[1]许少华,张曼,综述,等.晚钠电流与舒张性心力衰竭[J].心血管病学进展,2016,(2):213-216.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.030]
 XU Shaohua,ZHANG Man,ZHANG Jin,et al.Late Sodium Current and Diastolic Heart Failure[J].Advances in Cardiovascular Diseases,2016,(2):213-216.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.030]
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晚钠电流与舒张性心力衰竭()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2016年2期
页码:
213-216
栏目:
综述
出版日期:
2016-04-20

文章信息/Info

Title:
Late Sodium Current and Diastolic Heart Failure
作者:
许少华12张曼12综述张进12王礼琳12审校
1.昆明理工大学附属医院,云南 昆明 650032; 2.昆明理工大学医学院,云南 昆明 650550
Author(s):
XU Shaohua12ZHANG Man12ZHANG Jin12WANG Lilin12
1.Kunming University of Science and Technology Affiliated Hospital,Kunming 650032,Yunnan,China; 2.Medical College of Kunming University of Science and Technology,Kunming 650500,Yunnan,China
关键词:
心血管病学 晚钠电流 舒张性心力衰竭
Keywords:
Cardiovascular diseases Late sodium current Diastolic heart failure
分类号:
R541.6
DOI:
10.16806/j.cnki.issn.1004-3934.2016.02.030
文献标志码:
A
摘要:
近年来,临床有越来越多心力衰竭患者伴左室射血分数正常,这使舒张性心力衰竭迅速演变成一个临床重要的独立病症,引起人们的广泛关注。晚钠电流的异常增强会引起心肌细胞内的钙离子超载,从而导致心脏的舒张功能出现障碍。现就舒张性心力衰竭和晚钠电流之间的关系做一综述。
Abstract:
In recent years,more and more patients with heart failure with normal left ventricular ejection fraction.This makes the diastolic heart failure quickly evolved into an important independent clinical symptoms and aroused people's wide attention.Late sodium current cause myocardial intracellular calcium overload, causing problems to the diastolic function of the heart.In the study, we review the relationship between the late sodium current and diastolic heart failure.

参考文献/References:

[1] Owan TE,Hodge DO,Herges RM,et al.Trends in prevalence and outcome of heart failure with preserved ejection fraction[J].N Engl J Med,2006,355(3):251-259.
[2] Kitzman DW.Heart failure with normal systolic function[J].Clin Geriatr Med,2000,16(3):489-512.
[3] Trenor B, Cardona K, Gomez JF, et al.Simulation and mechanistic investigation of the arrhythmogenic role of the late sodium current in human[J].PLoS One, 2012,7(3):e32659.
[4] Denac H,Mevissen M,Scholtysik G.Structure,function and pharmacology of voltage-gated sodium channels[J].Naunyn Schmiedebergs Arch Pharmacol,2000,62(6):453-479.
[5] Schwarz N, Hahn A, Bast T,et al.Mutations in the sodium channel gene SCN2A cause neonatal epilepsy with late-onset episodic ataxia[J].J Neurol,2015,1(1):1-2.
[6] Todt H, Dudley SC Jr, Kyle JW,et al.Ultra-slow inactivation in mu1 Na+ channels is produced by a structural rearrangement of the outer vestibule[J].Biophys J,1999,76(3):1335-1345.
[7] Maltsev VA, Kyle JW, Mishra S, et al.Molecular identity of the late sodium current in adult dog cardiomyocytes identified by Nav1.5 antisense inhibition[J].Am J Physiol Heart Circ Physiol,2008,295(2):H667-676.
[8] Yang T,Atack TC,Stroud DM,et al.Blocking SCN10A channels in heart reduces late sodium current and is antiarrhythmic[J].Circ Res,2012,111(3):322-332.
[9] Kornyeyev D,El-Bizri N,Hirakawa R,et al.Contribution of the late sodium current to intracellular sodium and calcium overload in rabbit ventricular myocytes treated by anemone toxin[J].Am J Physiol Heart Circ Physiol,2015,37(62):27-32.
[10] London B.Whither art thou,SCN10A,and what art thou doing?[J].Circ Res,2012, 111(3):268-270.
[11] Noble D,Noble PJ.Late sodium current in the pathophysiology of cardiovascular disease:consequences of sodium-calcium overload[J].Heart,2006,92(suppl 4):iv1-iv5.
[12] Holm H,Gudbjartsson DF,Arnar DO,et al.Several common variants modulate heart rate, PR interval and QRS duration[J].Nat Genet,2010,42(2):117-122.
[13] Maier LS.New treatment options for late Na current, arrhythmias,and diastolic dysfunction[J].Curr Heart Fail Rep,2012,9(3):183-191.
[14] Ju YK, Saint DA, Gage PW.Hypoxia increases persistent sodium current in rat ventricular myocytes[J].J Physiol,1996,497(2):337-347.
[15] Chen Y,Yu FH,Surmeier DJ,et al.Neuromodulation of Na+ channel slow inactivation via cAMP-dependent protein kinase and protein kinase C[J].Neuron,2006,49(3):409-420.
[16] Moreno JD, Clancy CE.Pathophysiology of the cardiac late Na current and its potential as a drug target[J].J Mol Cell Cardiol,2012,52(3):608-619.
[17] Mishra S, Undrovinas NA, Maltsev VA, et al.Post-transcriptional silencing of SCN1B and SCN2B genes modulates late sodium current in cardiac myocytes from normal dogs and dogs with chronic heart failure[J].Am J Physiol Heart Circ Physiol,2011,301(4):H1596-1605.
[18] Bai Y,Morgan EE,Giovannucci DR,et al.Different roles of the cardiac Na+/Ca2+-exchanger in ouabain-induced inotropy, cell signaling, and hypertrophy[J].Am J Physiol Heart Circ Physiol,2013,304(3):H427-435.
[19] Wu Y, Wang L, Ma J,et al.Protein kinase C and Ca2+-calmodulin-dependent protein kinase Ⅱ mediate the enlarged reverse INCX induced by ouabain-increased late sodium current in rabbit ventricular myocytes[J].Exp Physiol,2015,100(4):399-409.
[20] Wagner S, Dybkova N, Rasenack EC,et al.Ca2+/calmodulin-dependent protein kinase Ⅱ regulates cardiac Na+ channels[J].J Clin Invest,2006,116(12):3127-3138.
[21] Zhang XQ, Yamada S,Barry WH.Ranolazine inhibits an oxidative stress-induced increase in myocyte sodiumand calcium loading during simulated-demand ischemia[J].J Cardiovasc Pharmacol,2008,51(5):443-449.
[22] Sossalla S, Maurer U, Schotola H, et al.Diastolic dysfunction and arrhythmias caused by overexpression of CaMKⅡδC can be reversed by inhibition of late Na+ current[J].Basic Res Cardiol, 2011,106(2):263-272.
[23] Sossalla S,Fluschnik N,Schotola H,et al.Inhibition of elevated Ca2+/calmodulin-dependent protein kinase Ⅱ improves contractility in human failing myocardium[J].Circ Res,2010,107(9):1150-1161.
[24] Anderson ME,Brown JH,Bers DM.CaMKⅡ in myocardial hypertrophy and heart failure[J].J Mol Cell Cardiol,2011,151(4):468-473.
[25] Pourrier M, Williams S, McAfee D,et al.CrossTalk proposal:the late sodium current is an important player in the development of diastolic heart failure[J].J Physiol,2014,592(3):411-414.
[26] Belardinelli L,Liu G,Smith-Maxwell C,et al.A novel,potent,and selective inhibitor of cardiac late sodium current suppresses experimental arrhythmias[J].J Pharmacol Exp Ther,2013,344(1):23-32.
[27] Sossalla S, Kallmeyer B, Wagner S, et al.Altered Nat-currents in atrial fibrillation: effects of ranolazine on arrhythmias and contractility in human atrial myocardium[J].J Am Coll Cardiol,2010,55(21):2330-2342.
[28] Sicouri S, Glass A, Belardinelli L,et al.Antiarrhythmic effects of ranolazine in canine pulmonary vein sleeve preparations[J].Europace,2008,5(7):1019-1026.
[29] Adakkak M, Camara AK, Heisner JS,et al.Ranolazine reduces Ca2+ overload and oxidative stress and improves mitochondrial intergrity to protect against ischemia reperfusion injury in isolated hearts[J].Pharmacol Res,2011,64(4):381-392.
[30] Figueredo VM, Pressman GS, Romero-Corral A, et al.Improvement in left ventricular systolic and diastolic performance during ranolazine treatment in patients with stable angina[J].Cardiovasc Pharmacol Ther,2011,16(2):168-172.
[31] Maier LS, Layug B, Karwatowska-Prokopczuk E,et al.RAnoLazIne for the treatment of diastolic heart failure in patients with preserved ejection fraction: the RALI-DHF proof-of-concept study[J].JACC Heart Fail,2013,1(2):115-122.
[32] Jacobshagen C,Belardinelli L,Hasenfuss G,et al.Ranolazine for the treatment of heart failure with preserved ejection fraction:background,aims,and design of the RALI-DHF study[J].Clin Cardiol,2011,34(7):426-432.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金项目(81360039); 云南省心律失常诊治研究中心研究基金项目(2014NS260,2014NS259) 作者简介:许少华(1988—),在读硕士,主要从事心肌细胞电生理、移植免疫学研究。Email:huashao412@163.com 通信作者:张进(1976—),住院医师,主要从事心肌电生理研究。Email:zhangjinxy@sina.com
更新日期/Last Update: 2016-03-25