: 35349080
doi: 10.1007/s12024-022-00466-5
pii: 10.1007/s12024-022-00466-5
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
156-164Informations de copyright
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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