起源于左侧希氏-浦肯野系统的特发性加速性室性自主心律

目的 介绍起源于左侧希氏-浦肯野系统的特发性加速性室性自主心律,揭示其临床特征并探讨可能的电生理机制.方法 回顾分析4例特发性加速性室性自主心律患者的心电图形态特征、临床表现、治疗方法及预后.结果 4例患者,男性2例,平均年龄48(40～54)岁,均无器质性心脏病.室性自主心律均呈右束支阻滞型,其QRS时限0.11～0.13 s,符合左侧希氏-浦肯野系统起源,其中3例电轴右偏,1例电轴左偏.自主心律RR间期不规则,平均频率为87(55～110)次/min,与窦性心律交替出现.所有患者临床均表现为发作性心悸.1例患者室性自主心律在短期服用普罗帕酮后消失,另1例短期服用维拉帕米后消失,余2例未予以特殊处理后自然消退.平均随访4.5(2～8)年,临床无心律失常发作,亦无其他心血管事件发生.结论 起源于左侧希氏-浦肯野系统的加速性室性自主心律是左侧希氏-浦肯野系统特发性室性心律失常的一种表现形式,多数为自限性,临床呈良性经过.     

起源于左侧希氏-浦肯野系统的特发性加速性室性自主心律

Objective To clarify the clinical manifestations of patients with idiopathic accelerated ventricular rhythm(AVR)originating from the left His-Purkinje system and to further explore the probable mechanisms of this special entity of cardiac arrhythmias. Methods Eletrogram( ECG)characteristics,clinical manifestations,medications and the prognosis of 4 patients with AVR were retrospectively reviewed. Results Four AVR patients(2 male,mean age 48 years)without structural heart disease were carefully analyzed. ECG indicated that the AVR was in right bundle branch block morphology with QRS width of 0. 11 ～0. 13 s. Right axis deviation during AVR was found in three patients while left axis deviation was found in the remaining one. RR interval of AVR was slightly irregular with the mean rate of 87bpm(55 ～ 110 bpm). AVR was frequently alternating with sinus rhythm. AVR automatically resolved in 2 patients without any medication and in the other 2 patients after a short period of respective medication of propafenone and varapamil. During the 4. 5 years follow-up period(2 ～8 years),no AVR recurred and no other cardiac events occurred in all the patients. Conclusion AVR originating from the left His-Purkinje system in structurally normal hearts is idiopathic with a benign clinical course. AVR in such patients will resolve automatically and not require special treatment.     

起源于左侧希氏-浦肯野系统的特发性加速性室性自主心律

Objective To clarify the clinical manifestations of patients with idiopathic accelerated ventricular rhythm(AVR)originating from the left His-Purkinje system and to further explore the probable mechanisms of this special entity of cardiac arrhythmias. Methods Eletrogram( ECG)characteristics,clinical manifestations,medications and the prognosis of 4 patients with AVR were retrospectively reviewed. Results Four AVR patients(2 male,mean age 48 years)without structural heart disease were carefully analyzed. ECG indicated that the AVR was in right bundle branch block morphology with QRS width of 0. 11 ～0. 13 s. Right axis deviation during AVR was found in three patients while left axis deviation was found in the remaining one. RR interval of AVR was slightly irregular with the mean rate of 87bpm(55 ～ 110 bpm). AVR was frequently alternating with sinus rhythm. AVR automatically resolved in 2 patients without any medication and in the other 2 patients after a short period of respective medication of propafenone and varapamil. During the 4. 5 years follow-up period(2 ～8 years),no AVR recurred and no other cardiac events occurred in all the patients. Conclusion AVR originating from the left His-Purkinje system in structurally normal hearts is idiopathic with a benign clinical course. AVR in such patients will resolve automatically and not require special treatment.     

不同房室传导阻滞部位患者的希氏-浦肯野系统起搏成功率

目的评估不同房室传导阻滞(AVB)部位患者行希氏-浦肯野系统起搏(HPSP)的成功率, 为AVB患者HPSP方案的选择提供依据。方法本研究为回顾性病例分析。选取2016年3月至2021年9月于北部战区总医院心血管内科接受心脏永久起搏器置入治疗且需要高比例心室起搏的637例AVB患者, 依据心脏电生理检查判断AVB部位。其中前130例(20.4%)进行了希氏束起搏(HBP)的患者为HBP组;后507例(79.6%)进行了HPSP的患者为HPSP组, 包括HBP和/或左束支起搏(LBBP)。收集两组的年龄、性别等基本临床信息, 分析不同AVB部位及QRS时限患者的HBP或HPSP的成功率。结果 HBP组年龄(66.4±15.9)岁, 男性75例(57.7%);HPSP组年龄(66.8±13.6)岁, 男性288例(56.8%)。637例AVB患者中, 63.0%(401/637)为房室结阻滞;22.9%(146/637)为希氏束内阻滞;14.1%(90/637)为希氏束远段或以下阻滞。总体上, HPSP较HBP的成功率高[93.9%(476/507)比86.9%(113/130), P&l...     

希氏-浦肯野系统和室性心律失常

近期研究提示希氏-浦肯野系统与室性心律失常的发生关系密切。作为左室的特殊传导组织,希氏-浦肯野系统的解剖与电生理特点,使其在正常或病理情况下易于参与折返型心律失常形成。目前资料提示浦肯野系统病变是短联律间期室性早搏相关心律失常和儿茶酚胺敏感性多形性室性心动过速的原因。随着对希氏-浦肯野系统与室性心律失常关系的认识,导管消融可作为此类心律失常的治疗途径。     

希氏-浦肯野系统电冲动与实验性室性心律失常的关系

以针电极探查 2 5只犬心脏希氏 浦肯野系统 (HPS)的电冲动 ,观察其与缺血和再灌注室性心律失常的关系。结果表明自发室性心律失常的最早激动点 ,其双极电图以Q波为起始 ,源于HPS者HPS电位在前 ,源于心肌者HPS电位在后。自发HPS电冲动未向周边传出时 ,仅见局部电图异常 ;向周边传出时 ,则触发或驱动室性早搏、单形与多形室性心动过速和心室颤动。心室颤动初期心脏电图有序 ,终末期心室电冲动分离 ,而HPS电冲动频率最快 ,提示起关键驱动作用。室性心律失常体表QRS波窄者提示起源于HPS或经HPS快速传导 ,QRS波宽者多起源于心肌 ,也见起源于HPS伴有心室内或束支缓慢传导。多形性室性心律失常常见于多个起源点 ,也见于单个起源点伴有冲动传导的逐搏变化。结论 :HPS电冲动参与器质性室性心律失常的触发和维持 ,以HPS电冲动为指导 ,可望改进器质性室性心律失常的消融技术和效果。     

起源于左侧希氏束-浦肯野系统的反复单形性室性心动过速

反复单形性室性心动过速（Repetitive monomorphic ventricular taehyeardia，RMVT）多见于右心室及左心室流出道部位，包括主动脉窦。近年，也有报道起源于左侧二尖瓣环。但起源于左侧希氏束-浦肯野系统的RMVT较为罕见，报道甚少。本文报道3例此类患者，介绍其临床特征并探讨其可能的电生理机制。     

心脏再同步治疗:双心室起搏还是希氏-浦肯野系统起搏?

希氏-浦肯野系统(希浦系统)起搏是近年出现的除传统双心室同步起搏外同样能达到心脏再同步治疗(CRT)的新方法。本文阐述了2种方法达到CRT的途径、机制、临床证据及各自的利弊,并对现阶段CRT方式的选择提出了建议。     

自制针电极记录急性缺血和再灌注犬希氏-浦肯野系统的电冲动

探讨针电极记录犬在体心脏希氏 浦肯野系统 (HPS)电冲动的可行性 ,观察其图形特点、规律与影响因素。以注射针头和不锈钢丝自制针电极 ,2 5只犬开胸后沿HPS的解剖行程探查电冲动。结扎冠状动脉前降支 ,观察缺血和再灌注时心脏电图与电生理参数的变化。结果 :HPS电冲动为高频、持续时间短暂的电位 ,HPS近心房插入端 ,电位隐含于心房电图尾部 ;中段游离于房室肌间 ,电位独立于房、室电图之间 ;远端插入心内、外膜下层心室肌 ,电位隐含于心室电图的内部。高通滤波衰减低频高幅电位 ,显露基线稳定的高频低幅电位。双极电极与HPS走行平行排列所记HPS电位的幅度最大。缺血区HPS电位迟于心肌电位消失 ,再灌注HPS电位最先恢复。结论 :以针电极记录HPS电冲动稳定可靠 ,其图形与记录部位HPS的解剖和电生理特性有关外并受记录技术的影响。     

起源于左室流出道的频发性室性早搏射频消融治疗

目的:观察左室流出道频发室性早搏的射频消融治疗效果。方法:8例频发室性早搏患者,药物治疗无效,采用激动标测和起搏标测法确定室性早搏的起源部位,并行射频消融治疗。结果:8例患者7例射频消融成功。7例中6例在主动脉瓣下方的左室流出道记录到提前(31±8)ms的心室激动,室性早搏形态与起搏心电图12导联QRS波形完全相同者5例,11导联相同者1例;1例在左冠窦内记录到提前33ms的心室激动,属左室流出道室性早搏特殊类型,消融成功。随访3～21个月未复发。1例左室流出道早搏因多处标测未找到理想的靶点,消融失败。结论:射频消融治疗左室流出道室性早搏安全有效。     

起源于左后分支的室性早搏临床心电图特点和射频消融治疗

目的报道起源于左后分支的室胜早搏（PVC）的临床心电图特点及射频消融经验。方法8例无器质性心脏病且频发PVC的患者（男5例,女3例）,其中5例伴有阵发性左心室室性心动过速（室速）,年龄19—54（42．7±10．6）岁。其中3例患者行常规射频导管消融治疗,5例在三维电解剖标测系统（Carto系统）指导下行射频消融治疗。在左后分支标测到最早心室激动点处给予温度控制下射频导管消融。结果8例患者术前均以体表心电图定位起源于左后分支处区域,其PVC或左心室室速的体表心电图均为典型特发性左心室室速（ILVT）表现（QRS波呈右束支阻滞图形,心电轴左偏,QRS时限≤160ms）。其中,QRS波I导联6例呈rS,2例呈Rs;aVL导联呈qR;II、Ⅲ、aVF导联呈rs。胸前导联多在V,～V,处移形,由R转为Rs或rs。在消融成功部位（最早激动点）消融导管均记录到融合有浦肯野电位（PP）的V波,V波提前于体表心电图QRS波时限20—48（33．0±10．2）ms,8例患者行射频消融即时成功。术后3～15（8．1±4．2）个月复查,8例患者动态心电图的PVC均小于10000／24h。所有患者术中、术后无并发症发生。结论起源于左后分支处的PVC,在消融导管标测到PVC最早激动点并融合有PP时可成功消融PVC。     

分支起源室早的射频消融

目的探讨左室传导分支起源的室性早搏（Premature Ventricular Contractions,PVCs）的心电生理特点及导管射频消融（RadioFrequencyCatheterAblation,RFCA）方法。方法 14例排除器质性心脏病的左室分支起源的PVCs患者,3例行常规导管射频消融治疗,11例在三维电解剖标测（Carto）下射频消融治疗。结果14例患者均表现为＂反复心悸＂,PVCs均大于10000次/24h,7例伴有阵发性左室室性心动过速。6例左前分支起源患者的标准12导联心电图PVCs表现为心电轴右偏、右束支阻滞图形并左后分支阻滞（left posterior hemiblock,LPH）。8例左后分支起源患者的标准12导联心电图PVCs表现为心电轴左偏、右束支阻滞图形及左前分支阻滞（leftanteriorhemiblock,LAH）。在成功消融靶点（最早或提前激动点）附近均记录到浦肯野氏分支电位（Purkinje Potential,PP）,位于左室前外侧间隔、左室中间隔高位或左室后间隔中部,V波提前于体表心电图QRS波（33.0±10.1）ms;11例患者采用冷盐水灌注消融或普通Carto消融导管消融,3例常规7F双弯消融导管消融,放电即刻成功消融,无并发症。术后随访11±5个月,5例患者PVCs完全消失,9例患者24h动态心电图的PVCs小于1000次。结论起源于左室传导前、后分支起源的PVCs各有其临床特征,在消融导管标测到PVC最早或提前激动点并伴有PP处成功消融。     

射频消融左后分支治疗维拉帕米敏感性特发性室性心动过速

目的报道消融左后分支治疗左室特发性室性心动过速(简称室速)。方法对57例维拉帕米敏感性左室特发性室速患者进行电生理检查及射频消融,以窦性心律时产生左后分支阻滞和/或室速不再被诱发作为消融成功终点。结果57例中41例室速诱发条件稳定(71.9%),9例诱发条件不稳定(15.8%),7例不能被诱发(12.3%),所有患者均达消融成功终点。术后全部患者体表心电图Ⅰ导联出现R波降低,S波加深,呈rS形态或RS形态,Ⅱ、Ⅲ、aVF导联出现小q波,或在原有q波基础上加深,R波振幅明显增高,呈qR形态,额面电轴度数显著增加(54.06°±38.24°vs 90.55°±7.88°,P<0.001)。27例出现完全性左后分支阻滞改变(47.4%),30例为不完全性左后分支阻滞(52.6%)。1例1年后室速再发,左后分支阻滞消失,重复消融直至再次出现左后分支阻滞,术后室速未有再发。结论射频消融产生左后分支阻滞可作为左室特发性室速的消融成功终点,尤其适用于不易被常规电生理检查诱发的患者。     

Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract in patients with left ventricular dilation and/or dysfunction

Left ventricular (LV) dysfunction caused by frequent premature ventricular complexes (PVCs) can be reversed by suppression of PVCs with antiarrhythmic agents or radiofrequency catheter ablation (RFA). However, there is a paucity of data on the efficacy and safety of RFA among the local population. We aimed in this study to evaluate the effect of RFA of frequent PVCs originating from right ventricular outflow tract (RVOT-PVCs) on cardiac function in patients with depressed cardiac function and/or LV dilation. The study included sixteen patients with monomorphic RVOT-PVCs without overt underlying structural heart disease. Frequency of PVCs by 24-h Holter monitoring, left ventricular ejection fraction (LVEF), end-diastolic diameter (LVEDD), end-systolic diameter (LVESD), mitral regurgitation (MR) by echocardiogram and NYHA functional class were evaluated before and 3 and 6 months after RFA. All patients underwent RFA.ResultsThe higher the number of PVCs/24 h, the bigger the LVESD and the lower the EF. Procedural success was achieved in 13 (81%) of the patients with no complications. Six months follow-up after successful ablation, LVEDD decreased significantly (from 56.62 ± 5.87 to 49.23 ± 5.31 mm; p = 0.002), LVESD decreased significantly (from 41.85 ± 7.82 to 33.69 ± 4.66 mm; p = 0.002), LVEF increased significantly (from 46.69 ± 4.92% to 60.54 ± 5.39%; p < 0.001) and NYHA functional class improved in all patients after successful ablation.ConclusionRF catheter ablation of frequent RVOT-PVC has a beneficial effect on cardiac function in patients with depressed cardiac function.It carries a high degree of success and safety. Frequent RVOT-PVCs are burden on LV function even in patients without overt underlying structural heart disease.     

Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: Comparison with a control group without intervention

BACKGROUND: Idiopathic premature ventricular complexes (PVCs) usually are considered benign, even when frequent. However, case reports have demonstrated a possible link between frequent PVCs and left ventricular (LV) dysfunction. In addition, frequent PVCs recently were demonstrated to be associated with increased LV dimensions and cardiomyopathy. METHODS: Among 60 consecutive patients with idiopathic, frequent PVCs (>10/hour), a reduced LV ejection fraction (EF; mean 34% +/- 13%) was present in 22 (37%) patients. Patients with decreased LV function had a greater PVC burden on a 24-hour Holter monitor than patients with normal EF (37% +/- 13% vs. 11% +/- 10% of all QRS complexes; P <.0001). There was a significant inverse correlation between the PVC burden and the EF before ablation (r = 0.73, P <.0001). RESULTS: The PVCs originated in the right ventricular outflow tract in 31 (52%) of 60 patients, the LV outflow tract in 9 (15%) of 60 patients, and in other sites in 13 (22%) of 60 patients. The site of PVC origin could not be determined in seven patients. Ablation was completely successful in 48 (80%) patients. In patients with an abnormal EF before ablation, LV function normalized in 18 (82%) of 22 patients from a baseline of 34% to 59% +/- 7% (P <.0001) within 6 months. In the four patients in whom ablation was ineffective, the EF further declined from 34% +/- 10% to 25% +/- 7% (P = .06) during follow-up. In a control group of 11 patients with a similar PVC burden (30% +/- 8%) and a reduced EF (28% +/- 13%) who did not undergo ablation, the EF remained unchanged in 10/11 patients over 19 +/- 17 months of follow-up and one patient underwent heart transplantation. CONCLUSION: LV dysfunction in the setting of frequent, idiopathic PVCs may represent a form of cardiomyopathy that can be reversed by catheter ablation of the PVCs.     

射频消融左前分支起源的室性早搏

目的 探讨左前分支起源的室性早搏(PVC)的心电生理特点及射频导管消融结果.方法 6例排除器质性心脏病的左前分支起源的PVC患者,均在三维电解剖(Carto)标测系统指导下消融.结果6例患者标准12导联心电图PVC均表现为:右束支阻滞(RBBB)+左后分支阻滞(LPFB);V1～V6呈Rs型,Ⅰ、aVL呈rS或QS型,Ⅱ、Ⅲ、aVF呈qR或qRs型,aVR呈Qr或QS型;电轴右偏;QRS时限为(118±17)ms;PVC的移行区指数(transitional zoneindex)平均为(-2.08±0.49).在成功消融靶点(最早或提前激动点)附近均记录到浦肯野电位(purkinje potential,PP),位于左心室前外侧间隔或左心室中间隔高位,Ⅴ波提前于体表心电图QRS波20 ～48(33.0±9.9)ms.6例患者采用冷盐水灌注消融或普通Carto导管消融,即刻成功,无并发症.术后随访(11±5)个月,5例患者PVC完全消失,1例患者24 h动态心电图的PVC ＜1000次.结论 起源于左前分支处的PVC可在消融导管标测到PVC最早或提前激动点并伴有PP处成功消融.