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|本期目录/Table of Contents|

心肌梗死后左室重构发病机制进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2018年第2期
页码:
222-224
栏目:
综述
出版日期:
2018-02-15

文章信息/Info

Title:
Progress in left ventricular remodeling after myocardial infarction
作者:
陈启龙1; 2; 王海昌1; 2; 孙冬冬1; 2
(第四军医大学:1.第二附属医院心血管内科,陕西 西安 710038，2.第一附属医院心血管内科,陕西 西安 710032)
Author(s):
CHEN Qi-long1; 2;  WANG Hai-chang1; 2;  SUN Dong-dong1; 2
(1.Department of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi’an 710038, Shaanxi, China; 2.Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
心肌梗死; 左室重构
Keywords:
myocardial infarction;  left ventricular remodeling
分类号:
R541.4
DOI:
-
文献标识码:
A
摘要:
急性心肌梗死(AMI)是威胁人类健康的重大疾病，心肌梗死(MI)后30 min，部分心肌细胞即发生不可逆的坏死，因此，MI有效救治的时间窗极为短暂，许多患者不能够得到及时有效的治疗，使得MI后心力衰竭(HF)的发生率仍然居高不下。最新调查研究表明，MI后1年HF的发生率约为14.2%。因MI后HF再次入院的患者，1年死亡率高达为45.5%。MI后HF的主要原因是部分心肌细胞坏死，左室重构，心脏扩张，继而引发HF。目前，MI后左室重构的机制尚未完全阐明。本文介绍了AMI后左室重构的发病机制主要进展。
Abstract:
Acute myocardial infarction is a major threat to human health. Cardiomyocytes develop irreversible death 30 minutes after myocardial infarction. Therefore, the time window of myocardial infarction treatment is very short. Many patients do not receive timely and effective treatment and, as a result, the incidence of heart failure after myocardial infarction is still high. The incidence of heart failure 1 year after myocardial infarction was about 14.2%. In patients with heart failure after myocardial infarction, the 1 year mortality rate is 45.5%. The main pathogenesis of heart failure after myocardial infarction includes cardiomyocyte death, left ventricular remodeling, cardiac dilatation and subsequent heart failure. However, the mechanism of left ventricular remodeling after myocardial infarction has not been fully elucidated. In this review, description of major research progress is discussed in the pathogenesis of left ventricular remodeling after acute myocardial infarction.

参考文献/References

[1] Hockman JS,Bulkley BH.Expansion of acute myocardial infarction:an experimental study[J].Circulation,1982,65(7):1446-1450.

[2]Pfeffer JM,Pfeffer MA,Braunwald E. Influence of chronic captopril therapy on the infarcted left ventricle of the rat[J].Circ Res,1985,57(1):84-95.

[3]Cohn JN,Ferrari R,Sharpe N. Cardiac remodeling-concepts and clinical implications:a consensus paper from an international forum on cardiac remodeling. Behalf of an International Forum on Cardiac Remodeling[J].J Am Coll Cardiol,2000,35(3):569-582.

[4]Rischpler C.Acute myocardial infarction[J].Q J Nucl Med Mol Imaging,2016,60(3):236-251.

[5]Benjamin EJ,Blaha MJ,Chiuve SE,et al.Heart Disease and Stroke Statistics-2017 Update:A Report From the American Heart Association[J].Circulation,2017,135(10):e146-e603.

[6]Cohn JN,Ferrari R,Sharpe N.Cardiac remodeling-concepts and clinical implications:a consensus paper from an international forum on cardiac remodeling. Behalf of an International Forum on Cardiac Remodeling[J].J Am Coll Cardiol,2000,35(3):569-582.

[7]Anand IS,Florea VG,Solomon SD,et al.Noninvasive assessment of left ventricular remodeling:concepts, techniques and implications for clinical trials[J].J Card Fail,2002,8(6 Suppl):S452-S464.

[8]Levine B,Klionsky DJ.Development by self-digestion:molecular mechanisms and biological functions of autophagy[J].Dev Cell,2004,6(4):463-477.

[9]Nakai A,Yamaguchi O,Takeda T,et al.The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress[J].Nat Med,2007,13(5):619-624.

[10]Matsui Y,Takagi H,Qu X,et al.Distinct roles of autophagy in the heart during ischemia and reperfusion:roles of AMP-activated protein kinase and Beclin 1 in mediating autophagy[J].Circ Res,2007,100(6):914-922.

[11]Zhu H,Tannous P,Johnstone JL,et al.Cardiac autophagy is a maladaptive response to hemodynamic stress[J].J Clin Invest,2007,117(7):1782-1793.

[12]Lavandero S,Chiong M,Rothermel BA,et al.Autophagy in cardiovascular biology[J].J Clin Invest,2015,125(1):55-64.

[13]Orogo AM,Gustafsson ?B.Therapeutic targeting of autophagy:potential and concerns in treating cardiovascular disease[J].Circ Res,2015,116(3):489-503.

[14]Gatica D,Chiong M,Lavandero S,et al.Molecular mechanisms of autophagy in the cardiovascular system[J].Circ Res,2015,116(3):456-467.

[15]Nishida K,Taneike M,Otsu K.The role of autophagic degradation in the heart[J].J Mol Cell Cardiol,2015,78:73-79.

[16]Maejima Y,Kyoi S,Zhai P,et al.Mst1 inhibits autophagy by promoting the interaction between Beclin1 and Bcl-2[J].Nat Med,2013,19(17):1478-1488.

[17]Hu J,Zhang L,Zhao Z,et al.OSM mitigates post-infarction cardiac remodeling and dysfunction by up-regulating autophagy through Mst1 suppression[J].Biochim Biophys Acta,2017,1863(8):1951-1961.

[18]Lopaschuk GD,Ussher JR,Folmes CD,et al.Myocardial fatty acid metabolism in health and disease[J].Physiol Rev,2010,90(1):207-258.

[19]Wan A,Rodrigues B.Endothelial cell-cardiomyocyte crosstalk in diabetic cardiomyopathy[J].Cardiovasc Res,2016,111(3):172-183.

[20]Campos DH,Leopoldo AS,Lima-Leopoldo AP,et al.Obesity preserves myocardial function during blockade of the glycolytic pathway[J].Arq Bras Cardiol,2014,103(4):330-337.

[21]Azevedo PS,Minicucci MF,Santos PP,et al.Energy metabolism in cardiac remodeling and heart failure[J].Cardiol Rev,2013,21(3):135-140.

[22]Deb A,Ubil E.Cardiac fibroblast in development and wound healing[J].J Mol Cell Cardiol,2014,70:47-55.

[23]Spinale FG,Janicki JS,Zile MR.Membrane-associated matrix proteolysis and heart failure[J].Circ Res,2013,112(1):195-208.

[24]Sayer G,Bhat G.The renin-angiotensin-aldosterone system and heart failure[J].Cardiol Clin,2014,32(1):21-32.

[25]Albuquerque FN, Brand?o AA,Silva DA,et al.Angiotensin-converting enzyme genetic polymorphism:its impact on cardiac remodeling[J].Arq Bras Cardiol,2014,102(1):70-79.

[26]Florea VG,Cohn JN.The autonomic nervous system and heart failure[J].Circ Res,2014,114(11):1815-1826.

备注/Memo

备注/Memo:
收稿日期：2017-06-01.通讯作者：孙冬冬，副教授，主要从事冠心病疾病研究 Email：51483696@qq.com 作者简介：陈启龙，住院医师，硕士生 Email：87163161@qq.com
更新日期/Last Update: 1900-01-01