| Objective:To study the changes of angiotensin-converting enzyme (ACE), angiotensinⅡtype 1 receptor (AT1R), extracellular signal-regulated kinase (ERK) , and atrial fibrosis in patients with rheumatic heart disease (RHD) and atrial fibrillation (AF) treated with or without angiotensin- converting enzyme inhibitor (ACEI) .Methods: Atrial tissue was obtained from the right appendage during open surgery in 25 patients with RHD. The mRNA of ACE and ERK2 and AT1R was semi-qualified by reverse transcription-ploymerase chain reaction (RT-PCR) and normalized to the glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Western blotting analysis was employed to examine the expression of ACE and ERK and AT1R. Atrial collagen volume fraction (CVF) was detected by Masson's stain. Result: The mRNA of ACE and ERK2 or the protein of ACE and ERK was significantly increased , the mRNA or protein of AT1R was significantly down-regulated , and CVF was significantly increased in patients with chronic atrial fibrillation(CAF) compared with sinus rhythm group(SR) (p＜0.01 or p＜0.05) . Compared with CAF patients treated without ACEI, the mRNA of ERK2 and protein of ERK were significantly decreased in CAF patients treated with ACEI (p＜0.05) , but there is no difference between ACE and AT1R, and decreased CVF was detected (p＞0.05).Conclusion: The expression of ACE , ERK2 and ERK was increased ,that of AT1R was decreased , and fibrosis was more severe in RHD patients with CAF compared with thoes with SR . Compared with CAF patients treated without ACEI , The expression of ERK2 and ERK was significantly decreased (p＜0.05) and decreased CVF was detected (p＞0.05) in CAF patients treated with ACEI . It sugests that the increasing expression of ERK2 and ERK resulting from local renal angiotensin-converting enzyme system activation mediates the development of atrial fibrosis, and ACEI may contribute to decrease the atrial fibrosis in RHD patients with AF.
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