, Yubing Wang 1
, Liangchen Shen 1
, Zhuang Shuai 1
, Wei Liu 1
, Qian Wen 1
, Hu Tang 1
, Yumei Chen 1
, You Yang 2
, Hanmei Li 2
2Department of Ultrasound Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, China
Abstract
Background: The initiation and maintenance of atrial fibrillation (AF) are predominantly driven by progressive atrial structural remodeling, characterized by fibrosis and electrical conduction abnormalities. While vericiguat has shown efficacy in attenuating cardiac remodeling in heart failure (HF), its impact on AF remains insufficiently characterized.
Methods: This study investigated the cardioprotective effects of vericiguat in a Sprague-Dawley rat model of AF. Twenty-four male SD rats (250-300 g, 8-10 weeks old) were randomly assigned to control, AF, and vericiguat-treated groups. Echocardiography and histological assessments were performed, along with quantification of NT-proBNP, Collagen I, CaMKII, Cx43, ATG7, P62, and LC3II/I in the left atrium.
Results: Compared to controls, AF rats exhibited atrial enlargement, elevated myocardial fibrosis, and significant alterations in molecular markers. Vericiguat treatment effectively reversed these pathological changes. Specifically, NT-proBNP, Collagen I, CaMKII, ATG7, and LC3II/I were upregulated, while Cx43 and P62 were downregulated in the AF group—changes that were mitigated by vericiguat.
Conclusion: Collectively, these findings suggest that vericiguat attenuates atrial remodeling and AF progression by modulating autophagy and suppressing fibrosis.