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Updated: Jan 16, 2026

Sterile Pericarditis in Aachener Minipigs As a Model for Atrial Myopathy and Atrial Fibrillation
Published on: September 24, 2021
Preoperative Activation of c-Src Kinase in Atrial Tissue in Patients Developing Postoperative Atrial Fibrillation
Tomasz Andrzej Bonda1, Magdalena Dziemidowicz1, Tomasz Hirnle2
1Department of General and Experimental Pathology, Medical University of Bialystok, ul. Mickiewicza 2c, 15-222 Białystok, Poland.
Abstract:
Background and Objectives: Atrial fibrillation (AF) is a common complication of cardiac surgery. c-Src has been implicated in atrial remodeling in chronic AF, but its role in the early postoperative setting remains unclear. We, therefore, investigated whether baseline c-Src expression in atrial tissue is associated with the subsequent development of postoperative AF (PoAF). The aim of the present work was the evaluation of atrial c-Src expression and activity in patients subjected to open heart surgery who were previously free from AF and to check if changes to the initial level of this protein predispose to the development of postoperative AF (PoAF). Materials and Methods: Forty-two patients without previous AF history we enrolled. Patients with an AF episode during postoperative in-hospital follow-up were assigned to the PoAF group, while the rest (in sinus rhythm-SR) constituted the control group. Samples of the right atrial appendage were harvested before the introduction of the extracorporeal circulation. The expression of c-Src and phospho-c-Src(Tyr416), as well as upstream regulators of c-Src kinase, STAT3, ERK1/2, PDGFRα, and PDGFRβ, was assessed using Western blot. Results: AF occurred in 14 subjects. Expression of c-Src and phospho-c-Src was significantly higher in the PoAF group than in the SR group (c-Src: 1.65×, p = 0.037, and phospho-c-Src: 2.75×, p = 0.003). In addition, in the right atrium of PoAF patients, there was significantly elevated expression of STAT3, ERK1/2, and PDGF receptors, which may facilitate activation of c-Src kinase in patients with PoAF. Conclusions: Our preliminary findings suggest that c-Src expression and activity may contribute to atrial vulnerability and could represent a molecular target for future therapeutic interventions to prevent PoAF.

