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Increased Inflammatory Cell Infiltration in the Atrial Myocardium of Patients With Atrial Fibrillation

  • Mien-Cheng Chen
    Correspondence
    Corresponding author: Tel: 886-7-731-7123 ext. 8300; fax: 886-7-732-2402
    Affiliations
    Division of Cardiology and Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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  • Jen-Ping Chang
    Affiliations
    Division of Cardiovascular Surgery, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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  • Wen-Hao Liu
    Affiliations
    Division of Cardiology and Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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  • Cheng-Hsu Yang
    Affiliations
    Division of Cardiology and Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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  • Yung-Lung Chen
    Affiliations
    Division of Cardiology and Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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  • Tzu-Hsien Tsai
    Affiliations
    Division of Cardiology and Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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  • Ya-Hui Wang
    Affiliations
    Division of Cardiology and Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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  • Kuo-Li Pan
    Affiliations
    Division of Cardiology and Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, Republic of China
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      Atrial fibrillation (AF) may be caused by structural and electrophysiological changes in the atria induced by inflammation. This study analyzed 35 adult patients with symptomatic severe mitral valve disease and moderate-to-severe tricuspid valve disease and without coronary artery disease who underwent valve operations for congestive heart failure; 18 patients had persistent AF and 17 patients had no history or electrocardiogram examination of AF before surgery. Atrial appendageal tissues obtained during surgery were evaluated for histopathological changes. The number of inflammatory cells identified as CD45-positive cells in the right atrial myocardium in the AF group (7.5 ± 7.5 cells per high power field) was significantly higher than that of normal controls (2.7 ± 1.5 cells per high power field, p = 0.0018). The number of inflammatory cells in the right atrial myocardium did not differ between the sinus group and normal controls (2.7 ± 1.5 vs 2.6 ± 2.2 cells per high power field, p >0.05). Additionally, the number of inflammatory cells in the atrial myocardium did not differ between the right and left atria in patients with AF (7.5 ± 7.5 cells per high power field for right atria vs 7.1 ± 4.2 cells per high power field for left atria, p = 0.7563). Moreover, correlation analysis revealed a significant association between the number of inflammatory cells in the right atrial myocardium and the number of inflammatory cells in the left atrial myocardium in patients with AF (r = 0.6145, p = 0.0067). In conclusion, inflammatory cell infiltration increases in the atrial myocardium of patients with AF.
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