曲美他嗪对陈旧性心肌梗死后室性心律失常影响的随机配对、交叉研究

目的：研究曲美他嗪（Trimetazidine）对于处于常规治疗中的心肌梗死后的心 律失常的作用。方法：冠心病陈旧心肌梗死病例（OMI）,共29对（58例）;男性27对,女性2对;配对主要条件：性别、年龄、梗死部位、梗死后时间、高血压病史及分级;糖尿病史;采用病例配对、随机进入试验、交叉、单盲的试验设计;结果分析采用方差分析（ANOV／F检验）。结果：综合交叉试验结果,Trimetazidine处理组室性心律失常的发生低于对照组（F＝4．20,P＜0．05）;对于清醒时间段即活动时间段的室性心律失常的分析显示：Trimetazidine也具有显著的抑制作用（F＝5．87,P＜0．05）;对于Lown3级以上室性心律失常的单独分析,也显示出其较明显的抑制作用（F＝7．61,P≈0．01）;对于OMI后LVEF≤40％患者组的室性心律失常,Trimetazidine也表现出明确的抑制作用（F＝5．43,P＜0．05）。结论：对于陈旧性心肌梗死所伴发的室性心律失常,除基础药物的处理外,应用曲美他嗪可对其产生显著地抑制作用,并减少抗心律失常药物的应用;改善缺血心肌的能量代谢可能是此作用的主要基础。     

Clinical and familial study of arrhythmogenic right ventricular cardiomyopathy

Objective　To explore the characteristics of arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods　Seven patients with arrhythmogenic right ventricular cardiomyopathy and 34 members of three families were studied. All patients and family members underwent history collection, clinical examination, electrocardiogram (ECG), two-dimensional echocardiography (2-DE) and a signal averaging electrocardiogram. Programmed ventricular stimulation was performed in five patients. Results　All patients and family members had normal morphologic characteristics and normal function of the left ventricular by 2-DE. Fourteen persons had abnormal findings indicating ARVC. Five had enlargement of the right ventricular with diffused hypocontractility, eight had thin and systolic bulging in the focal anterior wall with hypokinesia and one had bulging of the inferior wall. Twenty-five persons (seven patients and 18 family members) had abnormal findings in ECG. Positive ventricular late potential was recorded in 13 persons (six patients). Two to three monomorphic ventricular tachycardia (VT) with left bundle branch block (LBBB) configurations were induced in five patients. Ventricular fibrillation was induced in two patients during the electrophysiologic study (EPS). Five patients had very high pacing threshold and/or ineffective pacing in one or many regions of the right ventricle. Two members of one family died suddenly. One member was a dwarf with ARVC. Spontaneous VT with a left bundle branch block (LBBB) configuration was recorded in five patients, polymorphic VT with extremely short coupling interval in one, and premature ventricular complexes with LBBB configuration in 12 (six patients). Conclusion　Our familial study strongly suggests that ARVC may be a hereditary disease and it is helpful in the diagnosis and detection of ARVC. The most common manifestations were abnormal structure and function of the right ventricle and abnormal ECG of repolarization and ventricular arrhythmia which originates from the right ventricle.     

梗死前心绞痛对初次急性心肌梗死后QTd及严重室性心律失常的影响

目的 :观察 2 4h内心绞痛发作对初次急性心肌梗死 (AMI)患者住院期间严重室性心律失常及 QT离散度 (QTd)的影响。方法 :184例初次 AMI患者 ,分为梗死前心绞痛 (PA)组 ,5 8例 ;无梗死前心绞痛 (NPA)组 ,12 6例。观察住院期间心脏并发症及 QTd。结果 :两组间一般临床情况、冠心病危险因素、AMI前用药情况、AMI后抗心律失常药物使用、溶栓成功率及入院后肌酸磷酸激酶 (CK)及其 MB亚型 (CK- MB)峰值无显著差异。PA组及 NPA组早期 QTd分别为 (5 6 .2 2± 18.40 )及 (84.45±2 1.90 ) m s,(P<0 .0 5 ) ;晚期 QTd分别为 (5 0 .6 7± 16 .34 )及 (6 4.18± 16 .41) ms(P<0 .0 5 )。PA组严重室性心律失常、心力衰竭、心源性休克发生率及院内心源性病死率明显低于 NPA组。结论 :梗死前心绞痛显著降低 AMI患者住院期间 QTd值及严重室性心律失常的发生率。提示该结果可能与缺血预适应对心肌及心室泵功能的保护及改善心室肌复极的非同步性有关     

犬陈旧性心肌梗死时连接蛋白43的分布

目的：探讨陈旧性心肌梗死时心肌缝隙连接蛋白43（connexin 43,Cx43)的分布特征。方法：结扎犬冠状动脉造成心肌梗死,术后恢复40－50d,用改良的免疫细胞化学法显示心肌梗死区,边缘带及非缺血区Cx43的分布,半定量分析不同部位Cx43的分布密度。结果：与正常心肌相比,梗死病灶及其邻近区域Cx43的分布出现明显紊乱：梗死中心区Cx43完全消失;边缘带Cx43呈现不均匀消失,少量Cx43分布于岛状或半岛状尚存活的心肌;心肌细胞端－端相接处的Cx43严重消失,而细胞侧－侧相接处的Cx43仍有部分存在。非缺血区Cx43的密度和分布与正常心肌相比无明显改变。结论：陈旧性心肌梗死时Cx43的数量和分布呈现高度不均一性,尤其在边缘带Cx43的分布特点是形成局部传导阻滞和折返性心律失常的结构基础。     

胸科非心脏手术后心律失常高危因素分析

对 2 38例胸科非心脏手术后并发心律失常进行分析 ,结果显示 :发生心律失常 38例 ,年龄≥ 6 5岁、血氧饱和度 <0 .96、术前有合并症、术后有并发症、酸碱电解质紊乱者发病率明显升高 (P <0 .0 5 )。认为胸科非心脏手术后并发心律失常与高龄、低氧血症、术前合并症、术后并发症、酸碱电解质紊乱密切相关。     

QT离散度预测老年冠心病患者室性心律失常的发生

目的探讨QT离散度(QTd)作为预测室性心律失常发生指标的意义.方法对70例冠心病患者,包括34例室性心律失常患者及30例健康者的QTd进行比较.结果冠心痛组的QTd值(61.34±20.17)ms明显大于正常组,P＜0.001.其中室性心律失常患者的QTd值(76.94±22.19)ms明显高于冠心病组,P＜0.005.当QTd≥60ms时,心律失常组的阳性率明显大于冠心痛组.结论QTd可作为预测室性心律失常发生的指标之一.     

QT Dispersion Level and Its Clinical Significance.in Dilated Cardiomyopathy

［1］Richardson CP, Mckenna RM, Bristow CM, et al.Report of the 1995 Word Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation, 1996,93: 841 ［2］Barr CS, Naas A, Freeman M, et al. QT dispersion and sudden unexpected death in chronic heart failure. Lancet, 1994,343:327 ［3］Martin AB, Garson A, Perry JC, et al. Prolonged QT interval in hypertropic and dilated cardiomyopathy in children. Am Heart J, 1994,127(1):64 ［4］Pye M, Quinn AC, Cobble SM. QT dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?Br Heart J, 1994,71(5):51 ［5］Berger RD, Kasper EK, Baughman KL, et al. Beat to beat QT interval variability: novel evidence for repolarization lability in ischemic and non ischemic dilated cardiomyopathy. Circulation, 1997, 96 (5):1557 ［6］Wolfram G, Ulrike S, Volker M, et al. QT dispersion and arrhythmic events in idiopathic dilated cardiomyopathy. Am J Cardiol, 1997,78: 458 ［7］Fei L, Goldman JH, Prasal K, et al. QT dispersion and RR variations on 12-lead ECGs in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy. Eur Heart J, 1996,17: 258 ［8］Pan YZ, Guo NS, Xing ZF, et al. The relation between QT dispersion and ventricular arrhythmia of dilated cardiomyopathy. Chin J Inter Medi, 1996,35(11):73 ［9］Galinier M, Vialette JC, Fourcade J, et al. QT interval dispersion as a predictor of arrhythmic events in congestive heart failure. Importance of aetiology. Eur Heart J, 1998,19(7) :1054     

内皮素致心律失常作用的电生理特性

目的 :探讨内皮素 1在豚鼠乳头肌诱发异常电活动的特征及其离子机制。方法 :用常规微电极技术引导并记录心肌细胞内电活动 ,分析其各参数。结果 :ET 1浓度依赖地延长乳头肌细胞的APD ,并在低Mg2 + 灌流的条件下诱发EADs。ET 1所诱发EADs的幅度、触发发放时程TBD具有明显的浓度依赖性和刺激周长依赖性。ETA 受体拮抗剂BQ 12 3和Ca2 + 通道阻断剂硝苯吡啶可消除ET 1的上述作用。结论 :ET 1通过ETA 受体激活Ca2 + 通道 ,导致细胞内Ca2 + 超载进而诱发EADs。由于EADs的出现 ,致使心肌细胞复极化异常 ,可能是ET 1致心律失常作用的电生理基础。     

基于空洞卷积神经网络的心律失常分类算法

本文提出了一种基于卷积网络的心电信号分类算法,设计了空洞卷积池化金字塔模块,通过不同尺寸的空洞卷积提取信息,再将各通道的信息聚合,在增强网络的特征提取能力的同时可以降低参数量。本文聚焦于窦性心律、房性早搏、心动过速以及心动过缓4种分类,使用的心电图数据集来自医院的实测数据,数据集包含75000名不同检测者的心电记录。经过测试,本文提出的模型在该数据集上取得了0.89的F1值,另外在CinC2017数据集上也达到了0.87的F1值。实验结果表明该分类算法具有优秀的特征提取和分类能力,在心电信号的实时分类中具备应用前景。     

The inhibitory effect of the antipsychotic drug haloperidol on HERG potassium channels expressed in Xenopus oocytes

1. The antipsychotic drug haloperidol can induce a marked QT prolongation and polymorphic ventricular arrhythmias. In this study, we expressed several cloned cardiac K⁺ channels, including the human ether-a-go-go related gene (HERG) channels, in Xenopus oocytes and tested them for their haloperidol sensitivity.
2. Haloperidol had only little effects on the delayed rectifier channels Kv1.1, Kv1.2, Kv1.5 and I_sK, the A-type channel Kv1.4 and the inward rectifier channel Kir2.1 (inhibition <6% at 3 μM haloperidol).
3. In contrast, haloperidol blocked HERG channels potently with an IC₅₀ value of approximately 1 μM. Reduced haloperidol, the primary metabolite of haloperidol, produced a block with an IC₅₀ value of 2.6 μM.
4. Haloperidol block was use- and voltage-dependent, suggesting that it binds preferentially to either open or inactivated HERG channels. As haloperidol increased the degree and rate of HERG inactivation, binding to inactivated HERG channels is suggested.
5. The channel mutant HERG S631A has been shown to exhibit greatly reduced C-type inactivation which occurs only at potentials greater than 0 mV. Haloperidol block of HERG S631A at 0 mV was four fold weaker than for HERG wild-type channels. Haloperidol affinity for HERG S631A was increased four fold at +40 mV compared to 0 mV.
6. In summary, the data suggest that HERG channel blockade is involved in the arrhythmogenic side effects of haloperidol. The mechanism of haloperidol block involves binding to inactivated HERG channels.