Right Atrial Myocardial Remodeling in Children With Atrial Septal Defect Involves Inflammation, Growth, Fibrosis, and Apoptosis

Frontiers in Pediatrics

article

Hatem Rouatbi¹  Nesrine Farhat¹  Ruth Heying²  Arlette Gérard³  Jaime F. Vazquez-Jimenez⁴  Marie-Christine Seghaye¹ 

[1] Department of Pediatrics & Pediatric Cardiology, University Hospital Liège;Department of Pediatric Cardiology, University Hospital Leuven;Department of Pediatrics, University Hospital Liège;Department of Pediatric Cardiac Surgery, University Hospital Aachen

关键词: myocardial remodeling;    congenital heart disease;    atrial septum defect;    inflammation;    growth;    fibrosis;    apoptosis;   

DOI  :  10.3389/fped.2020.00040

学科分类：社会科学、人文和艺术（综合）

来源: Frontiers

【 摘 要 】

Introduction: Myocardial remodeling due to large atrial septum defect (ASD) is macroscopically characterized by dilation of the right-sided cardiac cavities secondary to volume overload, the cellular mechanisms of which are not yet understood. We postulated that inflammation, fibrosis, and cell death are actors of right atrial remodeling secondary to ASD. Patients and Methods: In 12 children with large ASD (median age: 63 months), expression of genes coding for proteins involved in the response to cell stress and -protection, inflammation, growth and angiogenesis, fibrosis, and apoptosis was assessed by RT-PCR in right atrial myocardial biopsies taken during cardiac surgery. The presence of cytokines in myocardial cells was confirmed by immunohistochemistry and effective apoptosis by TUNEL assay. Results: In all patients investigated, a cellular response to early mechanical stress with the initiation of early protective mechanisms, of inflammation (and its control), -growth, and -angiogenesis, of fibrosis and apoptosis was present. The apoptotic index assessed by TUNEL assay averaged 0.3%. Conclusions: In children with large ASD, macroscopic right atrial remodeling relates to cellular mechanisms involving the expression of numerous genes that either still act to protect cells and tissues but that also harm as they initiate and/or sustain inflammation, fibrosis, and cell death by apoptosis. This may contribute to long term morbidity in patients with ASD.

【 授权许可】

CC BY