选择性消融逆传快径治疗典型房室结折返性心动 …

设计一种新的射频消融方法（选择性消融逆传快径）对２５例反复发作的典型房这地折返性心动过速（ＡＶＮＲＴ）进行消融治疗。经股静脉插入１～２根大头电极至Ｋｏｃｈ氏三角区,于旁Ｈｉｓ束心室起搏下寻找逆传Ａ最早的靶点,靶点图上不能有或仅有极小Ｈ波,大头电极用力压向靶点出现：（１）ＶＡ分离或ＨＡ间期延长,说明逆传快径已机械刺激所阻断,立即放电１５～２５Ｗ,持续３０～９０ｓ;（２）ＡＨ间期延长,说明前传快快径已     

射频消融具有Mahaim纤维特性的左侧旁道一例

报道1例具有Mahaim纤维特性左侧旁道参与的宽QRS波心动过速:V1～V6均以R波为主,电轴左偏,呈右束支阻滞型。心内电生理检查:无典型预激图形,心房刺激出现与心动过速一致的宽QRS波,见旁道前传文氏现象;室房逆传呈向心性递减,心动过速时His束电图呈V-H-A顺序,逆传A波以His束部位最早;三磷酸腺苷可阻断旁道前传。窦性心律下,在左室中后间隔消融放电阻断旁道,术前极易发作的心动过速不再诱发,术后见房室传导跳跃现象。考虑该旁道起自房室结慢径或附近的心房肌,止于左室基底部。     

射频消融治疗房室结折返性心动过速的方法学研究——判断慢径阻断的新指标

改良房室结折返性心动过速 (AVNRT)慢径消融的方法学 ,以探讨判断慢径阻断的新指标。 6 0例AVNRT病人接受慢径射频消融术 ,根据X线影像部位和局部电图特点确定消融靶点 ,心房快速刺激 (S1S1)显示慢径前传放电消融 ,以 10s内慢径前传阻滞作为有效消融指标并以此连续放电达 30s。消融后房室结双径传导消失 ,不再诱发AVNRT为手术终点。 6 0例病人均达到消融终点。共消融 36 1个靶点 ,其中放电不足 10s者 2 80个、放电 30s者 81个 ,后者中 6 0个为有效消融靶点。有效阻断慢径者表现为放电 6 .9± 1.8(2 .8～ 10 )s慢径前传阻滞 ,S1刺激经快径前传。所有病人术后 3～ 7天食管电生理复查不再诱发AVNRT。随访 3～ 19个月无AVNRT复发。结论 :显示慢径前传消融可客观判断放电消融的有效性 ,避免盲目延长放电时间所造成的无效心肌损伤     

慢径消融时出现交界区心律伴室房逆传阻滞意义的再探讨

目的探讨慢径消融过程中出现交界区心律伴室房逆传阻滞的意义。方法房室结折返性心动过速经射频消融治疗患者,共91例。采用由低至高的逐点递进的方法进行消融,放电中注意观察交界区心律伴逆传阻滞现象的出现。结果所有病例均获得手术成功,其中3例首次消融后复发。91例手术中有47例曾出现交界区心律伴逆传阻滞,与无逆传阻滞组相比较,手术时间及曝光时间无明显差异,但放电次数多于后者;在共计309次有效放电中,95次有室房逆传阻滞,与214次无逆传阻滞者相比较,其靶点与His束电极间垂直距离明显小于后者,伴发一过性房室传导阻滞(AVB)的比例亦明显大于后者(12.63%vs 2.39%),多元Logistic回归分析发现靶点到HBE电极间垂直距离≤1.5 cm是房室前传阻滞的独立相关因素(OR=12.50,P=0.018),而交界区心律伴逆传阻滞与AVB间相关性不明确(P>0.05)。结论在消融慢径的过程中,出现交界区心律伴逆传阻滞与房室前向传导阻滞之间并无明确的相关性,而消融靶点过高则是出现AVB的独立危险因素。     

射频消融具有Mahaim纤维特性的左侧旁道一例

报道1例具有Mahaim纤维特性左侧旁道参与的宽QRS波心动过速：V1～V6均以R波为主，电轴左偏，呈右束支阻滞型。心内电生理检查：无典型预激图形，心房刺激出现与心动过速一致的宽QRS波，见旁道前传文氏现象；室房逆传呈向心性递减，心动过速时His束电图呈V-H-A顺序，逆传A波以His柬部位最早；三磷酸腺苷可阻断旁道前传。窦性心律下，在左室中后间隔消融放电阻断旁道，术前极易发作的心动过速不再诱发，术后见房室传导跳跃现象。考虑该旁道起自房室结慢径或附近的心房肌，止于左室基底部。     

从慢径消融发生的交界区心律试探房室结双径的本质

７６例慢－快型房室结折返性心动过速（ＡＶＮＲＴ）患者接受房室结慢径消融术。６５例慢径阻断、９例双径存在但ＡＶＮＲＴ不能诱发、２例快径阻断。慢径阻断后，除快径的前传有效不应期（ＥＲＰ）缩短（２８７．０±７９．０ｍｓｖｓ３４４．０±８７．０ｍｓ，Ｐ＜０．０１）外，房室传导的文氏点、２１阻滞点、室房传导的１１点、快径逆传ＥＲＰ、前传和逆传功能不应期均无明显改变。共放电８４１次，其中无交界区心律的３１７次放电，无一次消融成功。６５例慢径阻断者，交界区心律减少或消失。以上结果提示快径和慢径可能是两条各具电生理特性的传导纤维。     

快径间断逆传是房室结折返性心动过速的少见电生理表现

报道 4例房室结折返性心动过速 (AVNRT)的少见电生理表现———快径间断逆传。 4例经心电图和食管电生理检查证实为AVNRT的病人 ,心内电生理检查中心室刺激无快径逆传 ,遂静脉注射异丙肾上腺素和消融阻断慢径后观察室房 (VA)传导特点。结果 :4例病人基础电生理检查均无快径逆传。静脉注射异丙肾上腺素后心室刺激 ,3例显示快径逆传并诱发AVNRT ,1例仍不显示快径逆传。消融阻断慢径后 ,4例病人均显示良好的快径逆传。结论 :快径间断逆传是AVNRT的少见电生理特点 ,慢径和快径相互干扰是其产生的重要机制之一。     

射频消融慢径后房室结电生理特性变化的探讨

目的:探讨房室结折返性心动过速(AVNRT)患者消融慢径对房室结电生理特性的影响。方法:①比较34例患者射频消融术前及术后AH间期、房室结前传及逆传文氏周期、快径路及慢径路前传有效不应期。②根据术后慢径是否消失将34例患者分为:慢径消失组(n=24);慢径改良组(n=10),比较两组间快径及慢径前传有效不应期。结果:房室结改良前后文氏周期变化:34例患者在未分组前射频消融前后房室结文氏周期无明显变化。快径前传有效不应期:慢径消失组快径前传有效不应期术后较术前降低,有显著性差异(P<0．05);慢径改良组慢径前传有效不应期术后较术前延长,有显著性差异(P<0．05)。结论:快径前传有效不应期的缩短与消融后慢径是否残存有关;慢径的消融影响房室结的前向传导。     

房室结慢径消融靶点图特征预测发生房室阻滞的研究

本文通过对23例选择性消融房室结慢径放电前靶点图特征分析,旨在寻找一个更可靠的电生理参数,用来预测放电后发生房室阻滞的危险性。　　资料和方法　23例慢-快型房室结折返性心动过速(AVNRT)患者,其中男性7例,女性16例,平均年龄48.6±16.2(15～67)岁。慢-快型AVNRT的诊断通过程序心房刺激S1S2每缩短10ms,A2H2跃增50ms或以上,诱发心动过速。当呈现出清晰而稳定的希氏束电位时,以100mm/s或50mm/s走纸速度测量希氏束电图心房信号与大头电极标测心房信号之间的A(HBE)-A(ABL)间期;测量希氏束电图心房信号与固定在冠状静脉窦(冠状窦)口…     

左室起搏标测消融左侧隐匿性旁道靶点的探讨

探讨左侧旁道 (AP)构成的房室折返性心动过速 (AVRT)的标测及射频消融 (RFCA)靶点定位方法。 15 4例左侧隐匿性AP构成的AVRT随机分成A、B两组 ,两组均经股动脉逆行法进入大头电极 (ABL)于二尖瓣环下RFCA。A组经大头电极以S1S135 0～ 5 0 0ms沿二尖瓣环起搏 ;以起搏信号S到CS上最早逆传A波之间的间距S -A最小处为靶点。B组以AVRT和 /或右室心尖部起搏时CS最早逆传A波处为靶点。结果 :A组 75例均经 1～ 2次放电即成功阻断AP ,且V、A分离均在放电后 5s内出现。其中有 9例靶点与CS上最早逆行A波处相距 10～ 15mm ,其靶点处S-A较其余 6 6例明显延长。B组 79例中 6 8例在 1～ 2次放电 ,5s内V、A分离 ,另 11例放电无效在改用A组方法后均在一次放电后即阻断AP ,靶点距CS最早逆A波处 10～ 2 0mm ,S -A显著长于该组其他病例。 15 4例中 2 0例靶点与CS上最早逆行A波有距离 ,其S -A明显延长 (5 6± 2 3msvs 4 5± 12ms,P <0 .0 1)。结论 :以最短S -A为靶点能快速有效地阻断各种类型的左侧隐匿性AP ;尤其在以最早逆行A波为靶点无法阻断AP传导时推荐使用该方法。     

Retrograde fast pathway ablation for atrioventricular nodal reentry associated with markedly prolonged PR intervals

Three patients with typical atrioventricular nodal reentrant tachycardia (AVNRT) and markedly prolonged PR intervals (>300 ms) without dual pathway physiology at baseline or during isoproterenol infusion underwent successful fast pathway ablation and remained asymptomatic without recurrent AVNRT, atrioventricular block, or symptomatic bradycardia for a mean of 19 months. In patients with recurrent AVNRT and markedly prolonged PR intervals, selective ablation of the retrograde fast pathway can eliminate AVNRT without further impairment of anterograde atrioventricular nodal function.     

Conversion of typical to "atypical" atrioventricular nodal reentrant tachycardia after radiofrequency catheter modification of the atrioventricular junction.

Typical atrioventricular (AV) nodal reentry tachycardia (AVNRT) is characterized by anterograde activation over a slowly conducting pathway and by retrograde activation through a rapidly conducting pathway. Preliminary reports suggest that radiofrequency catheter modification can eliminate typical AVNRT while preserving anterograde conduction. Radiofrequency catheter modification was used to treat 88 patients with typical AVNRT. After baseline electrophysiologic evaluation, the ablation catheter was positioned proximal and superior to the site of maximal His deflection. Radiofrequency energy was applied until there was significant attenuation of retrograde conduction, and elimination of AVNRT inducibility. Eighty-one patients were successfully treated and form the basis of this report. A new paroxysmal supraventricular tachycardia with RP greater than PR interval was induced at electrophysiologic testing after successful ablation in 9 patients (11%). Mean atrial-His activation time was 140 +/- 31 ms, and the ventriculoatrial activation time was 170 +/- 46 ms. This arrhythmia was induced only with ventricular pacing during isoproterenol infusion and appeared to be mediated by AV nodal reentry. New retrograde dual AV nodal physiology after modification was more frequent in patients with atypical tachycardia than in those without (4 of 9 vs 2 of 72; p less than 0.0001). Although none of the patients were treated, only 1 of 9 had an episode of spontaneous atypical tachycardia during a mean follow-up of 12 months. Results of this study confirm that typical AVNRT can be rendered noninducible without the complete destruction of reentrant pathways. Because induction of "atypical" AVNRT was not predictive of spontaneous arrhythmia recurrence, it should not be an indication for additional ablation sessions or long-term drug therapy.     

特殊类型房室结折返性心动过速的电生理机制及其射频消融

报道２例特殊类型的房室结折返性心动过速（ＡＶＮＲＴ），１例为慢－慢型ＡＶＮＲＴ伴起始部多径路逆传；１例为两种不同电生理特性的慢径交替前传、快径逆传构成的ＡＶＮＲＴ。电生理检查均提示房室结三径路。２例病人均于冠状静脉窦口上方消融慢径改良房室结成功，心动过速不再被诱发。随访２个月心动过速均无复发。提示房室结多径路形成的特殊类型ＡＶＮＲＴ，需详细的电生理检查并仔细鉴别方能予以诊断。射频导管消融方法同典型ＡＶＮ－ＲＴ，且安全、有效。     

Gender Differences in the Clinical Characteristics and Atrioventricular Nodal Conduction Properties in Patients With Atrioventricular Nodal Reentrant Tachycardia

Gender Differences in Patients With AVNRT. Introduction: The detailed electrophysiological characteristics of the gender differences associated with atrioventricular nodal reentrant tachycardia (AVNRT) have not been clarified. This study investigated the gender‐related electrophysiological differences in a large series of patients undergoing radiofrequency catheter ablation. Methods and Results: A total of 2,088 consecutive AVNRT patients (men/women 869/1,219) who underwent catheter ablation were enrolled in this study. We evaluated the gender differences in their electrophysiological characteristics. Women had a significantly younger age of onset, higher incidence of multiple jumps, shorter AH interval, atrial effective refractory period (ERP), anterograde fast pathway ERP, anterograde slow pathway ERP, and retrograde slow pathway ERP, and longer ventricular ERP than men. The incidence of baseline ventriculoatrial dissociation was lower in women than in men. Women needed less isoproterenol/atropine to induce AVNRT. No gender differences in the radiation exposure time, procedure time, complication rate, acute success rate, or second procedure rate were noted. Both typical and atypical AVNRT were more predominant in women. In the patients with atypical AVNRT, there was no significant gender difference in incidence of baseline ventriculoatrial dissociation; however, the retrograde slow pathway ERP was significantly shorter in women than in men. Women of premenopausal age (≤50 years old) had a significantly higher incidence of anterograde multiple jumps and a retrograde jump phenomenon, and a shorter anterograde slow pathway ERP and retrograde slow pathway ERP than those of women over 50 years old. Conclusion: Gender differences in the anterograde and retrograde AV nodal electrophysiology were noted in the patients with AVNRT. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1114‐1119)     

Differential Effect of Adenosine on Anterograde and Retrograde Fast Pathway Conduction in Patients with Atrioventricular Nodal Reentrant Tachycardia

Adenosine and Retrograde Fast Pathway Conduction . Introduction : Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction.
Methods and Results : The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 ± 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients ( P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 ± 78 vs 333 ± 74 msec, P < 0.01), a shorter VA block cycle length (383 ± 121 vs 307 ± 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 ± 23 vs 41 ± 17 msec, P < 0.01).
Conclusion : Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.     

快慢型房室结折返性心动过速的电生理机制和经导管射频消融

目的探讨快慢型房室结折返性心动过速(AVNRT)的电生理机制和经导管射频消融。方法快慢型AVNRT消融患者42例。消融方法为在心室起搏或心动过速时标测最早逆传慢径心房激动部位,然后在窦性心律下或心动过速时消融。消融成功的标准为消除逆传慢径、1:1前传慢径及不能诱发任何类型AVNRT。结果所有42例均消融成功。逆传慢径消融成功部位在三尖瓣环和冠状静脉窦(CS)口之间(传统慢径区域)36例(86%),其最早逆传心房激动也位于上述区域;逆传慢径在CS近端或/和二尖瓣环心房侧消融成功6例(14%),其最早逆传心房激动多位于CS近端1～3cm处。结论多数快慢型AVNRT可在传统慢径区域(房室结右侧后延伸)消融成功,但部分病例需要在CS近端和/或二尖瓣环房侧(左侧后延伸)消融成功。     

Variable responsiveness of anterograde and retrograde fast pathway conduction to adenosine in patients with typical AV-nodal reentry tachycardia

Adenosine is known as a substance which depresses predominantly the slow pathway of the av-node. However, the effect of adenosine on the anterograde and retrograde fast pathway (FP) has not been studied in a large patient population. Ninety-one patients with inducible typical av-nodal reentrant tachycardias (AVNRT) were included. The clinically used dosage of 12 mg adenosine was administered subsequently as bolus injection during a constant atrial and ventricular pacing (500 ms) in all patients. Electrophysiological av-nodal parameters were determined. A higher responsiveness of the anterograde compared to the retrograde FP was observed: the majority of patients (76%) blocked anterogradely and 55% blocked retrogradely within the FP after the administration of 12 mg adenosine. Thirty-six percent of all patients revealed a differential behaviour to adenosine. Sixteen percent of all patients were completely resistant to adenosine (P=0.012). Electrophysiological parameters did not predict the responsiveness of the FP to adenosine. In patients with typical AVNRT the anterograde FP shows a higher sensitivity than the retrograde FP to adenosine.This might reflect an anatomical and/or functional distinction between anterograde and retrograde FP. The variable response to adenosine could be due to individual anatomical and electrophysiological heterogenity of the perinodal tissue and the av-node.     

多型房室结折返性心动过速的机制和射频导管消融

目的分析多型房室结折返性心动过速（AVNRT）并存的电生理机制和射频导管消融结果。方法18例经电生理检查后行射频导管消融的多型AVNRT患者。慢快型和慢慢型AVNRT的消融方法为首选消融前传慢径（房室结右侧后延伸）,快慢型AVNRT的消融方法为消融最早慢径逆传心房激动部位。消融成功的标准为消除1：1前传慢径,消除快慢型AVNRT的逆传慢径,不能诱发任何类型AVNRT。结果11例在消融前的电生理检查中诱发出2种类型AVNRT,均在三尖瓣环与冠状静脉窦口之间（房室结右侧后延伸）成功消融。7例在电生理检查中诱发出1种类型,消融此型后又诱发出另外1种类型,其中4例在房室结右侧后延伸进一步消融成功,另3例均经左侧后延伸进一步消融成功。消融术后随访6个月至8年,18例均无复发。结论对于大多数多型AVNRT,房室结右侧后延伸可能为其折返环的主要基质,消融可成功治愈多型AVNRT。在少部分多型AVNRT中,左侧后延伸与右侧后延伸可能分别作为不Ⅻ类型AVNRT折返环的主要基质,需要分别消融才能成功治愈。     

Electrophysiological mechanisms of conversion of typical to atypical atrioventricular nodal reentrant tachycardia occurring after radiofrequency catheter ablation of the slow pathway

This report presents an adult patient with conversion of typical to atypical atrioventricular nodal reentrant tachycardia (AVNRT) after slow pathway ablation. Application of radiofrequency energy (3 times) in the posteroseptal region changed the pattern of the atrioventricular (AV) node conduction curve from discontinuous to continuous, but did not change the continuous retrograde conduction curve. After ablation of the slow pathway, atrial extrastimulation induced atypical AVNRT. During tachycardia, the earliest atrial activation site changed from the His bundle region to the coronary sinus ostium. One additional radiofrequency current applied 5 mm upward from the initial ablation site made atypical AVNRT noninducible. These findings suggest that the mechanism of atypical AVNRT after slow pathway ablation is antegrade fast pathway conduction along with retrograde conduction through another slow pathway connected with the ablated antegrade slow pathway at a distal site. The loss of concealed conduction over the antegrade slow pathway may play an important role in the initiation of atypical AVNRT after slow pathway ablation.