Literature DB >> 21911268

The increase in sympathetic nerve density in the atrium facilitates atrial fibrillation in patients with rheumatic heart disease.

Yuanhong Li1, Zhibing Lu, Qizhu Tang, Hong Jiang, Congxin Huang, Bo He, Xiaorong Hu, Jinqi Huang, Xiaoqing Zhu, Hongli Wang.   

Abstract

BACKGROUND: Atrial fibrillation (Af) is frequently observed in patients with rheumatic heart disease (RHD). The hyperactivity of autonomic nervous system is known to contribute to the occurrence of Af in RHD patients. This study investigated the association between the autonomic density and the risk of Af in RHD patients.
METHODS: Seventy-five patients were enrolled: (1) RHD patients with Af (N = 25, Group 1); (2) RHD patients without Af (N = 25, Group 2); (3) congenital heart disease patients without Af (N = 25, Group 3). The baseline characteristics and the blood concentrations of renin, C-reaction protein and angiotensin II were collected from all patients. The tissues were obtained from the right atrial appendage during the open-heart surgery and then stained using immunohistochemical methods with autonomic antibodies.
RESULTS: The sympathetic nerve density was significantly higher in RHD patients with Af than RHD patients without Af and congenital heart disease patients, both endocardially and epicardially. The parasympathetic nerve density did not show significant difference among the three groups. The left atrial diameter was larger in RHD patients with Af than the other two groups. The blood concentrations of renin and angiotensin II were higher in RHD patients with Af than the other two groups. The erythrocyte sedimentation rate and blood concentrations of C-reaction protein did not show significant change among the three groups.
CONCLUSION: This study provided direct evidence of the increase in sympathetic nerve density in atrium in patients with RHD. This phenomenon may be associated with the development of Af in RHD patients.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

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Year:  2011        PMID: 21911268     DOI: 10.1016/j.ijcard.2011.08.058

Source DB:  PubMed          Journal:  Int J Cardiol        ISSN: 0167-5273            Impact factor:   4.164


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