目的：炎症反应在心房颤动（简称房颤）发生、发展和维持中扮演重要角色，但在房颤患者尤其是瓣膜性房颤患者中，究竟何种因素促进了炎症反应尚不清楚。文中探讨多配体蛋白聚糖-4（ Syndecan-4）脱落在瓣膜性房颤患者左心房炎症反应中的作用。方法选取先天性心脏病但无瓣膜病变及房颤患者为对照组（ n＝10），60名择期行瓣膜置换术或瓣膜成形术的瓣膜性心脏病患者，分为窦性心律组（n＝20）、阵发性房颤组（n＝20）及持续性房颤组（n＝20）。记录患者基本临床资料，术中获取患者少量左心房组织，采用Western blot检测左心房中诱导型一氧化氮合酶（ inducible nitric oxide synthase ， iNOS）、高迁移率族蛋白B1（high mobility group protein B1， HMGB1）和Syndecan-4含量，HE染色观察左心房组织病理学变化。结果经Western blot检测，阵发性房颤组和持续性房颤组 iNOS表达水平（1．61±0．10）、（1．67±0．08）较对照组（1．02±0．12）和窦性心律组（1．06±0．11）明显升高，HMGB1表达水平（0．63±0．05）、（0．95±0．10）也较对照组（0．46±0．06）和窦性心律组（0．45±0．07）明显升高，炎症细胞浸润增加，Syndecan-4表达水平明显降低，差异有统计学意义（P＜0．05）。结论瓣膜性房颤患者左心房组织Syndecan-4表达降低，炎症反应增加，提示Syndecan-4脱落可能是左心房局部炎症反应发生发展的潜在机制。%Objective Inflammation plays a critical role in the presence , development and maintenance of atrial fibrillation ( AF) , but it remains unclear what factors induce inflammation in AF patients , especially in those with valvular heart disease ( VHD) . The aim of this paper was to investigate the role of the shedding of Syndecan -4 in left atrial inflammation in patients with valvular atrial fibrillation. Methods Sixty VHD patients scheduled for valvuloplasty or valve replacement surgery were divided into three groups of equal number:sinus rhythm (SR), paroxysmal atrial fibrillation (PaAF), and persistent atrial fibrillation (PeAF).Another 10 pa-tients with congenital heart disease but no valve damage and atrial fibrillation were included in a control group .Baseline clinical data were recorded and tissues were obtained from the left atrial appendage during operation .The expressions of iNOS , HMGB1, and Syn-decan-4 in the left atrium were detected by Western blot , and the pathological changes of the left atrial tissue observed by HE staining . Results Western blot analysis was performed to detect expression levels of proteins .The iNOS level was significantly higher in pa-tients from the paroxysmal AF group (1.61 ±0.10) and persistent AF group (1.67 ±0.08) than those from sinus group (1.06 ± 0.11) and control group (1.02 ±0.12), as was the protein level of HMGB1 (0.63 ±0.05, 0.95 ±0.10, 0.45 ±0.07 and 0.46 ± 0.06 in paroxysmal AF group, persistent AF group, sinus group and controlgroup respectively ).Inflammatory cell infiltration in-creased, while syndecan 4 was down-regulated in AF groups.All these comparisons were significant (P<0.05). Conclusion The decreased expression of Syndecan-4 and enhanced inflammatory response in the left atrial tissue indicate that the shedding of Synde-can-4 may play a role in the presence and development of inflamma-tion in the left atrium .
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