Patient-specific modeling of atrial fibrosis increases the accuracy of sinus rhythm simulations and may explain maintenance of atrial fibrillation

2014 ◽  
Vol 47 (3) ◽  
pp. 324-328 ◽  
Author(s):  
Martin W. Krueger ◽  
Kawal S. Rhode ◽  
Mark D. O‘Neill ◽  
C. Aldo Rinaldi ◽  
Jaswinder Gill ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Sinus Rhythm ◽  
Patient Specific ◽  
Atrial Fibrosis ◽  
Patient Specific Modeling ◽  
Specific Modeling

scholarly journals Methodology for patient-specific modeling of atrial fibrosis as a substrate for atrial fibrillation

2012 ◽  
Vol 45 (6) ◽  
pp. 640-645 ◽  
Author(s):  
Kathleen S. McDowell ◽  
Fijoy Vadakkumpadan ◽  
Robert Blake ◽  
Joshua Blauer ◽  
Gernot Plank ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Patient Specific ◽  
Atrial Fibrosis ◽  
Patient Specific Modeling ◽  
Specific Modeling

scholarly journals B-PO05-012 PREDICTING ATRIAL FIBRILLATION RECURRENCE BY COMBINING POPULATION DATA & PATIENT-SPECIFIC MODELING

Heart Rhythm ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. S375-S376
Author(s):  
Caroline H. Roney ◽  
Iain Sim ◽  
Jin Yu ◽  
Marianne Beach ◽  
Arihant Mehta ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Population Data ◽  
Patient Specific ◽  
Atrial Fibrillation Recurrence ◽  
Patient Specific Modeling ◽  
Specific Modeling

scholarly journals Increased α-Actinin-2 Expression in the Atrial Myocardium of Patients with Atrial Fibrillation Related to Rheumatic Heart Disease

Cardiology ◽  
2016 ◽  
Vol 135 (3) ◽  
pp. 151-159 ◽  
Author(s):  
Lei Zhang ◽  
Nan Zhang ◽  
Xuejiao Tang ◽  
Fajin Liu ◽  
Suxin Luo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Sinus Rhythm ◽  
Rheumatic Heart Disease ◽  
Collagen Content ◽  
Atrial Fibrosis ◽  
Smad Pathway ◽  
Smad Signaling Pathway ◽  
Tgf Β1 ◽  
Rheumatic Heart

Objectives: Atrial fibrosis, a marker of atrial structural remodeling, plays a critical role in atrial fibrillation (AF). α- Actinin-2 is associated with structural remodeling related to stretching. The transforming growth factor-β1 (TGF-β1)/Smad pathway plays an important role in atrial fibrosis. We investigated the effects of the TGF-β1/Smad signaling pathway on α-actinin-2 in atrial fibrosis in patients with AF. Methods: Forty-one right atrial specimens obtained from patients with rheumatic heart disease (RHD) were divided into a chronic (c)AF group, i.e. RHD + cAF (n = 29), and a sinus rhythm group, i.e. RHD + sinus rhythm (n = 12). Patients with congenital heart disease (CHD) and sinus rhythm who underwent heart surgery served as controls (n = 10). Fibrosis was assessed by histological examination, and expression of α-actinin-2, TGF-β1 and Smad2/phosphorylated Smad2 (p-Smad2) was evaluated by immunohistochemistry, quantitative real-time PCR and Western blotting. In rat atrial fibroblasts treated with TGF-β1, the collagen content was measured using hydroxyproline detection, and α-actinin-2 and p-Smad2 were evaluated by semiquantitative reverse-transcription PCR and Western blotting. Results: The histology results revealed a significant increase in atrial fibrosis in AF patients. The collagen content, mRNA and protein expression levels of α-actinin-2 and the components of the TGF-β1/Smad signaling pathway were significantly gradually increased in the CHD + sinus rhythm, RHD + sinus rhythm and RHD + cAF groups (p < 0.05). The mRNA and protein levels of α-actinin-2 and TGF-β1 in RHD patients were positively correlated with the collagen volume fraction. A positive correlation between the expression of α-actinin-2 and TGF-β1 was also observed. In rat atrial fibroblasts treated with TGF-β1, the collagen content was greater than that in the control group (p < 0.05), and the expression levels of α- actinin-2 and p-Smad2 were also upregulated (p < 0.05). Conclusions: α-Actinin-2 expression was increased in the atrial tissues of patients with AF secondary to RHD. α-Actinin-2 was upregulated via the TGF-β1/Smad pathway in atrial fibroblasts, which suggests that it may be involved in TGF-β1/Smad pathway-induced atrial fibrosis in patients with AF.

Characterization of hemodynamics in anomalous aortic origin of coronary arteries using patient-specific modeling

2022 ◽  
pp. 110919
Author(s):  
Simbarashe G. Chidyagwai ◽  
Madhurima Vardhan ◽  
Michael Kaplan ◽  
Reid Chamberlain ◽  
Piers Barker ◽  
...  
Keyword(s):  
Coronary Arteries ◽  
Patient Specific ◽  
Patient Specific Modeling ◽  
Specific Modeling

scholarly journals Towards patient-specific modeling of brain tumor growth and formation of secondary nodes guided by DTI-MRI

2018 ◽  
Vol 20 ◽  
pp. 664-673 ◽  
Author(s):  
Stelios Angeli ◽  
Kyrre E. Emblem ◽  
Paulina Due-Tonnessen ◽  
Triantafyllos Stylianopoulos
Keyword(s):  
Brain Tumor ◽  
Tumor Growth ◽  
Patient Specific ◽  
Patient Specific Modeling ◽  
Specific Modeling

Galectin-3 Induces Atrial Fibrosis by Activating the TGF-β1/Smad Pathway in Patients with Atrial Fibrillation

Cardiology ◽  
2020 ◽  
Vol 145 (7) ◽  
pp. 446-455 ◽  
Author(s):  
Minghan Xiao ◽  
Meixia Zhang ◽  
Mengjun Bie ◽  
Xiaowen Wang ◽  
Jingwen Guo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Sinus Rhythm ◽  
Rheumatic Heart Disease ◽  
Atrial Fibrosis ◽  
Smad Pathway ◽  
Galectin 3 ◽  
The Relationship ◽  
Tgf Β1 ◽  
Rheumatic Heart

Background: Atrial fibrosis plays a critical role in the occurrence and maintenance of atrial fibrillation. The role of TGF-β1 in mediating atrial fibrosis is well documented. The β-galactoside-binding lectin galectin-3 (Gal-3) is mainly produced by macrophages in biological events such as inflammation and angiogenesis. Previous studies have shown that Gal-3 is associated with atrial fibrosis, but the relationship between TGF-β1 and Gal-3 in atrial fibrosis remains unclear. Objective: To determine whether Gal-3 induces atrial fibrosis and atrial fibrillation by activating the TGF-β1/Smad pathway and whether the expression of Gal-3 is mediated by TGF-β1, which can enable assessing the relationship between Gal-3 and TGF-β1 in atrial fibrosis. Methods: In this study, 30 patients’ right atrial appendages were collected and divided into 3 groups: congenital heart disease sinus rhythm group (n = 10, as a control group), rheumatic heart disease sinus rhythm group (n = 10), and rheumatic heart disease atrial fibrillation group (n = 10). Rat atrial fibroblasts were cultured in vitro, and recombinant Gal-3 and recombinant TGF-β1 proteins were added to the cell culture. The expression of Gal-3, TGF-β1, Smad2, and collagen I was detected by Western blotting and quantitative real-time PCR. Atrial tissues were stained with Masson’s trichrome stain to evaluate the extent of atrial fibrosis. The expression of Gal-3 and TGF-β1 was detected by immunohistochemical staining and immunofluorescence staining. Gal-3 and TGF-β1 interaction was demonstrated by immunoprecipitation. Results: The expression levels of Gal-3, TGF-β1, Smad2, and collagen I were elevated in the rheumatic heart disease atrial fibrillation group compared with the congenital heart disease sinus rhythm group and the rheumatic heart disease sinus rhythm group. In cultured atrial fibroblasts, there is a synergistic interaction between Gal-3 and TGF-β1. Gal-3 stimulated the TGF-β1/Smad pathway, and overexpression of TGF-β1 induced Gal-3 expression. Conclusions: Gal-3 and TGF-β1 interact with each other and stimulate the downstream TGF-β1/Smad pathway. This finding suggests that Gal-3 could be an important factor in TGF-β1-induced fibrosis in atrial fibrillation.

Sign in / Sign up

Export Citation Format

Share Document