Detailed Study of Collagen, Vasculature, and Innervation in the Human Cardiac Conduction System.

autonomic innervation blood vessels human cardiac conduction system interstitial collagen lymphatic vessels morphometry

Journal

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
ISSN: 1879-1336
Titre abrégé: Cardiovasc Pathol
Pays: United States
ID NLM: 9212060

Informations de publication

Date de publication:
15 Dec 2023
Historique:
received: 12 10 2023
revised: 12 12 2023
accepted: 13 12 2023
medline: 18 12 2023
pubmed: 18 12 2023
entrez: 17 12 2023
Statut: aheadofprint

Résumé

The cardiac conduction system (CCS) creates and propagates electrical signals generating the heartbeat. This study aimed to assess the collagen content, vasculature, and innervation in the human sinoatrial and atrioventricular CCS, and surrounding tissue. Ten sinoatrial and 17 atrioventricular CCS samples were collected from 17 adult human autopsied hearts. Masson trichrome stain was used to examine collagen, cardiomyocytes, and fat proportions. Immunohistochemically, vessels and lymphatics were studied by CD31 (pan-endothelial marker) and D2-40 (lymphatic endothelium marker) antibodies. General nerve densities were assessed by S100, while sympathetic nerves were studied using tyrosine hydroxylase, parasympathetic nerves with choline acetyltransferase, and GAP43 (neural growth marker) antibodies looked at these components. All components were quantified with QuPath software. Interstitial collagen was more than two times higher in the sinoatrial vs. atrioventricular CCS (55% vs. 22%). The fat content was 6.3% in the sinoatrial CCS and 6.5% in the atrioventricular CCS. The lymphatic vessel density was increased in the sinoatrial and atrioventricular CCS compared to the surrounding tissue and was lower in the sinoatrial vs. atrioventricular CCS (P=0.043). The overall vasculature density did not differ between the SA and AV CCS. The overall innervation and neural growth densities were significantly increased in the CCS compared to the surrounding tissue. The overall innervation was higher in the atrial vs. ventricular CCS (P=0.018). The neural growth was higher in the atrial vs. ventricular CCS (P=0.018). The sympathetic neural supply was dominant in all the studied regions with the highest density in the sinoatrial CCS. Our results provide new insights into the unique morphology of the human CCS collagen, fat, vasculature, and innervation. A deeper understanding of the CCS anatomical components and morphologic substrates' role will help in elucidating the causes of cardiac arrhythmias and provide a basis for further therapeutic interventions.

Sections du résumé

BACKGROUND BACKGROUND
The cardiac conduction system (CCS) creates and propagates electrical signals generating the heartbeat. This study aimed to assess the collagen content, vasculature, and innervation in the human sinoatrial and atrioventricular CCS, and surrounding tissue.
MATERIALS AND METHODS METHODS
Ten sinoatrial and 17 atrioventricular CCS samples were collected from 17 adult human autopsied hearts. Masson trichrome stain was used to examine collagen, cardiomyocytes, and fat proportions. Immunohistochemically, vessels and lymphatics were studied by CD31 (pan-endothelial marker) and D2-40 (lymphatic endothelium marker) antibodies. General nerve densities were assessed by S100, while sympathetic nerves were studied using tyrosine hydroxylase, parasympathetic nerves with choline acetyltransferase, and GAP43 (neural growth marker) antibodies looked at these components. All components were quantified with QuPath software.
RESULTS RESULTS
Interstitial collagen was more than two times higher in the sinoatrial vs. atrioventricular CCS (55% vs. 22%). The fat content was 6.3% in the sinoatrial CCS and 6.5% in the atrioventricular CCS. The lymphatic vessel density was increased in the sinoatrial and atrioventricular CCS compared to the surrounding tissue and was lower in the sinoatrial vs. atrioventricular CCS (P=0.043). The overall vasculature density did not differ between the SA and AV CCS. The overall innervation and neural growth densities were significantly increased in the CCS compared to the surrounding tissue. The overall innervation was higher in the atrial vs. ventricular CCS (P=0.018). The neural growth was higher in the atrial vs. ventricular CCS (P=0.018). The sympathetic neural supply was dominant in all the studied regions with the highest density in the sinoatrial CCS.
CONCLUSIONS CONCLUSIONS
Our results provide new insights into the unique morphology of the human CCS collagen, fat, vasculature, and innervation. A deeper understanding of the CCS anatomical components and morphologic substrates' role will help in elucidating the causes of cardiac arrhythmias and provide a basis for further therapeutic interventions.

Identifiants

pubmed: 38104850
pii: S1054-8807(23)00087-X
doi: 10.1016/j.carpath.2023.107603
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

107603

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Denis Depes (D)

Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, 33520 Tampere, Finland. Electronic address: denis.depes@tuni.fi.

Ari Mennander (A)

Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, 33520 Tampere, Finland; Division of Cardiothoracic Surgery, Tampere University Heart Hospital, Elämänaukio 1, 33520 Tampere, Finland. Electronic address: ari.mennander@sydansairaala.fi.

Timo Paavonen (T)

Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, 33520 Tampere, Finland; Department of Pathology, Fimlab Laboratories, Arvo Ylpön katu 4, 33520 Tampere, Finland. Electronic address: timo.paavonen@tuni.fi.

Mary N Sheppard (MN)

Department of Cardiovascular Pathology, Cardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's Medical School, London, United Kingdom. Electronic address: msheppar@sgul.ac.uk.

Ivana Kholová (I)

Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, 33520 Tampere, Finland; Department of Pathology, Fimlab Laboratories, Arvo Ylpön katu 4, 33520 Tampere, Finland. Electronic address: ivana.kholova@tuni.fi.

Classifications MeSH