TGF-beta1 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.