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

BACKGROUND: Atrial fibrosis was considered a structural basis for the development and sustaining of atrial fibrillation (AF). Transforming growth factor-beta1 (TGF-beta1) was one of the main factors for accelerating collagen production. The contribution of TGF-beta1 in the pathogenesis of AF needs further investigation. HYPOTHESIS: The altered expression and distribution of TGF-beta1 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-beta1 were detected. RESULTS: The collagen content, serum level, TGF-beta1 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-beta1 and the degree of atrial fibrosis was also demonstrated (P < 0.05). CONCLUSION: The TGF-beta1 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-beta1 is possibly involved in the pathogenesis of AF in RHD patients.