我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

心房颤动患者心房组织醛固酮和心房基质重构研究

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第1期
页码:
41-45
栏目:
基础研究
出版日期:
2009-02-28

文章信息/Info

Title:
Atrial tissue aldosterone level and atrial extracellular matrix remodeling in patients with atrial fibrillation
作者:
裴德安1; 李莉2; 徐志云2; 黄进宇1; 徐正明1; 王敏1; 姚强1; 黄世恩1; 黄琪1
1.杭州市红十字会医院心内科，浙江 杭州 310003； 2.第二军医大学附属上海长海医院胸心外科，上海 200433
Author(s):
PEI De-an;  LI Li;  XU Zhi-yun;  HUANG Jin-yu;  XU Zheng-ming;  WANG Min;  YAO Qiang;  HUANG Shi-en;  HUANG Qi
Department of Cardiology, Hangzhou Red Cross Hospital, Hangzhou 310003, Zhejiang, China
关键词:
心房颤动;  醛固酮; 心房基质重构; 胶原
Keywords:
atrial fibrillation;  aldosterone;  atrial remodeling;  collagen
分类号:
R541.75
DOI:
-
文献标识码:
A
摘要:
目的 探讨心房颤动患者心房组织醛固酮水平和心房基质重构的相关关系。方法 入选行人工瓣膜置换术的风湿性心脏病患者25例，其中窦性心律者12例，慢性心房颤动者（房颤时程≥6月）13例。术前进行经胸超声心动图检查并留取有关资料，于手术时取左右心房侧壁组织，用放射免疫法测定心房组织醛固酮水平；用VG染色法对总胶原容量分数（CVF）半定量分析；RT-PCR检测Ⅰ型和Ⅲ型胶原mRNA表达改变。结果 与窦性心律者比较心房颤动组左房内径显著扩大（均P<0.01）；心房肌组织醛固酮［右房：(310.3±69.6) vs (154.5±35.8)pg/g,左房：(334.2±76.6) vs (166.5±38.6)pg/g，均P<0.01］、Ⅰ型胶原mRNA表达［右房：(1.95±0.22) vs (0.71±0.11)，左房：(2.05±0.28) vs (0.74±0.16),均P<0.01］和CVF［右房：(13.0±1.9)％ vs (6.5±1.1)％，左房：(14.1±1.7)％ vs (6.7±1.2)％，均P<0.01］均明显增加；Ⅲ型胶原mRNA表达在房颤组和窦性心律组间无差异；上述指标在左、右心房之间无差异。Ⅰ型胶原mRNA与左心房直径（r＝0.885，P<0.01）、CVF和左心房直径（r＝0.845，P<0.01）均显著正相关；心房组织醛固酮水平与左心房内径（r＝0.814，P<0.01）和CVF（r＝0.885，P<0.01）均呈明显正相关。结论 心房组织醛固酮水平可能在心房颤动心房基质重构中起重要作用，并可能参与了心房颤动的发生和维持。
Abstract:
AIM To investigate atrial tissue aldosterone level and atrial extracellular matrix remodeling in patients with atrial fibrillation and to evaluate the effects of aldosterone on the progress of atrial structural remodeling. METHODS Twenty-five patients with rheumatic heart valve disease, 12 in sinus rhythm and 13 in chronic atrial fibrillation (≥6 months), underwent transthoracic echocardiography and right and left atrial lateral wall tissue samples were obtained from these patients during mitral/aortic valve replacement operation. Radioimmunoassay was used to determine tissue aldosterone level in local atria. The mRNA expression of Type Ⅰor Ⅲ collagen and total collagen volume fraction (CVF) were analyzed by RT-PCR and VG staining respectively. RESULTS The left atrial diameters increased markedly in the atrial fibrillation as compared to sinus rhythm (P<0.01). The results suggested that atrial tissue aldosterone level \[(310.3±69.6) vs (154.5±35.8) pg/g in right atria, (334.2±76.6) vs (166.5±38.6) pg/g in left atria, both P<0.01\], the mRNA expression of TypeⅠcollagen \[(1.95±0.22) vs (0.71±0.11) in right atria, (2.05±0.28) vs (0.74±0.16) in left atria, both P<0.01) and total CVF \[(13.0±1.9)％ vs (6.5±1.1)％ in right left, (14.1±1.7)％ vs (6.7±1.2)％ in left atria, both P<0.01) all increased significantly in atrial fibrillation groups compared with those in sinus rhythm, whereas the mRNA expression of type Ⅲ collagen remained compatible within groups. No significant difference was found in aldosterone, the mRNA expression of typeⅠcollagen and total CVF between left atria and right atria both in fibrillation and sinus groups. There were significant positive correlation between typeⅠ collagen mRNA expression and left atrial dimension, CVF and left atrial dimension, and the correlation coefficient r was 0.885 and 0.845 respectively (both P<0.01). Tissue aldosterone in local atria also significantly was correlated with left atrial dimension（r＝0.814， P<0.01） and CVF（r＝0.885， P<0.01）. CONCLUSION Aldosterone in local atria may promote the process of atrial matrix remodeling and probably participate in the mediation and persistence of atrial fibrillation.

参考文献/References

[1］ Spach MS. Mounting evidence that fibrosis generates a major mechanism for atrial fibrillation［J］. Circ Res, 2007, 101(8):743-745.
［2］ Healey JS, Morillo CA, Connolly SJ. Role of the renin-angiotensin-aldosterone system in atrial fibrillation and cardiac remodeling［J］. Cur Opin Cardiol, 2005, 20(1):31-37.
［3］ Birnie DH, Gollob M, Healey JS. Clinical trials, the renin angiotensin system and atrial fibrillation［J］. Curr Opin Cardiol, 2006, 21(4):368-375.
［4］ Connell JM, Davies E. The new biology of aldosterone［J］. J Endocrinol, 2005, 186(1):1-20.
［5］ Goette A, Haffmanns P, Enayati W, et al. Effect of successful electrical cardioversion on serum aldosterone in patients with persistent atrial fibrillation［J］. Am J Cardiol, 2001, 88(8):906-909.
［6］ 裴德安，李莉. 心房颤动总是引发心房颤动吗［J］. 国际心血管病杂志（原国外医学心血管病分册）, 2006, 33（3）：166-169.
［7］ Kostin S, Klein G, Szalay Z, et al. Structural correlate of atrial fibrillation in human patients［J］. Cardiovasc Res, 2002, 54(2):361-379.
［8］ Everett TH 4th, Li H, Mangrum JM, et al. Electrical, morphological and ultrastructural remodeling and reverse remodeling in a canine model of chronic atrial fibrillation［J］. Circulation, 2000, 102(12):1454-1460.
［9］ Verheule S, Sato T, Everett T 4th, et al. Increased vulnerability to atrial fibrillation in transgenic mice with selective atrial fibrosis caused by overexpression of TGF-beta1［J］. Circ Res, 2004, 94(11):1458-1465.
［10］Lombes M, Alfaidy N, Eugene E, et al. Prerequisite for aldosterone action: mineralocorticoid receptor and 11beta-hydroxysteroid dehydrogenase in the human heart［J］. Circulation, 1995, 92(2):175-182.
［11］Milliez P, Girerd X, Plouin PF, et al. Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism［J］. J Am Coll Cardiol, 2005, 45(8):1243-1248.
［12］Lee YS, Kim JA, Kim KL, et al. Aldosterone upregulates connective tissue growth factor factor gene expression via p38 MAPK pathway and mineralocorticoid receptor in ventricular myocytes［J］. J Korean Med Sci, 2004, 19(6):805-811.
［13］Rude MK, Duhaney TA, Kuster GM, et al. Aldosterone stimulates matrix metalloproteinases and reactive oxygen species in adult rat ventricular cardiomyocytes［J］. Hypertension, 2005, 46(3):555-561.
［14］Sugiyama T, Yoshimoto T, Tsuchiya K, et al. Aldosterone induces angiotensin converting enzyme (ACE) gene expression via JAK2-dependent pathway in rat endothelial cells［J］. Endocrinology, 2005, 146(9):3900-3906.
［15］Shroff SC, Ryu K, Martovitz NL, et al. Selective aldosterone blockade suppresses atrial tachyarrhythmias in heart failure［J］. J Cardiovasc Electrophysiol, 2006, 17(5):534-541.

备注/Memo

备注/Memo:
收稿日期：2007-10-31.通讯作者：裴德安，副主任医师，博士，主要从事心律失常和心电生理研究Email:smmu.peidean@126.com
更新日期/Last Update: 2009-04-02