Abstract
Background: The current paradigm is that fibrosis promotes electrophysiological disorders and drives atrial fibrillation (AF). In this current study, we investigated the relation between the degree of fibrosis in human atrial tissue samples of controls and patients in various stages of AF and the degree of electrophysiological abnormalities. Methods: The degree of fibrosis was measured in the atrial tissue and serum of patients in various stages of AF and the controls. Hereto, picrosirius and H&E staining were performed to quantify degree of total, endo-perimysial fibrosis, and cardiomyocyte diameter. Western blot quantified fibrosis markers: neural cell adhesion molecule, tissue inhibitor of metalloproteinase, lysyl oxidase, and α-smooth muscle actin. In serum, the ratio carboxyl-terminal telopeptide of collagen/matrix-metalloproteinase1 was determined. High-resolution epicardial mapping evaluated low-voltage areas and conduction abnormalities. Results: No significant differences were observed in the degree of fibrosis between the groups. Finally, no significant correlation—absolute nor spatial—was observed between all electrophysiological parameters and histological fibrosis markers. Conclusions: No differences in the degree of fibrosis were observed in patients from various stages of AF compared to the controls. Moreover, electrophysiological abnormalities did not correlate with any of the fibrosis markers. The findings indicate that fibrosis is not the hallmark of structural remodeling in AF.
Highlights
The parameters of age, sex, body mass index (BMI), hypertension, dyslipidemia, diabetes mellitus, thyroid disease, and left ventricular function were similar among the control and atrial fibrillation (AF) groups
No significant difference in the degree of fibrosis were observed between patients with and without post-operative AF (Supplementary Figure S5)
We observed in human atrial appendage tissue samples that fibrosis, the tissue fibrosis markers α-smooth muscle actin (αSMA), TIMP, neural cell adhesion molecule (NCAM), and lysyl oxidase (LOX), and the serum fibrosis histological fibrosis markers including cardiomyocyte size, total, and endo and perimarker carboxy terminal telopeptide (CITP)/matrix metalloproteinase 1 (MMP1) ratio are comparable between various stages of AF and the control mysial fibrosis, the tissue fibrosis markers αSMA, TIMP, NCAM, and LOX, and the serum group
Summary
Electropathology is defined as structural remodeling in atrial myocardium, which causes electrical conduction impairment. It has been hypothesized that altered extra-cellular matrix (ECM), especially fibrosis, is the key aspect of structural remodeling that underlies these electrical conduction and voltage changes [5]. The current paradigm is that fibrosis promotes electrophysiological disorders and drives atrial fibrillation (AF) In this current study, we investigated the relation between the degree of fibrosis in human atrial tissue samples of controls and patients in various stages of AF and the degree of electrophysiological abnormalities. Methods: The degree of fibrosis was measured in the atrial tissue and serum of patients in various stages of AF and the controls. Conclusions: No differences in the degree of fibrosis were observed in patients from various stages of AF compared to the controls. The findings indicate that fibrosis is not the hallmark of structural remodeling in AF
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
