三尖瓣环游离壁起源房速的电生理特征

目的报道一组起源于三尖瓣环(TA)游离壁房性心律失常的心电生理特征及射频消融治疗。方法7例患者经心内电生理检查和射频消融证实的起源于三尖瓣环游离壁的房性心律失常,对其心电生理特点及射频消融进行分析。结果三尖瓣环房速表现为阵发性,为心房程序刺激诱发(4例)或静滴异丙肾上腺素后自发(3例)。三尖瓣环房速有独特的体表心电图特征,所有患者I,aVL导联P波直立,TA11点起源房速II,III,aVF导联P波直立;TA9点起源房速II,III,aVF导联P波低幅直立;TA7点起源房速II,III,aVF导联P波倒置。TA11点起源房速胸导V1导为负向,V2～V6导P波逐渐移行为正向。其余部位TA房速V1～V6P波均为负向。7例患者均消融成功,随访12月均无房速复发。结论三尖瓣环房速有独特的心电图特征和房内激动顺序,长期随访这类房速射频消融有较好的治疗效果。     

起源于冠状静脉窦口的房性心动过速九例

目的报道9例起源于冠状静脉窦口附近的房性心动过速(简称房速)。方法回顾分析2005年11月至2009年1月行射频消融治疗的59例房速患者,发现9例起源于冠状静脉窦口。其定义为标测的最早激动点位于冠状静脉窦口周1 cm范围以内的区域并在此消融成功。结果9例靶点局部A波激动时间领先体表P波起点39±12(30~53)m s。房速体表P波具有以下特点:Ⅱ、Ⅲ、aVF导联P波呈负向波,I导联呈等电位线或低幅正向波,aVL导联呈正向波,多数病例V1导联P波前半部分为等电位线,后半部分为正向波,胸前导联P波由右向左在V3~V6导联逐渐移行为负向。结论冠状静脉窦口是右房房速的一个重要起源点,其体表心电图有明确特征。     

经主动脉无冠状窦内射频消融房性心动过速四例

4例经主动脉无冠状窦内射频消融成功的房性心动过速(简称房速),其体表心电图P波特点:4例Ⅰ和aVL导联P′波正向;2例Ⅱ、Ⅲ、aVF导联P波呈负正双向,1例呈浅倒置,1例在基线水平;4例V1导联P′波呈负正双向。房速时无冠状窦标测到最早的A波,较His束电位提前15～20ms,较体表P波起始领先32～40ms。在无冠状窦内消融成功,随访3～21个月,房速无复发。     

Carto标测指导下射频导管消融左心耳房性心动过速

目的探讨三维电解剖Carto指导下标测消融源于左心耳部位房性心动过速(房速)的方法和可行性。方法结合电生理和空间信息,首先利用Carto系统建立左心房三维解剖结构。对3例起源于左心耳的房速进行Carto标测,根据Carto标测来确定最早激动点,并以此为靶点进行射频消融。同时分析心动过速时体表心电图的P波特点。结果电解剖标测证实3例房速均为局灶性房速,其最早激动点起源于左心耳,并向左心房前壁、房间隔和后下壁激动。左心耳放电成功消融3例房速。体表心电图分析显示房速时Ⅱ、Ⅲ、aVF和V1导联P波为正向,I、aVL导联为完全负向。结论三维电解剖标测可以清楚显示左心耳解剖结构以及源于其中的房速的激动顺序并有利于经导管进行射频消融。     

经射频导管消融起源于心耳的局灶性房速

目的起源于左、右心耳处的局灶性房性心动过速(房速)比较少见,本研究报告14例起源于左、右心耳的局灶性房速的电生理特性和射频导管消融结果。方法 14例患者年龄为12～55岁,均有反复发作心悸和心动过速的病史,11例心动过速呈无休止发作,抗心律失常药物难以控制,其中3例伴明显左心室增大。电生理检查明确局灶性房速机制,其它机制的室上性心动过速经详细的的电生理检查和心内标测排除。对14例患者均在房速时进行体表心电图分析和激动标测,在心动过速时双极和单极标测所示的最早心房激动部位处行射频导管消融。14例患者中,5例应用CARTO三维标测系统引导标测和消融;除3例患者外,其他11例患者均应用盐水灌注导管消融。结果 10例起源于右心耳的局灶性房速患者,房速时的P’波形态Ⅰ导联和Ⅱ、Ⅲ、aVF导联均为正向波,aVL导联P’波负向、正向、双向者分别是3例、3例和4例;V1导联负向波为主(7/10),V3～V6导联正向波为主(9/10),1例V1～V6导联P波全部为正向波。4例左心耳局灶性房速的P’波形态,Ⅰ和aVL导联均为负向波,Ⅱ、Ⅲ和aVF导联均为正向波,V1～V6导联均为正向波。10例右心耳起源房速均消融成功;4例左心耳起源房速2例消融成功,2例消融失败。14例均无围术期相关并发症发生。在随访期间,右心耳起源房速复发1例,经再次消融成功;其他成功消融患者在未服用抗心律失常药物下无房速复发,3例左心室增大患者随访中左心室基本恢复正常。结论起源于左、右心耳局灶性房速多呈无休止特点,可导致心动过速性心肌病。经射频导管消融心耳部(尤其是右心耳)起源局灶性房速有较高的成功率、较低的复发率和较好的安全性。     

经射频导管消融起源于心耳的局灶性房速

目的起源于左、右心耳处的局灶性房性心动过速(房速)比较少见,本研究报告14例起源于左、右心耳的局灶性房速的电生理特性和射频导管消融结果。方法 14例患者年龄为12～55岁,均有反复发作心悸和心动过速的病史,11例心动过速呈无休止发作,抗心律失常药物难以控制,其中3例伴明显左心室增大。电生理检查明确局灶性房速机制,其它机制的室上性心动过速经详细的的电生理检查和心内标测排除。对14例患者均在房速时进行体表心电图分析和激动标测,在心动过速时双极和单极标测所示的最早心房激动部位处行射频导管消融。14例患者中,5例应用CARTO三维标测系统引导标测和消融;除3例患者外,其他11例患者均应用盐水灌注导管消融。结果 10例起源于右心耳的局灶性房速患者,房速时的P’波形态Ⅰ导联和Ⅱ、Ⅲ、aVF导联均为正向波,aVL导联P’波负向、正向、双向者分别是3例、3例和4例;V1导联负向波为主(7/10),V3～V6导联正向波为主(9/10),1例V1～V6导联P波全部为正向波。4例左心耳局灶性房速的P’波形态,Ⅰ和aVL导联均为负向波,Ⅱ、Ⅲ和aVF导联均为正向波,V1～V6导联均为正向波。10例右心耳起源房速均消融成功;4例左心耳起源房速2例消融成功,2例消融失败。14例均无围术期相关并发症发生。在随访期间,右心耳起源房速复发1例,经再次消融成功;其他成功消融患者在未服用抗心律失常药物下无房速复发,3例左心室增大患者随访中左心室基本恢复正常。结论起源于左、右心耳局灶性房速多呈无休止特点,可导致心动过速性心肌病。经射频导管消融心耳部(尤其是右心耳)起源局灶性房速有较高的成功率、较低的复发率和较好的安全性。     

射频消融治疗起源于心房下部局灶房性心动过速

对6例起源于右房下部及3例起源于冠状静脉窦口局灶性房性心动过速(简称房速),行常规心内电生理检查,明确房速时心房激动顺序,寻找心房激动最早起源点标测与消融,临床随访评价疗效。结果:6例右房下部房速心电图Ⅱ、Ⅲ、aVF、V1导联P′为负,Ⅰ、aVL为正,3例冠状窦口部房速心电图Ⅱ、Ⅲ、aVF及V1导联P′波为负\正双向,Ⅰ、aVL P′低平,不易区别。成功消融靶点双极电图A-P间期40±15 m s。结论:体表心电图可大致区分房速起源部位。     

起源于右心耳局灶性房性心动过速电生理特点及射频消融

目的探讨起源于右心耳局灶性房性心动过速（RAAT）心电图、电生理特点及射频消融。方法138例经射频消融治疗的局灶性房性心动过速（房速）中有7例（5．0％）起源于右心耳,通过10极冠状静脉窦（CS）电极导管、高位右心房（HRA）电极导管、希氏束（HBE）电极导管和消融导管（ABL）记录其电生理检查结果、靶点位置,并记录和观察体表心电图房性P波形态（正向、负向、低平和双向）。结果7例RAAT患者平均年龄为（41．1±19．6）岁,病史（5．4±4．0）年,其中男性4例,女性3例。房速持续性4例,阵发性2例,通过心房程序刺激诱发1例。体表心电图房性P波形态特征：所有患者V,导联P波负向,绝大多数下壁导联P波正向或双向,胸前导联P波由负向逐渐变为正向。心内电生理检查提示房速时HRA处A波最早,有效消融靶点较体表心电图P波提前（38．4±12．6）ms。6例患者消融成功,其中4例使用盐水灌注消融导管,随访3～12个月无房速复发,未见并发症发生。结论RAAT相对少见（5．0％）,有特殊的心电图和心内电生理表现,盐水灌注消融导管能提高消融成功率,远期效果好。     

心房后间隔局灶性房性心动过速的电生理特征及射频消融

目的 探讨起源于心房后间隔及邻近区域局灶性房性心动过速（房速）心脏电生理特点及射频导管消融特点.方法 入选23例患者,男12例,女11例,平均年龄（48.3±19.3）岁,自发或心房程序刺激诱发房速后,分析体表心电图P＆#39;波特点并于后间隔各个部位进行激动标测和射频消融治疗.结果 23例心房刺激均能反复诱发或终止房速,平均周长（346.7±61.8） ms,房速时P＆#39;波时限明显短于窦性心律时P波时限[（86.2±14.0）ms对（115.4±19.9） ms,P＜0.05].体表P＆#39;波表现为Ⅰ导联多呈等电位线,下壁导联呈深倒负向波,aVR和aVL导联呈正向波,V3～W5导联呈负向波.常规激动标测,所有患者于冠状静脉窦口（CSO）附近标测到相对提前的心房激动,其中12例起源于右后间隔,6例起源于CSO及近端,2例起源于心中静脉,3例起源于左后间隔.靶点提前体表P＆#39;波平均（34.4±18.0） ms,放电开始至心动过速终止时间为（6.2±4.2）s,11例患者放电过程中出现交界区心律.所有患者均消融成功,其中3例需应用盐水灌注导管.随访4个月～ 10年,无复发病例及手术相关并发症.结论 后间隔局灶性房速P＆#39;波形态具有特异性,对导管消融定位意义较大.由于解剖的复杂性,部分病例标测和消融困难,需结合右心房后间隔、冠状静脉窦（CS）内和/或其分支、左心房后间隔等多部位标测和/或消融方能获得成功.     

无冠窦起源房速的电生理特征与射频消融

目的进一步分析起源于主动脉无冠窦房性心律失常的心电生理特征及射频消融治疗。方法11例患者经心内电生理检查和射频消融证实的起源于主动脉无冠窦局灶性房速,对其临床特征,心电生理特点及射频消融进行分析。结果无冠窦房速大多为女性,表现为阵发性,为心房或心室程序刺激诱发和终止。所有患者房速心电图P波窄而低幅,Ⅱ,Ⅲ,aVF和v,导联P波负正双向,Ⅰ,aVL导联直立,V2～V6导联P波负向。心内最早激动位于希氏束远端,并领先于体表P波起始（15±3）ms。无冠窦内标测最早激动等于或早于希氏束远端,局部电位特征为大A小V（或大V）,无希氏束电位,11例患者无冠窦内放电均在8秒内终止心动过速,均无并发症,无抗心律失常药物随访12±5月所有患者均无心动过速复发。结论主动脉无冠窦房速有独特的临床特征,心电图特征及心房内激动顺序,长期随访这类房速射频消融有良好的治疗效果。     

无冠窦起源房性心动过速的电生理特点及射频消融治疗五例分析

目的研究无冠窦起源房性心动过速(房速)的电生理特点。方法 5例无冠窦起源房速患者,其中男性2例,女性3例,年龄37～68岁。观察心动过速时P波形态,心内标测心房最早激动部位,并行射频消融治疗。结果 5例无冠窦起源房速的周长平均为(363±44)ms。P波形态主要表现为在Ⅱ、Ⅲ和aVF导联上直立和双向,aVR导联倒置,在aVL导联上全为正向。胸前导联中,V_1～V_2为负正双向,V_3～V_5为负正双向或正向,V_6为正向。5例患者均于无冠窦内成功消融,术后随访6个月均未见复发。结论无冠窦起源房速P波形态的特征可能为右胸导联先负后正,下壁导联直立或双向。此类房速的射频消融安全有效。     

Electrocardiographic and electrophysiologic characteristics of ventricular tachycardia originating within the pulmonary artery

OBJECTIVES: We investigated the electrocardiographic (ECG) and electrophysiologic characteristics of ventricular tachycardia (VT) originating within the pulmonary artery (PA). BACKGROUND: Radiofrequency catheter ablation (RFCA) is routinely applied to the endocardial surface of the right ventricular outflow tract (RVOT) in patients with idiopathic VT of left bundle branch block morphology. It was recently reported that this arrhythmia may originate within the PA. METHODS: Activation mapping and ECG analysis were performed in 24 patients whose VTs or ventricular premature contractions (VPCs) were successfully ablated within the PA (PA group) and in 48 patients whose VTs or VPCs were successfully ablated from the endocardial surface of the RVOT (RV-end-OT group). RESULTS: R-wave amplitudes on inferior ECG leads, aVL/aVR ratio of Q-wave amplitude, and R/S ratio on lead V(2) were significantly larger in the PA group than in the RV-end-OT group. On intracardiac electrograms, atrial potentials were more frequently recorded in the PA group than in the RV-end-OT group (58% vs. 12%; p < 0.01). The amplitude of local ventricular potentials recorded during sinus rhythm within the PA was significantly lower than that recorded from the RV-end-OT (0.62 +/- 0.56 mV vs. 1.55 +/- 0.88 mV; p < 0.01). CONCLUSIONS: Ventricular tachycardia originating within the PA has different electrocardiographic and electrophysiologic characteristics from that originating from the RV-end-OT. When mapping the RVOT area, the catheter may be located within the PA if a low-voltage atrial or local ventricular potential of <1-mV amplitude is recorded. Heightened attention must be paid if RFCA is required within the PA.     

Focal atrial tachycardia arising from the tricuspid annulus: electrophysiologic and electrocardiographic characteristics

INTRODUCTION: Focal right atrial tachycardia (RAT) arising from the crista terminalis, para-Hisian, and coronary sinus os regions are well described. Less information exists regarding RAT arising from the nonseptal region of the tricuspid annulus (TA). METHODS AND RESULTS: From a consecutive series of 64 patients who had undergone successful radiofrequency ablation (RFA) of 67 RATs, the characteristics of 9 (13%) patients (6 men; mean age 50 +/- 20 years) with a TA focus were reviewed. The annular focus was localized to the inferoanterior TA in 7 and the superior TA in 2. Mean tachycardia cycle length was 371 +/- 66 msec. Mean activation time at the site of successful RFA in 9 of 9 patients was -43 +/- 11 msec. At 9.3 +/- 5.6 months of follow-up, 1 of 9 patients had recurrent tachycardia successfully treated with repeat RFA. In 7 of 9 patients with RAT from the inferoanterior TA, the surface ECG P wave morphology was upright in aVL, inverted in III and VI, and either inverted or biphasic with an initial negative deflection from V2 to V6. CONCLUSION: The TA is an important site of origin of RAT. In the present study, the inferoanterior region of the TA was a preferential site of origin with resulting characteristic P wave morphology. Knowledge of this anatomic distribution and P wave morphology allows targeted mapping and may facilitate successful RFA.     

P wave polarities of an arrhythmogenic focus in patients with paroxysmal atrial fibrillation originating from superior vena cava or right superior pulmonary vein

INTRODUCTION: The superior vena cava (SVC) and right superior pulmonary vein (RSPV) are anatomically close structures. Using 12-lead ECG may facilitate identification of ectopic foci from SVC or RSPV. The aim of this study was to assess whether P wave polarity on surface ECG is helpful in distinguishing an arrhythmogenic focus of paroxysmal atrial fibrillation (AF) from SVC or RSPV. METHODS AND RESULTS: Thirty-four patients with paroxysmal AF from the SVC (group I: 17 patients, 10 men and 7 women; mean age 57 +/- 12 years) or RSPV (group II: 17 patients, 15 men and 2 women, mean age 62 +/- 14 years) underwent electrophysiologic study and radiofrequency (RF) catheter ablation. All of the AF foci were confirmed by successful ablation. P wave polarities on surface ECG inferior leads were positive during sinus rhythm and ectopic beats in both groups. Leads I, aVR, aVL, and V1 were further analyzed. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) in predicting an arrhythmogenic focus of AF from SVC or RSPV were provided. P wave polarity in lead aVR was negative in all 34 patients. P wave polarity in lead V1 was positive in 47.1% of SVC ectopy but positive in all RSPV ectopy. The combination of a biphasic or isoelectric P wave polarity in lead V1 or a biphasic P wave polarity in lead aVL had a sensitivity of 71%, specificity of 82%, PPV of 80%, and NPV of 74% in predicting an arrhythmogenic focus of AF from SVC. CONCLUSION: P wave polarity in leads V1 and aVL may predict an arrhythmogenic focus of AF from SVC or RSPV.     

Atrial tachycardia initiating atrial fibrillation successfully ablated in the non-coronary cusp of the aorta

A 60-year-old woman was referred for catheter ablation of atrial fibrillation (AF). Atrial flutter and atrial tachycardia (AT) also had been clinically documented. During the electrophysiological study, the clinical AT was induced by burst atrial pacing during isoproterenol infusion and exhibited negative P waves in the inferior leads, positive P waves in leads I, aVL, and aVR, and biphasic P waves in lead V1. The AT repeatedly and spontaneously accelerated to initiate AF by causing fibrillatory conduction in the atria. Successful catheter ablation of the AT was achieved in the non-coronary cusp of the aorta (NCC) where the local atrio-ventricular electrogram amplitude ratio was >1 during both the AT and sinus rhythm. The tailored approach targeting the NCC AT alone without left atrial ablation completely eliminated the AF. In catheter ablation of AF in a patient with a co-existing clinical AT, it may be recommended to examine the clinical AT first. If the clinical AT initiates the AF and local atrial activations in the His bundle region precede the P wave onset during AT, mapping in the NCC should be considered prior to left atrial catheterization.     

常规心电图对急性前壁心肌梗死时前降支闭塞部位预测价值的临床研究

目的探讨急性前壁心肌梗死时的常规心电图（ECG）对前降支（LAD）闭塞部位的预测价值。方法根据冠状动脉造影的结果，以第一间隔支（S1）为标志将患者分为S1近端病变（PS）组（61例）和S1远端病变（DS）组（40例）。分别测量常规ECG12导联ST段的偏移程度及出现的频率，以计算、比较两组之间的差异及其对近、远段病变部位的预测性诊断价值。结果（1）各导联诊断LAD近端病变的敏感性和特异性分别为：aVR导联ST段抬高为43％和85％（P=0．004）；aVL导联ST段抬高≥1．5mm为16％和97％（P=0．031）；Ⅱ导联ST段下移≥1．0mm为39％和85％（P=0．009）；Ⅲ导联ST段下移≥2．0mm为23％和98％（P=0．005）；aVF导联ST段下移≥1．0mm为38％和88％（P=0．006）；V5导联ST段下移为20％和86％（P=0．037）；aVR导联ST段抬高同时伴V5导联ST段下移为18％和100％（P=0．005）；aVR导联ST段抬高同时伴V6导联ST段下移为30％和93％（P=0．008）；（2）各导联诊断LAD远端病变的敏感性和特异性分别为：Ⅲ导联ST段居于等电位线或抬高为53％和90％（P=0．000）；V5导联ST段抬高≥1．5mm为50％和82％（P=0．001）；（3）近、远端患者的梗死面积和心功能水平未见明显差异。结论（1）aVR导联ST段抬高同时出现V5、V6导联ST段下移；下壁导联Ⅱ、Ⅲ、aVF导联ST段明显下移（Ⅱ，aVF导联ST段下移≥1．0mm，STⅢ下移≥2．0mm）以及Ⅰ，aVL导联ST段抬高，尤其是aVL导联ST段抬高≥1．5mm均提示LAD近端病变。（2）下壁导联（尤其是Ⅲ导联）ST段居于等电位线或升高，V5导联ST段抬高≥1．5mm均提示LAD远端病变。     

Role of surface electrocardiogram precordial leads in localizing different anatomic sites of ectopic atrial tachycardia arising from lower right atrium in pediatric population

Background

The study was designed to examine P wave morphology (PWM) in precordial leads (V₁–V₆) during ectopic atrial tachycardia (EAT) originating from low right atrium (RA) to identify the anatomic sites of these foci in children.

Methods

Twenty‐three consecutive pediatric patients (56% females, mean age 8.5 ± 2.5) with EAT originating from the low RA underwent detailed atrial endocardial activation mapping and radiofrequency ablation. PWM during EAT was analyzed using standard 12‐lead ECG in relation to successful ablation sites in RA.

Results

Ectopic atrial tachycardia originated from coronary sinus ostium (CSo) in 12 patients, nonseptal tricuspid annulus (TA) in five, lower crista terminalis (CT) in three and lower free wall in three. In lead V₁, PWM showed a positive pattern during EAT originating from CSo (8/12) [91.7% sensitivity, 100% specificity, 100% positive predictive value (PPV), 100% negative predictive value (NPV)]. A negative pattern was observed in EAT originating from lower free wall (1/3) and nonseptal TA (5/5) [50% sensitivity, 100% specificity, 100% PPV, 75% NPV], while isoelectric pattern was in EAT originating from lower CT (3/3) [100% sensitivity, 100% specificity, 100% PPV, 100% NPV]. In leads V₃–V₆, PWM showed a negative pattern in at least two consecutive leads during EAT from CSo (12/12), nonseptal TA (5/5) and lower free wall (3/3) while it was positive in EAT originating from lower CT (3/3) [100% sensitivity, 95% specificity, 75% PPV and 100% NPV].

Conclusions

P wave morphology in precordial leads can help differentiate the anatomic sites of EAT from lower RA with high PPVs and NPVs.