36例乌头碱中毒致室性心律失常的临床研究

目的:研究乌头碱中毒致室性心律失常是为了提高对室性心律失常的诊疗水平.方法:36例乌头碱中毒患者入院,立即洗胃,心电监护.根据心电图情况及时纠正心律紊乱,选用利多卡因、硫酸镁、氯化钾静滴及电除颤抢救.结果:36例患者有效30例,显效4例,无效2例.总有效率94.44%,乌头碱中毒时间与治疗早搏消失时间的疗效比较P值<0.05,有显著性差异.结论:乌头碱中毒所致室性心律失常治疗关键:及早药物及电复律,可提高其治愈率.     

CRT_D介导室性心动过速的研究进展

心室再同步心脏转复除颤器（CRT）可有效改善心力衰竭（CHF）患者的运动耐量和生活质量,预防猝死,提高生存率,但_DCHFCRTD植入后由于心室激动顺序的改变,使QT间期延长、跨室壁复极离散度（TDR）增加,潜在致室性心律失常风险;且CHF患者通常存在心肌解剖改变,传导的不均一性,也为折返性心动过速的发生提供了维持的机制;而多次电击也可导致肌钙蛋白升高,引起心肌损伤,局部心肌复极离散度增加（DRVR）和QT间期延长,以及电除颤后心肌纤维化和急性细胞损伤,反复室速、室颤也会引起进行性左心功能不全、心肌细胞凋亡、恶化心律失常基质和增加心律失常易感性。CRT_D潜在致室性心律失常作用逐渐引起人们的重视,本文就近年来CRTD致室性心律失常的电生理机制与临床防治对策等做一综述。     

CRT_D介导室性心动过速的研究进展

心室再同步心脏转复除颤器(CRT_D)可有效改善心力衰竭(CHF)患者的运动耐量和生活质量,预防猝死,提高生存率,但CRT_D植入后由于心室激动顺序的改变,使QT间期延长、跨室壁复极离散度(TDR)增加,潜在致室性心律失常风险;且CHF患者通常存在心肌解剖改变,传导的不均一性,也为折返性心动过速的发生提供了维持的机制;而多次电击也可导致肌钙蛋白升高,引起心肌损伤,局部心肌复极离散度增加(DRVR)和QT间期延长,以及电除颤后心肌纤维化和急性细胞损伤,反复室速、室颤也会引起进行性左心功能不全、心肌细胞凋亡、恶化心律失常基质和增加心律失常易感性。CRT_D潜在致室性心律失常作用逐渐引起人们的重视,本文就近年来CRT_D致室性心律失常的电生理机制与临床防治对策等做一综述。     

68例服胺碘酮的75岁以上老年心律失常患者甲功变化分析

目的：探讨口服小剂量胺碘酮对老年心律失常患者甲状腺功能的作用和影响。方法：回顾性分析老年器质性心脏病心律失常患者68例,记录胺碘酮治疗方案与疗效、甲状腺变化及随访干预措施情况。结果：老年人服用胺碘酮引起甲状腺疾病发生率为31．8％（22／68）,以甲状腺功能减退25．7％（18／68）为主,大致为甲状腺功能亢进（6．1％,4／68）的4倍。采用小剂量胺碘酮方案出现的甲状腺功能紊乱多数经过减量或停药逆转或恢复。结论：老年人服用胺碘酮甲状腺功能紊乱发生率高,但临床表现不典型,应更密切地监测甲状腺功能;甲状腺功能紊乱经胺碘酮及时减量或停药等措施多能逆转或恢复。     

68例服胺碘酮的75岁以上老年心律失常患者甲功变化分析

目的:探讨口服小剂量胺碘酮对老年心律失常患者甲状腺功能的作用和影响。方法:回顾性分析老年器质性心脏病心律失常患者68例,记录胺碘酮治疗方案与疗效、甲状腺变化及随访干预措施情况。结果:老年人服用胺碘酮引起甲状腺疾病发生率为31.8%(22/68),以甲状腺功能减退25.7%(18/68)为主,大致为甲状腺功能亢进(6.1%,4/68)的4倍。采用小剂量胺碘酮方案出现的甲状腺功能紊乱多数经过减量或停药逆转或恢复。结论:老年人服用胺碘酮甲状腺功能紊乱发生率高,但临床表现不典型,应更密切地监测甲状腺功能;甲状腺功能紊乱经胺碘酮及时减量或停药等措施多能逆转或恢复。     

神经系统与心律失常

焦虑、悲伤、情绪紧张等可使儿茶酚胺分泌过多、心电图出现ST段T波变化、心肌纤维断裂及各种室性心律失常。电刺激或将药物注入动物脑内不同部位可产生各种心律失常。在中脑中央灰质内注入微量去甲肾上腺素或乙酰胆硷均可增加刺激下丘脑引起的室性期前收缩。脑内吗啡样物质、5-羟色胺水平增加可降低交感中枢紧张性,导致交感神经传出冲动减少,降低心室易颤性,减少刺激下丘脑引起的室性期前收缩。躯体传入冲动对刺激下丘脑诱发期前收缩的抑制作用与脑内吗啡样物质的释放及下丘脑弓状核区、中脑中央灰质等处阿片受体的激活有关,且部分通过5-羟色胺途径。     

神经系统与心律失常

焦虑、悲伤、情绪紧张等可使儿茶酚胺分泌过多、心电图出现 ST 段 T 波变化、心肌纤维断裂及各种室性心律失常.电刺激或将药物注入动物脑内不同部位可产生各种心律失常.在中脑中央灰质内注入微量去甲肾上腺素或乙酰胆硷均可增加刺激下丘脑引起的室性期前收缩.脑内吗啡样物质、5-羟色胺水平增加可降低交感中枢紧张性,导致交感神经传出冲动减少,降低心室易颤性,减少刺激下丘脑引起的室性期前收缩.躯体传入冲动对刺激下丘脑诱发期前收缩的抑制作用与脑内吗啡样物质的释放及下丘脑弓状核区、中脑中央灰质等处阿片受体的激活有关,且部分通过5-羟色胺途径.     

电场引起心肌组织兴奋的特点

恶性心律失常仍然是心脏病人死亡的主要原因之一。由于恶性心律失常的药物有效率仅40％,故目前国内外正开展恶性心律失常的非药物性治疗,常用的方法之一是电击治疗。尤其是心室颤动,电击是唯一的治疗方法。此外,在科研中引起心室颤动、室性心动过速以及进行多数电生理实验时,采用的是细胞外电刺激,其实质是电场与心肌组织电生理特性的相互     

室性心律失常的基因诊疗

在一些发达国家,心脏骤停已成为最主要的死亡原因.快速性室性心律失常是导致心脏骤停最主要的原因,且快速性室性心律失常会增加结构性心脏病患者发病的风险.通过药物和器械治疗方法,存在较大的局限性.心脏电活动的细胞基础是动作电位.动作电位是由于时间和电压依赖性激活各种钠、钙和钾离子通道和泵产生的.心律失常机制包括折返,自律性异常和触发活动.折返是在组织水平发生的.异常的自动性和触发活动是细胞现象,能够存在于单个心肌细胞或细胞群.心律失常的发生就是上述电冲动传播从这个局部激动由细胞间传导至更多的心肌中.故研究人员提出开展基因治疗心律失常替代现有的治疗方法.在本文中,我们讨论应用基因治疗快速性室性心律失常的基本机制并总结方法.     

电刺激杏仁复合体诱发心律失常及其下行神经通路的初步探讨

电刺激杏仁复合体能诱发心律失常。心律失常的类型为心动过缓伴室性或结性期外收缩。刺激杏仁复合体不同亚核均能诱发心律失常,不同类型的心律失常在核内具有相应的代表点。心律失常发作与杏仁局部区域诱发的爆发性后放电有关。推测杏仁复合体内神经元过度激活可能通过杏仁-迷走神经运动背核及杏仁-下丘脑外侧区等通路下行,使心率减慢、房室传导阻滞而导致心律失常。     

A clinical approach to arrhythmias revisited in 2018

Understanding arrhythmias and their treatment is not always easy. The current straightforward approach with catheter ablation and device therapy is an amazing achievement, but does not make management of underlying or other cardiac disease and pharmacological therapy unnecessary. The goal of this paper is to describe how much of the knowledge of the 1980s and early 1990s can and should still be applied in the modern treatment of patients with arrhythmias. After an introduction, this review will focus on paroxysmal atrial fibrillation and a prototype of ‘idiopathic’ ventricular arrhythmias, two diseases with a striking similarity, and will discuss the arrhythmogenesis. The ECG continues to play an important role in diagnostics. Both diseases are associated with a structurally normal heart; the autonomic nervous system plays an important role in triggering arrhythmias at both the atrial and ventricular level.     

起搏器术后新发房性心律失常的影响因素分析

目的:探讨起搏器术后新发房性心律失常的发生情况及其相关影响因素。方法:选择2006年1月至2007年12月于沈阳军区总医院首次植入永久起搏器的107例患者,男性50例,平均年龄65.0±11.9岁,术前通过追问病史及相关检查均排除房性心律失常(房颤、房扑、房速),术后平均随访3.9年,观察新发房性心律失常情况。按术后是否出现房性心律失常,将患者分为新发房性心律失常组和无房性心律失常组,比较两组患者术前和术后心脏超声结果的变化、心室起搏比例、起搏部位及起搏模式,并通过logistic回归分析起搏器术后发生房性心律失常的影响因素。结果:新发房性心律失常组26例(24.3%),其中房颤17例(15.9%),房扑2例(1.9%),房速7例(6.5%);无房性心律失常组81例。与无房性心律失常组比较,新发房性心律失常组左房内径明显增加(P=0.040)、二尖瓣返流程度较重(P=0.032)及左室射血分数明显下降(P=0.001),心室起搏百分比(VP%)显著升高(P=0.017)。心尖部起搏患者房性心律失常的发生率明显高于间隔部起搏(33.3%vs 16.9%,P<0.05),双腔起搏组患者房性心律失常发生率明显低于单腔起搏器组(18.7%vs 37.5%,P<0.05)。Logistic回归分析显示术后新发房性心律失常的发生与高比例的心室起搏(P=0.006)、VVI(R)起搏模式(P=0.014)及右心室起搏电极导线植于心尖部(P=0.024)显著相关。结论:起搏模式、心室起搏百分比、起搏部位是起搏器术后发生房性心律失常的影响因素。     

活性氧诱导心律失常的分子生物学机制研究

心律失常特别是室性心律失常可能导致心源性猝死,已经成为临床上常见和重点问题。多种原因可能诱发心律失常如:冠状动脉粥样硬化性心脏病,瓣膜病,肥厚性心肌病等心脏源性病变,很多代谢性物质改变也可能增加心律失常的发生概率。近年发现活性氧可能是诱发各种心律失常的一个重要因素,活性氧不仅参与重要离子通道和转运受体的调控,同时本身也作为一个重要的第二信来调节一些关键酶的活性如:蛋白激酶A(PKA),蛋白激酶C(PKC),钙离子依赖性蛋白激酶II(CaMKII)。最近有研究发现长期的活性氧代谢紊乱可能引起细胞遗传物质如miRNA的改变,引起长期的心律失常如房颤。本文主要对活性氧导致心律失常的可能机制做一总结,为心律失常的防治提供一些可能潜在方向。     

Alpha-adrenoceptor blockade modifies neurally induced atrial arrhythmias

Our objective was to determine whether neuronally induced atrial arrhythmias can be modified by alpha-adrenergic receptor blockade. In 30 anesthetized dogs, trains of five electrical stimuli (1 mA; 1 ms) were delivered immediately after the P wave of the ECG to mediastinal nerves associated with the superior vena cava. Regional atrial electrical events were monitored with 191 atrial unipolar electrodes. Mediastinal nerve sites were identified that reproducibly initiated atrial arrhythmias. These sites were then restimulated following 1 h (time control, n = 6), or the intravenous administration of naftopidil (alpha(1)-adrenergic blocker: 0.2 mg/kg, n = 6), yohimbine (alpha(2)-adrenergic blocker: 1 mg/kg, n = 6) or both (n = 8). A ganglionic blocker (hexamethonium: 1 mg/kg) was tested in four dogs. Stimulation of mediastinal nerves sites consistently elicited atrial tachyarrhythmias. Repeat stimulation after 1 h in the time-control group exerted a 19% decrease of the sites still able to induce atrial tachyarrhythmias. Hexamethonium inactivated 78% of the previously active sites. Combined alpha-adrenoceptor blockade inactivated 72% of the previously active sites. Bradycardia responses induced by mediastinal nerve stimulation were blunted by hexamethonium, but not by alpha(1,2)-adrenergic blockade. Naftopidil or yohimbine alone eliminated atrial arrhythmia induction from 31% and 34% of the sites (similar to time control). We conclude that heterogeneous activation of the intrinsic cardiac nervous system results in atrial arrhythmias that involve intrinsic cardiac neuronal alpha-adrenoceptors. In contrast to the global suppression exerted by hexamethonium, we conclude that alpha-adrenoceptor blockade targets intrinsic cardiac local circuit neurons involved in arrhythmia formation and not the flow-through efferent projections of the cardiac nervous system.     

Cocaine-enhanced arrhythmogenesis: neural and nonneural mechanisms.

Cocaine abuse increases the susceptibility to cardiovascular complications and sudden cardiac death in man. We used programmed electrical stimulation of the heart to examine the arrhythmogenic influence of cocaine. Twenty-three pentobarbital-anesthetized adult dogs underwent programmed electrical stimulation using one to four extrastimuli before and during cocaine infusion. Autonomic decentralization was performed prior to the protocol in eight dogs. Induced ventricular arrhythmias included single premature ventricular depolarizations, doublets, triplets, ventricular tachycardia, and ventricular fibrillation. Intravenous cocaine, and subsequent adrenergic and muscarinic receptor blockade, or calcium channel blockade were evaluated for their influence on arrhythmogenesis. The incidence of induced ventricular arrhythmias was significantly elevated following cocaine and was reduced following propranolol and atropine. Verapamil, however, did not reduce the incidence of induced arrhythmias. In addition, cocaine significantly increased arrhythmia induction in decentralized animals, but propranolol, atropine, and phentolamine failed to reduce the proarrhythmic effects of cocaine in these animals. Thus, cocaine has a proarrhythmic effect on the heart with multiple mechanisms. The adrenergic mechanism appears to be a result of neurotransmitter uptake blockade, whereas the likely ionic mechanism is a neurally independent, direct effect on the heart.     

Comparison of arrhythmia detection by conventional Holter and a novel ambulatory ECG system using patch and Android App,over 24 h period

BackgroundAmbulatory electrocardiogram (AECG) is done for evaluation of arrhythmia. Commonly used AECG system is 24 h Holter. Patch based second generation AECG monitoring devices, which can record for longer periods, are now available.ObjectiveAndroid App based WebCardio using WiPatch is a new AECG system which records ECG in two leads for 72 h. Our study compared the arrhythmia detection by WebCardio and conventional Holter by simultaneously connecting both for 24 h in patients having indication for AECG.MethodsThe AECG of patients who had simultaneous recording with WebCardio and conventional Holter, in the department of Cardiology, Medical College, Thrissur were evaluated. Ability to detect any of the 6 arrhythmias :1) atrial fibrillation (AF), 2) atrioventricular (AV) block, 3) sinus pause of ≥3 s (SP), 4) supraventricular tachycardia (SVT), 5) premature ventricular complex (PVC) and 6) ventricular tachycardia (VT)/ventricular fibrillation (VF) was compared. Detection of each arrhythmia was also compared.Results141 patients had simultaneous recordings by both systems of AECG. The WebCardio picked up at least one of the 6 arrhythmias; AF, AV block, SP, SVT, PVC or VT/VF in 98 cases compared to 88 in the Holter (McNemars test, two tail P = 0.006). In eleven cases WebCardio detected an arrhythmia where Holter could not. In one case Holter identified an arrhythmia and WebCardio could not. Individual arrhythmias; AF, SP, SVT and VT/VF were detected equally by both systems. AV block (23 Vs 18, p = 0.0625) and PVCs (83 Vs 74, p = 0.0636) were detected in more number of cases in WebCardio. In the five cases where WebCardio alone identified AV block, four had poor quality of P wave in the Holter.ConclusionArrhythmia was picked up in more number of patients by the WebCardio compared to Holter. This was due to higher pickup of AV block and PVCs by WebCardio. Difference in AV block identification was due to better quality of P in WebCardio. WebCardio is a good alternative to Holter for AECG.     

15例儿童心动过速性心肌病的诊疗体会

目的:探讨儿童完全性心动过速性心肌病(pTIC)的临床特点、治疗及预后。方法:回顾分析2009年1月至2016年10月安徽省儿童医院心内科收治的15例完全性心动过速性心肌病患儿的临床表现、心功能、心电图、心脏彩超的特点,观察心律失常控制后的心室率、心脏左室内径大小及心功能恢复情况。结果:15例pTIC患儿以室上性快速心律失常多见(14例),10例单纯药物治疗,3例接受射频消融转为窦性心律,2例失访。随访半年至3年与治疗前比较心室率明显下降[(116±27)次/分vs.(189±28)次/分]、NT-proBNP降低[(404±355)pg/mL vs.(6280±3155)pg/mL]、心脏左室舒张末内径变小[(3.12±0.48)cm vs.(3.69±0.70)cm]、左室射血分数升高[(57.9±9.3)%vs.(42.2±9.5)%]、改良ROSS评分下降[1(0-5)分vs.7(4-10)分]。结论:儿童pTIC由各种快速心律失常引起,心脏扩大和心功能障碍可完全恢复,早期识别、有效治疗的儿童pTIC长期预后良好。     

Angiotensin in the brain suppresses epinephrine-induced cardiac arrhythmias through CNS opioid mechanisms.

To test the hypothesis that angiotensin II (Ang II) in the central nervous system modulates catecholamine-induced cardiac arrhythmias and to determine whether endogenous opioids are operative in this action, arrhythmias were produced in male Wistar rats, by continuous infusion of epinephrine at incremental doses until the development of fatal arrhythmias that were usually ventricular fibrillation. Rats were instrumented with catheters in the lateral cerebral ventricle, femoral vein and femoral artery. Ang II, 0.5 microgram, in the lateral cerebral ventricle (ICV) markedly and significantly (p less than 0.05) increased the epinephrine dose, at the occurrence of ventricular premature beats compared to the control group 228 +/- 11 (SEM) vs 116 +/- 7 micrograms epinephrine/kg and at the onset of fatal arrhythmias 225 +/- 13 vs 185 +/- 9 micrograms epinephrine/kg. Ang II, 0.5 microgram i.v., did not affect arrhythmia threshold. The angiotensin converting enzyme inhibitor captopril, 1 mg/kg, decreased arrhythmia threshold as ventricular arrhythmias were first noted at 106 +/- 4 and fatal arrhythmias occurred at 118 +/- 4 micrograms epinephrine/kg. The Ang II receptor antagonist saralasin 150 micrograms/kg ICV, blunted and 300 micrograms/kg ICV reversed the effect of Ang II. The mu opioids antagonist naloxone and the kappa opioid antagonist MR 2266, 50 micrograms/kg ICV, prevented the effect of Ang II on fatal arrhythmias. The action Ang II on arrhythmias could not be explained by the effects of Ang II on blood pressure or heart rate. These data indicate a role for Ang II within the CNS to modulate cardiac arrhythmias and that this is mediated in part, by endogenous opioids.     

Mechanically induced electrical storm as a complication of cardiac resynchronization therapy: A case report

BackgroundCardiac resynchronization therapy (CRT) has been shown to improve both the functional status and mortality of heart failure patients with left bundle branch block. Multiple recent studies suggest several mechanisms for proarrhythmia associated with CRT device.Case summaryA 51-year-old male with symptomatic non-ischemic cardiomyopathy and no previous history of ventricular arrhythmias underwent placement of a biventricular cardioverter-defibrillator. The patient developed sustained monomorphic ventricular tachycardia (VT) soon after implantation. The VT recurred despite reprogramming to right ventricular only pacing. The electrical storm resolved only after a subsequent discharge from the defibrillator caused inadvertent dislodgement of the coronary sinus lead. No recurrent VT occurred throughout 10-years follow up after urgent coronary sinus lead revision.DiscussionWe describe the first reported case of mechanically induced electrical storm due to the physical presence of the CS lead in a patient with a new CRT-D device. It is important to recognize mechanical proarrhythmia as a potential mechanism of electrical storm, as it may be intractable to device reprogramming. Urgent coronary sinus lead revision should be considered. Further studies on this mechanism of proarrhythmia are needed.     

基于多尺度快速样本熵与随机森林的心电图分析

目的:探讨基于多尺度快速样本熵与随机森林的心电图分析方法对常见心律失常(房性早搏、室性早搏)的自动诊断的可行性和有效性。方法:利用不同心律失常疾病的心电信号存在复杂性差异的特点,通过多尺度熵计算心电信号在不同尺度下的样本熵值以组成特征向量;利用kd树提高多尺度熵的计算效率,增强算法的实时性。利用训练样本的特征向量构建随机森林分类器,再根据众多决策树的分类结果结合投票原则确定测试样本心律失常疾病的类型。结果:本文提出的心电图分析方法能够有效地识别正常心律、房性早搏(APB)及室性早搏(VPB),平均识别准确率达到91.60%。结论:本文提出的心电图分析方法对常见心律失常(APB,VPB)具有较高的识别准确率及临床实用价值。