尖端扭转型室性心动过速与临床
摘要
尖端扭转型室性心动过速临床并不少见,虽建立在心脏异质性增大基础上的Q-T间期延长被认为是其发生的主要原因,但对其发生机制仍意见不一。该现象是触发于心肌动作电位时程超常期,原发于心内膜的病变在心脏异质性增大时,因兴奋频率低于心外膜,心脏自身调节抑制心肌电紊乱的基础上,出现心律失常起源点游移于心内膜与心外膜之间,进而出现相应心电图改变。心肌缺血、缺氧、离子通道变异、内环境紊乱及药物因素等均可致心脏异质性增大。如何去除诱因,降低心脏异质性,保证心脏复极同步是治疗的关键。
引文
[1]Khan Q,Ismail M,Haider I,et al.QT interval prolongation in hospitalized patients on cardiology wards:a prospective observational study[J].Eur J Clin Pharmacol,2017,73(11):1511-1518.
[2]Pourmand A,Mazer-Amirshahi M,Chistov S,et al.Emergency department approach to QTc prolongation[J].Am J Emerg Med,2017,35(12):1928-1933.
[3]丁绍祥,王智杰.心肌除复极的非同步与心律失常[J].中国老年学杂志,2017,37(9):2338-2340.
[4]Dressler FF,Brado J,Odening KE.Electromechanical heterogeneity in the heart:a key to long QT syndrome?[J].Herzschrittmacherther Elektrophysiol,2018,29(1):43-47.
[5]丁绍祥.恶性心律失常与心肌动作电位时程3相[J].医学争鸣,2018,9(5):30-33.
[6]Badri M,Patel A,Yan GX.Cellular and ionic basis of J-wave syndromes[J].Trends Cardiovasc Med,2015,25(1):12-21.
[7]Boukens BJ,Walton R,Meijborg VM,et al.Transmural electrophysiological heterogeneity,the T-wave and ventricular arrhythmias[J].Prog Biophys Mol Biol,2016,122(3):202-214.
[8]Maoz A,Christini DJ,Krogh-Madsen T.Dependence of phase-2 reentry and repolarization dispersion on epicardial and transmural ionic heterogeneity:a simulation study[J].Europace,2014,16(3):458-465.
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[11]Nˇemec J,Kim JJ,Salama G.The link between abnormal calcium handling and electrical instability in acquired long QTsyndrome--does calcium precipitate arrhythmic storms?[J].Prog Biophys Mol Biol,2016,120(1-3):210-221.
[12]丁绍祥,王智杰,王青,等.“R-on-T”现象的发生机制[J].中华心血管病杂志,2017,45(8):673-675.
[13]Aggarwal S,Randhawa PK,Singh N,et al.Role of ATP-sensitive potassium channels in remote ischemic preconditioning induced tissue protection[J].J Cardiovasc Pharmacol Ther,2017,22(5):467-475.
[14]Dunnink A,Stams TRG,Bossu A,et al.Torsade de pointes arrhythmias arise at the site of maximal heterogeneity of repolarization in the chronic complete atrioventricular block dog[J].Europace,2017,19(5):858-865.
[15]丁绍祥,祁国荣,刘品发,等.尖端扭转型室性心动过速的扭转机制[J].中华心血管病杂志,2015,43(8):670-672.
[16]Morand J,Arnaud C,Pepin JL,et al.Chronic intermittent hypoxia promotes myocardial ischemia-related ventricular arrhythmias and sudden cardiac death[J].Sci Rep,2018,8(1):2997.
[17]Lancaster MC,Sobie EA.Improved prediction of drug-induced torsades de pointes through simulations of dynamics and machine learning algorithms[J].Clin Pharmacol Ther,2016,100(4):371-379.
[18]Marill KA,Miller ES.Hypokalemia in women and methadone therapy are the strongest non-cardiologic factors associated with QT prolongation in an emergency department setting[J].J Electrocardiol,2017,50(4):416-423.
[19]Minetto D,Serratrice J,Stirnemann J.Magnesium in daily practice[J].Rev Med Suisse,2016,12(535):1761-1765.
[20]Cubeddu LX.Drug-induced inhibition and trafficking disruption of ion channels:pathogenesis of QT abnormalities and druginduced fatal arrhythmias[J].Curr Cardiol Rev,2016,12(2):141-154.
[21]Tse G,Chan YW,Keung W,et al.Electrophysiological mechanisms of long and short QT syndromes[J].Int J Cardiol Heart Vasc,2016,14:8-13.
[22]Hondeghem LM.Drug-Induced QT Prolongation and torsades de pointes:an all-exclusive relationship or time for an amicable separation?[J].Drug Saf,2018,41(1):11-17.
[23]Lazzerini PE,Laghi-Pasini F,Bertolozzi I,et al.Systemic inflammation as a novel QT-prolonging risk factor in patients with torsades de pointes[J].Heart,2017,103(22):1821-1829.
[24]丁绍祥,张宏考.β-受体阻滞剂不再降低患者死亡率吗?[J].医学争鸣,2016,7(5):28-31,33.
[25]Thomas SH,Behr ER.Pharmacological treatment of acquired QT prolongation and torsades de pointes[J].Br J Clin Pharmacol,2016,81(3):420-427.
[26]丁绍祥,张宏考,王智杰,等.利多卡因能相对延长心肌有效不应期吗?[J].医学争鸣,2017,8(1):49-52.
[27]Pourmand A,Mazer-Amirshahi M,Chistov S,et al.Emergency department approach to QTc prolongation[J].Am J Emerg Med,2017,35(12):1928-1933.
[28]Said TH,Wilson LD,Jeyaraj D,et al.Transmural dispersion of repolarization as a preclinical marker of drug-induced proarrhythmia[J].J Cardiovasc Pharmacol,2012,60(2):165-171.
[29]白玉云,赵子霞,李晨刚.尖端扭转型室性心动过速三例[J].实用心脑肺血管病杂志,2015,23(3):118-119.
[2]Pourmand A,Mazer-Amirshahi M,Chistov S,et al.Emergency department approach to QTc prolongation[J].Am J Emerg Med,2017,35(12):1928-1933.
[3]丁绍祥,王智杰.心肌除复极的非同步与心律失常[J].中国老年学杂志,2017,37(9):2338-2340.
[4]Dressler FF,Brado J,Odening KE.Electromechanical heterogeneity in the heart:a key to long QT syndrome?[J].Herzschrittmacherther Elektrophysiol,2018,29(1):43-47.
[5]丁绍祥.恶性心律失常与心肌动作电位时程3相[J].医学争鸣,2018,9(5):30-33.
[6]Badri M,Patel A,Yan GX.Cellular and ionic basis of J-wave syndromes[J].Trends Cardiovasc Med,2015,25(1):12-21.
[7]Boukens BJ,Walton R,Meijborg VM,et al.Transmural electrophysiological heterogeneity,the T-wave and ventricular arrhythmias[J].Prog Biophys Mol Biol,2016,122(3):202-214.
[8]Maoz A,Christini DJ,Krogh-Madsen T.Dependence of phase-2 reentry and repolarization dispersion on epicardial and transmural ionic heterogeneity:a simulation study[J].Europace,2014,16(3):458-465.
[9]Tokatli A,Yiginer O,Degirmencioglu G.et al.Transmural dispersion of repolarization and atrial electromechanical coupling:complementary indices for quantifying cardiac electrical heterogeneity in patients with conversion disorder[J].Ther Clin Risk Manag,2015,11:1077-1080.
[10]丁绍祥,王智杰,崔涛.2相折返是触发于心肌动作电位时程2相吗?[J].医学争鸣,2017,8(4):51-54.
[11]Nˇemec J,Kim JJ,Salama G.The link between abnormal calcium handling and electrical instability in acquired long QTsyndrome--does calcium precipitate arrhythmic storms?[J].Prog Biophys Mol Biol,2016,120(1-3):210-221.
[12]丁绍祥,王智杰,王青,等.“R-on-T”现象的发生机制[J].中华心血管病杂志,2017,45(8):673-675.
[13]Aggarwal S,Randhawa PK,Singh N,et al.Role of ATP-sensitive potassium channels in remote ischemic preconditioning induced tissue protection[J].J Cardiovasc Pharmacol Ther,2017,22(5):467-475.
[14]Dunnink A,Stams TRG,Bossu A,et al.Torsade de pointes arrhythmias arise at the site of maximal heterogeneity of repolarization in the chronic complete atrioventricular block dog[J].Europace,2017,19(5):858-865.
[15]丁绍祥,祁国荣,刘品发,等.尖端扭转型室性心动过速的扭转机制[J].中华心血管病杂志,2015,43(8):670-672.
[16]Morand J,Arnaud C,Pepin JL,et al.Chronic intermittent hypoxia promotes myocardial ischemia-related ventricular arrhythmias and sudden cardiac death[J].Sci Rep,2018,8(1):2997.
[17]Lancaster MC,Sobie EA.Improved prediction of drug-induced torsades de pointes through simulations of dynamics and machine learning algorithms[J].Clin Pharmacol Ther,2016,100(4):371-379.
[18]Marill KA,Miller ES.Hypokalemia in women and methadone therapy are the strongest non-cardiologic factors associated with QT prolongation in an emergency department setting[J].J Electrocardiol,2017,50(4):416-423.
[19]Minetto D,Serratrice J,Stirnemann J.Magnesium in daily practice[J].Rev Med Suisse,2016,12(535):1761-1765.
[20]Cubeddu LX.Drug-induced inhibition and trafficking disruption of ion channels:pathogenesis of QT abnormalities and druginduced fatal arrhythmias[J].Curr Cardiol Rev,2016,12(2):141-154.
[21]Tse G,Chan YW,Keung W,et al.Electrophysiological mechanisms of long and short QT syndromes[J].Int J Cardiol Heart Vasc,2016,14:8-13.
[22]Hondeghem LM.Drug-Induced QT Prolongation and torsades de pointes:an all-exclusive relationship or time for an amicable separation?[J].Drug Saf,2018,41(1):11-17.
[23]Lazzerini PE,Laghi-Pasini F,Bertolozzi I,et al.Systemic inflammation as a novel QT-prolonging risk factor in patients with torsades de pointes[J].Heart,2017,103(22):1821-1829.
[24]丁绍祥,张宏考.β-受体阻滞剂不再降低患者死亡率吗?[J].医学争鸣,2016,7(5):28-31,33.
[25]Thomas SH,Behr ER.Pharmacological treatment of acquired QT prolongation and torsades de pointes[J].Br J Clin Pharmacol,2016,81(3):420-427.
[26]丁绍祥,张宏考,王智杰,等.利多卡因能相对延长心肌有效不应期吗?[J].医学争鸣,2017,8(1):49-52.
[27]Pourmand A,Mazer-Amirshahi M,Chistov S,et al.Emergency department approach to QTc prolongation[J].Am J Emerg Med,2017,35(12):1928-1933.
[28]Said TH,Wilson LD,Jeyaraj D,et al.Transmural dispersion of repolarization as a preclinical marker of drug-induced proarrhythmia[J].J Cardiovasc Pharmacol,2012,60(2):165-171.
[29]白玉云,赵子霞,李晨刚.尖端扭转型室性心动过速三例[J].实用心脑肺血管病杂志,2015,23(3):118-119.