三维标测系统指导射频消融治疗三尖瓣环游离壁起源的室性心律失常临床分析

目的探讨三尖瓣环游离壁起源的室性心律失常(VAs)体表心电图特点及三维标测系统指导下射频消融治疗的效果。方法回顾性分析2016年10月至2017年10月在北京安贞医院住院的连续9例起源于三尖瓣环游离壁的VAs患者。所有患者均在三维标测系统指导下采用压力监测导管进行激动标测和基质标测,行射频消融治疗,分析患者12导联心电图QRS波特征。结果 9例VAs患者经射频消融即刻成功8例(8/9),失败1例(1/9),后经心外膜标测消融,心内膜、心外膜均可见大片异常电压区,所有患者均无并发症发生。起源于三尖瓣环游离壁的VAs患者心电图特征表现为左束支传导阻滞,V1、V2导联呈r S型,Ⅰ、V5及V6导联呈R型,胸前导联移行区通常在V4或之后,由三尖瓣环后侧壁到侧壁再到前侧壁,下壁导联R(r)波逐渐增高,而S(s)波逐渐变浅甚至消失,同时R(r)波呈Ⅱa VFⅢ,S(s)波呈ⅢaVFⅡ。结论三维标测系统指导射频消融治疗三尖瓣环游离壁起源的VAs安全有效,该部位起源的VAs患者有典型心电图特征,部分超声心动图结构正常的患者继发于致心律失常性右心室心肌病,可能为其早期表现。     

起源于三尖瓣环的特发性室性心律失常体表心电图特点及射频导管消融治疗

目的 评估起源于三尖瓣环的室性心动过速(室速)和室性早搏(室早)的体表心电图特点及射频导管消融治疗效果.方法 共12例特发性室速/室早患者接受常规电生理检查及射频导管消融治疗,对所有病例的12导联体表心电图进行分析.结果 12例室速/室早均消融成功,并证实均起源于三尖瓣环附近,7例起源于三尖瓣环游离壁侧,5例起源于三尖瓣环间隔侧.三尖瓣环游离壁侧室速/室早QRS波平均时限长于三尖瓣环间隔侧室速/室早;游离壁侧室速/室早比间隔侧室速/室早QRS终末部更多见切迹.间隔侧室速/室早比游离壁侧室速/室早V1导联更多见QS型.结论 起源于三尖瓣环的室速/室早是特发性室速/室早的一个亚组,射频导管消融治疗可取得良好效果,掌握其体表心电图特点有助于消融术前判定室速/室早具体起源部位.     

起源于三尖瓣环附近的室性心律失常的射频消融及心电图特征

目的总结起源于三尖瓣环附近的室性心律失常的射频消融及心电图特征。方法 15例患者,根据心电图和/或动态心电图诊断为室性心动过速(VT)或频发室性早搏(VPC),均接受心脏电生理检查及射频消融治疗。消融成功后,结合靶点分布区域分析体表心电图。结果 15例消融均获成功,根据消融导管的X线影像特征及腔内电图判断均起源于三尖瓣环附近,不同区域起源的VT/VPC心电图表现各具特征,QRS波时限140 ms、肢体导联见切迹、V1导联可见正向起始波及胸前导联移行区间≥V4判断起源于游离壁的特异度分别为100%、100%、100%、91.7%,敏感度分别为81.8%、90.9%、81.8%、100%。结论射频消融是治疗三尖瓣环附近起源的室性心律的安全、有效方法,心电图表现具其特征。     

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。     

三尖瓣环不同部位起源的特发性室性心律失常患者心电图QRS波特征分析

目的 分析三尖瓣环不同部位起源的特发性室性期前收缩(IPVCs)/特发性室性心动过速(IVT)患者体表12导联心电图QRS波特征及变化规律。方法 收集2013年1月至2018年12月仙桃市第一人民医院210例行射频消融术(RA)治疗的三尖瓣环起源的IPVCs/IVT患者的临床资料,分析患者不同起源部位的体表心电图特征和RA的治疗效果。结果 本组210例患者中,行RA治疗成功192例,成功率为91.43%。随访3～36个月,平均(19.94±3.24)个月,期间复发6例。将发病部位为前侧壁、侧壁、后侧壁作为游离壁组(99例),前间隔、中间隔、后间隔为间隔组(111例)。相比间隔组,游离壁组QRS平均时限明显增宽差异有统计学意义(t=13.500,P 0.01)。三尖瓣环游离壁各个部位起源的IPVCs/IVT患者在心电图Ⅰ导联的比较,并无统计学意义(χ2=6.876,P 0.05);Ⅰ、aVL导联呈现R型,V1～V3导联呈现rS型,V5～V6导联呈现R型,胸前导联移行区多见于V3导联或之后,下壁导联呈现R型或Rs型或rS型。三尖瓣环间隔部各个部位起源的IPVCs/IVT患者在心电图Ⅰ导联呈现R型,Ⅱ导联呈现Rs型或R型,Ⅲ导联呈现QS型或rS型或Rs型,aVF导联呈现rS型或rs型或R型,V1导联呈现QS型,V5～V6导联呈现R型,胸前导联移行区多见于V2～V3导联之间,或V3导联之后。结论 三尖瓣环不同部位起源的IPVCs/IVT患者体表12导联心电图QRS波特征存在一定差异,亦存在一定变化规律,这些心电图特征有助于术前评估其起源部位和有效靶点,有助于减少手术时间,降低RA治疗的失败率。     

起源于主动脉窦与二尖瓣环交界处的室性心律失常心电图特征及射频消融

目的研究起源于主动脉窦与二尖瓣环交界处(AMC)室性心律失常的心电图特点及射频消融。方法观察6例起源于AMC的室性心律失常患者心电图特征及射频消融。结果 41例室性心律失常患者成功完成射频消融并且证实其起源部位,其中6例起源于AMC。仅有起源于AMC的室性心律失常心电图表现为右束支传导阻滞,QRS波电轴右偏,V1～V6导联中见到R或Rs波形,下壁导联振幅较高,Ⅰ导联呈Rs或rs形,RⅡ/RⅢ<1。三维激动扩布图可见始于AMC的波阵扩布,随后沿AMC传导至主动脉根部及左室,成功靶点消融时间短于左、右室流出道室性心律失常。结论室性心律失常时V1～V6出现R或Rs波形提示其起源于AMC,射频消融治疗安全、有效。     

经右锁骨下静脉途径导管射频消融三尖瓣环下的室性心律失常

目的探讨经右锁骨下静脉途径结合应用长鞘(SR0)导管射频消融三尖瓣环下起源的室性心律失常有效性及安全性。方法 8例患者,根据心电图和/或动态心电图诊断为三尖瓣环附近起源室性早搏(PVC)/室性心动过速(VT),均接受心脏电生理检查及射频消融治疗。术前曾经或术中采取常规下腔静脉途径消融失败后,改经右锁骨下静脉途径并辅用长鞘SR0进行标测与消融。消融成功后,结合靶点位置分析心电图及消融结果。结果 8例消融均获成功。根据消融导管的X线影像特征、电解剖证实其起源于三尖瓣环下6～9点。12导联体表心电图的PVC/VT的QRS波均呈左束支传导阻滞伴电轴左偏图形,Ⅰ、aVL导联主波向上,Ⅱ、Ⅲ、aVF导联主波向下,2例肢体导联见切迹,QRS波时限174.75±13.44 ms,消融靶点局部V波较体表心电图QRS波提早27.5±3.16 ms。8例成功消融靶点图只见V波,6例有峰电位。随访2～12个月,1例PVC复发。结论在长鞘辅助下,经右锁骨下静脉途径能够安全、有效地消融治疗三尖瓣环下PVC/VT,是经股静脉途径消融失败的有效补充。     

右心室间隔部希氏束附近室性期前收缩心电图与射频消融

目的 报道右心室流入道间隔部希氏束附近起源室性期前收缩体表心电图特征及射频消融效果。方法 无器质性心脏病频发性室性期前收缩5例,分析其12导联体表心电图室性期前收缩特点;病人接受心内电生理检查,于右心室流入道行激动与起搏标测,以心室激动较体表QRS波提早、消融导管远端起搏图形与体表心电图室性期前收缩相似部位为消融靶点。结果 室性期前收缩QRS波形态：5例病人Ⅰ导联和Ⅱ导联QRS波均呈R型,Ⅲ导联、aVF导联以低振幅波为主,V1导联均呈QS型,胸导联较早转变成qR或R型（发生于V2或V3）,V5、V6均呈高R型;室性期前收缩QRS波时限为110～120ms。5例病人分别于前间隔（2例）、中间隔（1例）、后间隔（2例）标测到消融靶点,放电后前间隔部、后间隔部病人室性期前收缩均消失,中间隔病人消融失败。无房室传导阻滞并发症。随访8～30个月,成功病例未应用抗心律失常药物,无室性期前收缩发作。结论 右心室流入道间隔部希氏束附近起源室性期前收缩体表心电图具有明显的特征,认识这些特征有助于导管标测与射频消融,消融此部位室性期前收缩安全、有效。     

起源于主动脉窦频发室性期前收缩的心电生理特征及射频消融治疗

目的报道11例起源于主动脉窦的频发室性期前收缩（premature ventricular contraction,PVC）患者的心电生理特征、射频消融（radiofrequency catheter ablation,RFCA）方法及疗效。方法分析患者术前体表心电图和动态心电图PVC的特点,测量V1或V2导联r波时限和振幅,计算r波与QRS波时限的比值及r波于S波振幅的比值。术中行主动脉窦内激动标测和起搏标测确定PVC起源部位,并行冠状动脉造影辅助定位后行RFCA。结果11例均有频发PVC,5例有反复短阵室性心动过速。下壁导联QRS波呈R形且高大直立,V1导联呈rS型,胸前导联多移行于V3以前,V6导联多呈Rs型或无S波。V1导联r波时限（84.6±9.8）ms,占QRS波时限的50%以上;r/S振幅比值0.72±0.31。有效消融靶点局部电图V波较体表心电图的QRS波明显提前（35.6±8.9）ms,有效靶点放电2～8 s见PVC减少至消失。结论起源于主动脉窦的PVC其下壁导联QRS波呈R形且高大直立,V1或V2导联r波时限宽（〉50%同导联QRS波）,r波振幅高（〉30%同导联S波）;主动脉窦内PVC的射频消融治疗是安全、有效的。     

起源于三尖瓣环非间隔部位的房性心动过速体表心电图特点及射频消融治疗

目的报道起源于三尖瓣环非间隔部位的房性心动过速(简称房速)体表心电图特点及射频消融结果。方法13例房速均被证实起源于三尖瓣环非间隔部位并射频消融成功。影像学消融靶点位于三尖瓣环,局部电图可见A波和V波,且A∶V<2,V波的振幅>0.5 mV。结果9例消融成功部位位于三尖瓣环下侧壁,4例位于三尖瓣环上侧壁,靶点局部A波激动时间领先体表心电图P波起点41±15 ms,AV比值0.5±0.4。三尖瓣环下侧壁起源的房速P波特点:Ⅰ、aVL、aVR导联P波正向,Ⅱ、Ⅲ、aVF导联P波负向,V1～V6导联P波负向。三尖瓣环上侧壁起源的房速P波特点:Ⅰ、aVL导联P波正向,aVR导联P波负向或呈等电位线,Ⅱ、Ⅲ、aVF导联P波低幅正向波或呈等电位线,V1导联负向,胸前导联由右向左P波逐渐移行为正向。结论三尖瓣环非间隔部位是右房房速的一个重要起源点,其体表心电图有明确特征。     

Calcification of the tricuspid annulus

Tricuspid annular calcification was observed on cardiac screening of a 50 year old woman with congenital valvular pulmonary stenosis and confirmed by angiography. At operation, the tricuspid annular calcification was palpable but there was no interference with valvular function. There was no associated disease process in this patient. Phosphate and calcium metabolism was normal. Tricuspid annular calcification is very rare: 7 other reported cases, aged 42 to 51 years old. All patients had right ventricular hypertension usually caused by pulmonary stenosis. Tricuspid valve function was normal in all cases. The pathogenesis is discussed: a premature degenerative process favored by right ventricular hypertension may be responsible. This would appear to be the first case to be published in France.     

Mitral annulus motion versus long-axis fractional shortening

BACKGROUND: In most echocardiographic studies concerning mitral annulus motion (MAM) in the assessment of left ventricular (LV) systolic function, comparisons have been performed between MAM, which represents a distance, and ejection fraction (EF), which represents a ratio between volumes. However, in theory, it is probably more suitable to compare the long-axis fractional shortening (FS(L)) (the ratio between the change in length [ie, MAM] and the end-diastolic length of the left ventricle) with EF. OBJECTIVES: To compare EF with MAM and EF with FS(L) in the assessment of LV systolic function. METHODS: Thirty healthy subjects were investigated using echo-cardiography, and the linear correlations between EF and MAM, and EF and FS(L) were calculated. RESULTS: The linear correlation (r) was found to be higher between EF and FS(L) (r=0.65; P<0.001) than between EF and MAM (r=0.49; P<0.01). CONCLUSIONS: The higher correlation between EF and FS(L) than between EF and MAM suggests that FS(L), which includes a correction for ventricular length, may be a more suitable index of LV systolic function than MAM per se.     

Atrial tachycardia originating at the tricuspid annulus

We report a patient with re-entrant atrial tachycardia that originated at the inferolateral tricuspid annulus. Single atrial extra-stimulation reproducibly induced the atrial tachycardia with an inverse relationship between the coupling interval of extra-stimulation and the return cycle of the first tachycardia beat. A real-time three-dimensional electroanatomical mapping showed focal atrial activation spreading semi-radially from the tricuspid annulus. The tachycardia was successfully eliminated by radiofrequency ablation at the earliest atrial activation site, preceding by 27 ms the arbitrary determined onset of surface P wave. An accelerated atrial rhythm with similar P-wave morphology to that of the tachycardia was observed at the successful ablation site during radiofrequency application. The mechanism of this tachycardia seems to be due to re-entry originating in or around the possible accessory atrioventricular node without ventricular connection.     

Myxoma on a mechanical mitral valve annulus

To date, myxoma on a mechanical valve annulus has not been reported. The case is reported of a 74-year-old woman who was admitted to hospital following the identification of an intracardiac tumor mass. Six years previously, the patient had received a mechanical valve implanted in the mitral position. Transesophageal echocardiography revealed a mobile hypoechogenic tumorous mass attached to the anterior annulus of the prosthesis. The tumor was successfully treated by surgical excision, and a diagnosis of myxoma was confirmed both clinically and pathologically.     

A larger aortic annulus causes aortic regurgitation and a smaller aortic annulus causes aortic stenosis in bicuspid aortic valve

A bicuspid aortic valve (BAV) often causes aortic stenosis (AS) or regurgitation (AR). In 54 patients with a BAV (48 +/- 16 years), transthoracic and transesophageal echo were performed to measure aortic annulus diameter (AAD), to evaluate the severity of aortic valve disease (AVD) and to calculate the area eccentricity index (AEI) of a BAV defined as a ratio of the larger aortic cusp area to a smaller aortic cusp area. By multiple linear regression analysis, the severity of AR correlated significantly with the AAD (r = 0.38) and AEI (r = 0.35) (P < 0.05) and that of AS correlated significantly with the AAD (r =-0.40) and AEI (r = 0.34) (P < 0.05). Thirty-six patients showed anteroposteriorly (A-P) located BAVs and 18 patients showed right-left (R-L) located BAVs. The AAD was larger in A-P type than in R-L type (15 +/- 3 vs 13 +/- 2 mm/BSA, P < 0.05) and there was no difference in the age and AEI between the two groups. AR was more severe in A-P type than in R-L type while AS was more severe in R-L type than in A-P type (P < 0.05). Twenty-nine patients showed raphes. The AEI was larger in raphe (+) type than in raphe (-) type (1.83 +/- 0.53 vs 1.51 +/- 0.47, P < 0.05) and there was no difference in the AAD and severity of AVD between the two groups. In conclusion, a BAV with larger aortic annulus or A-P located will tend to cause AR while a BAV with smaller aortic annulus or R-L located will tend to cause AS.     

Aortic valve replacement with anterior and posterior enlargement of small aortic annulus is comparable to surgery with normal annulus.

OBJECTIVE: To compare results of aortic valve replacement in patients with normal annulus and in those undergoing anterior and posterior enlargement of a small annulus to implant a larger prosthesis. METHODS: The study included 22 patients with enlargement of a small aortic annulus and 23 with a normal aortic annulus, with similar demographic characteristics and selected from a large surgical population. For normal annulus, simple valve replacement was performed. For annular enlargement, the posterior approach required incision in the mid portion of the non-coronary sinus, up to the anterior mitral leaflet; anterior enlargement was achieved by an incision between the left and right coronary ostium, extended to the ventricular septum for 2 cm. The aorta was reconstructed with bovine pericardium patches. The results analyzed included diameter of aortic annulus at surgery, clinical evolution (2 to 11 years of follow-up), left outflow tract obstruction and left ventricular mass (by Doppler echocardiography). RESULTS: Enlargement increased the aortic annulus from 18.3 +/- 2.2 mm to 24.8 +/- 2.0 mm (p < 0.001), a value similar to aortic annulus considered normal: 24.9 +/- 1.5 mm (NS). For annular enlargement, the peak systolic gradient at the prosthesis decreased from 83.6 +/- 22.3 mmHg (preoperative) to 26.7 +/- 11.4 mmHg (p < 0.01) at the last evaluation. For normal annulus, a reduction from 68.2 +/- 28.7 mmHg to 32.8 +/- 16.2 mmHg occurred (p < 0.001) (final values similar between groups; NS). Left ventricular mass at the last evaluation was 147.2 +/- 45.9 for patients with enlargement and 148.1 +/- 70.4 for those with normal annulus. CONCLUSION: Anterior and posterior aortic annulus enlargement enabled increases in annular diameter and valve prosthesis size, providing clinical and echocardiographic results similar to patients with valve replacement in a normal annulus.