Effect of left atrial enlargement on expression of the angiotensinⅡ, signal transducers and activators of transcription 3 and Rac GTPase activating protein 1 signaling pathways in patients with persistent atrial fibrillation and rheumatic heart disease
10.7507/1007-4848.201710021
- VernacularTitle:风湿性心脏病合并持续性心房颤动患者左心房内径增大对心房肌组织 AngⅡ/Rac1/STAT3 途径表达的影响
- Author:
LAN Huai
1
;
WANG Huishan
1
;
XUE Xiaodong
1
;
YIN Zongtao
1
;
ZHU Yan
1
;
HAN Jinsong
1
;
MA Dongchu
2
;
PU Feifei
2
Author Information
1. Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, Shenyang, 110016, P.R.China
2. Department of Experimental Medicine, General Hospital of Shenyang Military Area Command, Shenyang, 110016, P.R.China
- Publication Type:Journal Article
- Keywords:
Atrial fibrillation;
rheumatic heart disease;
angiotensinⅡ;
Rac GTPase activating protein 1;
signal transducers and activators of transcription 3
- From:
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery
2018;25(11):993-999
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of left atrial enlargement on atrial myocardial fibrosis degree and levels of the angiotensinⅡ (AngⅡ)/Rac GTPase activating protein 1 (Rac1)/signal transducersand activators of transcription 3 (STAT3) signaling pathways expressing in patients with persistent atrial fibrillation and rheumatic heart disease (RHD). Methods From March to December 2011, 30 patients with RHD who underwent prosthetic valve replacement in our hospital were enrolled, including 16 males and 14 females, aged 42-70 (56.9±6.8) years. Twenty RHD patients with persistent atrial fibrillation as a research group and ten RHD patients with sinus rhythm as a control group (group A) underwent transthoracic echocardiography and right atrial appendage (RAA) tissue samples were obtained from these patients during mitral/aortic valve replacement operation. The research group according to left atrial diameter (LAD) was divided into two groups, ten patients in each group: a group B with LAD of 50–65 mm and a group C with LAD of LAD>65 mm. For each sample, histological examination was performed by hematoxylin-eosin and Masson’s trichrome staining. Light-microscopic pictures of atrial tissues samples were stained and tissue fibrosis degree in each group was analyzed. AngⅡ concentration was measured by enzyme linked immunosorbent assay. Rac1 and STAT3 were measured by western blotting. Results LAD was significantly greater in AF patients with RHD than in the control group. Hematoxylin-eosin staining demonstrated highly organized arrangement of atrial muscles in the control group and significant derangement in both group B and group C with reduced cell density and increased cell size. Moreover, Masson’s trichrome staining showed that atrial myocytes were surrounded by large trunks of collagen fibers in both group B and group C, but not in the group A. There was a positive correlation between atrial tissue fibrosis and LAD. AngⅡ content was positively correlated with LAD. Similarly, Rac1 and STAT3 protein levels were found considerably higher in the group C and group B than in the group A with excellent correlation to LAD. Conclusion In patients with RHD complicated with persistent atrial fibrillation, the degree of atrial fibrosis and the expression level of AngⅡ/Rac1/STAT3 signaling pathways significantly increase with the left atrialenlargement.
