Arrhythmias and conduction disturbance
Increased Inflammatory Cell Infiltration in the Atrial Myocardium of Patients With Atrial Fibrillation

https://doi.org/10.1016/j.amjcard.2008.05.038Get rights and content

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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Patient population

This study examined consecutives series of patients with severe symptomatic mitral valve disease and moderate-to-severe tricuspid valve disease who underwent valve surgery for congestive heart failure. Exclusion factors included previous myocardial infarction, febrile disorder, infectious or inflammatory disease, autoimmune disease, malignancy, chronic renal failure (serum creatinine >2.5 mg/dl), acute or chronic viral hepatitis, or use of immunosuppressive drugs; 18 patients had persistent AF

Baseline characteristics of patients studied

Table 1, Table 2 list the clinical characteristics of the study patients. The 2 groups did not significantly differ in age, gender, body mass index, or heart failure status. The percentage of patients taking angiotensin-converting enzyme inhibitor or type I angiotension receptor blocker was significantly higher in the sinus group than in the AF group. The percentages of patients taking β blocker and digitalis were significantly higher in the AF group than in the sinus group. The preoperative

Discussion

This study examined the association of inflammatory cell infiltration in the atrial myocardium with AF in patients with mitral and tricuspid valve disease. This study is the first to demonstrate increased inflammatory cell infiltration (identified by a specific marker, i.e., CD45 for inflammatory cells) in the right and left atrial myocardium in patients with AF.

Whether inflammation is a cause of AF or merely a consequence is currently unknown. The contribution of the inflammatory cascade to

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This study was supported by program grants from the National Science Council, Taiwan, Republic of China under the contract number NSC 93-2314-B-182A-138.

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