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|本期目录/Table of Contents|

肥厚梗阻型心肌病猝死家族史患者心肌中Cx43表达变化

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第5期
页码:
552-555
栏目:
临床研究
出版日期:
2016-04-25

文章信息/Info

Title:
Clinical significance of Cx43 expression of myocardium from patients with obstructive hypertrophic cardiomyopathy and family history of sudden death
作者:
王晓武; 梁宏亮; 支伟伟; 苏 洁; 卢林鹤; 张金洲; 俞世强
（第四军医大学西京医院心血管外科，陕西 西安 710032）
Author(s):
WANG Xiao-wu;  LIANG Hong-liang;  ZHI Wei-wei;  SU Jie;  LU Lin-he;  ZHANG Jin-zhou;  YU Shi-qiang
(Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
肥厚梗阻型; 心肌病; 猝死; 家族史; 连接蛋白43
Keywords:
obstructive hypertrophy;  cardiomyopathy;  sudden death;  family history;  connexin 43
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的 通过观察猝死家族史肥厚型心肌病患者心肌中Cx43和TGFβ-1表达的改变，初步研究肥厚型心肌病猝死的可能机制。方法 分别选取猝死家族史肥厚型心肌病患者心肌组织（FHSD组,n=5）,非猝死家族史肥厚型心肌病患者心肌组织（NFHSD组,n=5）和非肥厚型心肌病患者心肌组织（NHCM组,n=5）作为研究样本（均获患者家属知情同意），应用Western blot和免疫组织化学方法检测心肌组织Cx43和TGFβ-1表达。结果 Western blot结果显示，FHSD组、NFHSD组心肌组织Cx43表达与NHCM组患者相比均显著性增高（P<0.01），NFHSD组Cx43表达明显高于FHSD组（P<0.05）；FHSD组、NFHSD组心肌组织TGF-β1表达与NHCM相比均显著性降低（P<0.01）；NFHSD组TGF-β1表达与FHSD组相比较无显著性差异。免疫组织化学结果与Western blot相同。结论 肥厚型心肌患者猝死的机制是否与心肌细胞Cx43表达在代偿期突然降低有关，尚需进一步研究。
Abstract:
AIM To preliminarily investigate the mechanisms underlying sudden death (SD) of hypertrophic cardiomyopathy (HCM) through analysis of the expression of Cx43 and TGFβ-1 in myocardium from patients with HCM and family history of sudden death (FHSD). METHODSSamples included five patients with HCM and FHSD, five patients with HCM and non-FHSD (NFHSD) and five patients with non-HCM (NHCM). Western blot and immunohistochemistry were used to detect the expression of Cx43 and TGFβ-1. RESULTSFor Western blot, expression of Cx43 in the FHSD and NFHSD group was much higher than in the NHCM group (P<0.01), and Cx43 in the NFHSD group was higher than in the FHSD group (P<0.05). However, expression of TGF-β1 in FHSD and NFHSD group was much lower than in the NHCM group (P<0.01), but there was no statistical significance between NFHSD and FHSD group. For immunohistochemistry, the findings were similar to Western blot. CONCLUSIONChanges of Cx43 in myocardium may be one of the causes leading to sudden death of HCM and TGF-β1 may mediate the changes of Cx43 in hypertrophic cardiomyopathy.

参考文献/References

[1]Maron BJ.Contemporary insights and strategies for risk stratification and prevention of sudden death in hypertrophic cardiomyopathy[J].Circulation,2010,121(3):445-456.
[2]O’Mahony C,Elliott P,McKenna W.Sudden Cardiac Death in Hypertrophic Cardiomyopathy[J].Circ Arrhythm Electrophysiol,2013,6(2):443-451.
[3]Severs NJ,Coppen SR,Dupont E,et al.Gap junction alterations in human cardiac disease[J].Cardiovasc Res,2004,62(2):368-377.
[4]Fontes MS, van Veen TA, de Bakker JM, et al. Functional consequences of abnormal Cx43 expression in the heart[J].Biochim Biophys Acta,2012,1818(8):2020-2029.
[5]Gersh BJ,Maron BJ,Bonow RO,et al.2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy:A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in collaboration with the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons[J].JACC,2011,58(25):e212-e260.
[6]O'Mahony C,Jichi F,Pavlou M, et al. A novel clinical risk prediction model for sudden cardiac death in hypertrophic cardiomyopathy (HCM risk-SCD)[J].Eur Heart J,2014,35(30):2010-2020.
[7]杨金保,梁宏亮,孟 欣,等.改良Morrow手术治疗21例肥厚梗阻型心肌病临床分析[J].心脏杂志,2015,27(4):467-469.
[8]Maron BJ,Spirito P,Ackerman MJ,et al.Prevention of Sudden Cardiac Death With Implantable Cardioverter-Defibrillators in Children and Adolescents With Hypertrophic Cardiomyopathy[J].J Am CollCardiol,2013,61(14):1527-1535.
[9]O'Mahony C,Lambiase PD,Quarta G,et al.The long-term survival and the risks and benefits of implantable cardioverter defibrillators in patients with hypertrophic cardiomyopathy[J].Heart,2012,98(30):116-125.
[10]Kostin S,Dammer S,Hein S,et al.Connexin 43 expression and distribution in compensated anddecompensated cardiac hypertrophy in patients with aortic stenosis[J].Cardiovasc Res,2004,62(2):426-436.
[11]Rosenkranz S.TGF-h1 and angiotensin networking in cardiac remodeling[J].Cardiovasc Res,2004,63(3):423- 432.
[12]Saffitz JE,Kléber AG.Effects of Mechanical Forces and Mediators of Hypertrophyon Remodeling of Gap Junctions in the Heart[J].Circ Res,2004,94(5):585-591.

备注/Memo

备注/Memo:
收稿日期：2015-07-30.基金资助：国家自然科学基金项目资助(81170058)；西京医院临床新技术新业务项目资助（XJGX13LC08）
通讯作者：张金洲，副教授，主要从事肥厚梗阻型心肌病外科治疗研究 Email：jinzhouzhang2006@126.com 共同
通讯作者：俞世强，教授，主要从事微创心脏疾病外科治疗研究 Email：yushiq@fmmu.edu.cn
作者简介：王晓武，高级实验师，博士 Email：1774754900@qq.com
更新日期/Last Update: 2016-04-13