TGF‐β1 Expression and Atrial Myocardium Fibrosis Increase in Atrial Fibrillation Secondary to Rheumatic Heart Disease

Abstract

Background: Atrial fibrosis was considered a structural basis for the development and sustaining of atrial fibrillation (AF). Transforming growth factor‐β1 (TGF‐β1) was one of the main factors for accelerating collagen production. The contribution of TGF‐β1 in the pathogenesis of AF needs further investigation. Hypothesis: The altered expression and distribution of TGF‐β1 will be associated with the changes in atrial fibrosis in different types of AF patients with rheumatic heart disease (RHD). Methods: Right atrial specimens obtained from 38 RHD patients undergoing mitral valve replacement surgery were divided into 3 groups: the sinus rhythm group (n = 8), the paroxysmal AF group (pAF; n = 10), and the chronic AF group (cAF; AF lasting ≥ 6 mo; n = 20). The degree of atrial fibrosis, collagen content, serum levels, messenger RNA (mRNA), and protein expression of TGF‐β1 were detected. Results: The collagen content, serum level, TGF‐β1 mRNA, and protein expression of the atrial tissue increased gradually in sinus rhythm, for both pAF and cAF groups, respectively. A positive correlation between TGF‐β1 and the degree of atrial fibrosis was also demonstrated (P < 0.05). Conclusion: The TGF‐β1 expression in atrial tissue increased gradually in proportion to the degree of atrial fibrosis in AF and was associated with the type of AF, which suggests that TGF‐β1 is possibly involved in the pathogenesis of AF in RHD patients. Copyright