从慢慢型和慢快型房室结折返性心动过速电生理特性的差异分析折返环的不同

目的从慢慢型房室结折返性心动过速（AVNRT）和慢快型AVNRT的电生理特性的差异分析两型AVNRT间折返环的不同.方法在500例AVNRT患者中的59例慢慢型和60例慢快型之间,比较部分电生理特性的异同;同时在部分慢慢型和慢快型患者中应用2种方法（1）比较起搏时和心动过速时的HA间期的长度;（2）比较心动过速时心室刺激重整心动过速的不同.比较下传共径（LCP）的异同.结果慢慢型的前传慢径和逆传慢径有明显不同的传导时间;慢慢型的逆传慢径与慢快型的逆传快径有明显不同的传导时间和递减特性;和慢快型相比,2种方法均显示慢慢型有较长的LCP.结论 （1）慢慢型AVNRT中前传慢径和逆传慢径的传导时间明显不同;慢慢型较慢快型有较长的下传共径;（2）研究结果支持慢慢型AVNRT可能应用房室结的右侧后延伸和左侧后延伸分别形成心动过速的前传和逆传支而形成折返.     

依赖异丙肾上腺素逆传的房室结折返性心动过速

目的探讨房室结双径路中的室房逆传和对房室结双径路的快径逆传间歇性的认识。方法对401例AVNRT者中,在基础状态下RVAS1S1>500ms为无室房逆传的13例患者进行异丙肾试验,重复电生理检查。结果401例AVNRT为慢快型,其中388例(96.8%)RVAS1S1<300ms,为有室房逆传组,而13例(3.2%)RVAS1S1>500ms,为无室房逆传组。结论AVNRT的病人中行电生理检查示房室结存在双径路而室房分离或室房传导时间长,在不能诱发心动过速时,应使用异丙肾上腺素以明确存在快径间歇性逆传的可能性。     

心动过速发作时不同剂量的三磷酸腺苷对房室结快、慢径阻断作用的研究

在心动过速发作时 ,观察不同剂量的三磷酸腺苷 (ATP)对房室结 (AVN)快、慢径的阻断作用 ,进一步探讨快、慢径的电生理特性。对符合诊断的 2 4例房室结双径且可诱发出房室结折返性心动过速 (AVNRT)的病人进行研究 ,用食管调搏或心内电生理检查方法重复诱发心动过速。静脉给予不同剂量ATP ,以 0 .0 5mg/kg为起始剂量 ,0 .0 2 5mg/kg为递增量 ,直至ATP用量达 0 .2 0mg/kg。在AVNRT发作时 ,观察不同剂量的ATP对同一病人房室结快、慢径的阻断情况。在 2 0例 (83.3% )的患者中 ,ATP终止AVNRT于前传慢径 ,其ATP用量为 0 .119± 0 .0 43mg/kg;在 3例(12 .5 % )的患者中 ,ATP终止AVNRT于逆传快径 ,其用量为 0 .175± 0 .0 2 9mg/kg;在 1例 (4 .2 % )的患者中 ,较小剂量ATP终止AVNRT于前传慢径 ,递增剂量则终止于逆传快径。结论 :心动过速发作时较小剂量的ATP多使前传慢径阻断而较大剂量的ATP多使逆传快径阻断     

慢慢型房室结折返性心动过速的电生理机制和射频导管消融治疗

目的　探讨慢慢型房室结折返性心动过速 (AVNRT)的电生理机制和不同射频导管消融方法的治疗效果。方法　812例AVNRT患者分为两组,第 1组 500例,比较慢慢型中前传慢径和逆传慢径的成功消融部位的异同、比较在慢慢型和快慢型中选择性地消融逆传慢径部位的异同。第 2组312例,在设想慢慢型AVNRT折返机制的基础上,前瞻性地对慢慢型仅选择性消融前传慢径而不消融逆传慢径。结果　第 1组 59例慢慢型AVNRT的前传和逆传慢径的传导时间和成功消融的部位明显不同,逆传慢径多在冠状静脉窦(CS)窦口内或CS近端消融成功,而前传慢径多在三尖瓣环和CS窦口之间消融成功;慢慢型与快慢型的逆传慢径有明显不同的传导时间、递减特性和解剖分布。在第 2组前瞻性地仅消融前传慢径治疗 22例慢慢型组中,在三尖瓣环和CS窦口之间成功消融前传慢径并治愈AVN RT后, 21例逆传慢径功能不变,其逆传慢径最早心房插入点部位与前传慢径消融部位不同。所有 812例AVNRT均消融成功,第 1组在 3年以上的随访中, 387例慢快型复发 1例 (0 3% ), 59例慢慢型复发6例(10% ), 54例快慢型无复发。第 2组 312例 3 ~48 ( 23±12 )个月的随访中,慢快型复发 2例(0 5% ),慢慢型和快慢型无复发。结论　(1)慢慢型AVNRT应用电生理特性和解剖分布不同的两条慢径形     

从射频消融探讨房室结双径路的本质和房室结改良的机制

采用两种方法对142例房室结折返性心动过速(AVNRT)患者进行房室结改良。128例慢—快型AVNRT中,83例单纯慢径改良,33例慢径前传和快径逆传同时改良,3例单纯快径逆传改良,7例快径前传和慢径或快径逆传同时改良,2例失败。1例发生永久性Ⅲ度房室传导阻滞;10例快—慢型和4例慢—慢型AVNRT患者均慢径改良成功。总成功率98.6％。平均随访6±4月,4例(2.8％)复发,均再次消融成功。慢径改良后,快径前传有效不应期、维持1:1快径前传最短的心房刺激周期明显缩短(P<0.05),而逆向快径有效不应期、维持1:1快径逆传最短的心室刺激周期无明显变化(P>O.05)。本研究提示:快径和慢径可能是解剖上不同的纤维。慢径前传和逆传可以是同一条纤维,也可以是不同的纤维;快径亦然。     

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。     

房室结折返性心动过速与房室结双径路的相关性研究

目的　探讨房室结折返性心动过速 (AVNRT)与房室结双径路 (DAVNP)的相关性。方法　回顾性分析成功射频导管消融的单一类型 AVNRT的心内电生理和食管心房调搏 (GEAP)资料。结果　10 7例单一类型的 AVNRT,存在 DAVNP者 10 1例 ,其中慢 -快型 AVNRT99例 ,慢 -慢型 AVNRT2例 ;DAVNP阴性者 6例 ,其中慢 -快型 AVNRT1例 ,慢 -慢型 AVNRT3例 ,快 -慢型 AVNRT2例 ;慢 -快型 AVNRT DAVNP阳性检出率明显高于慢 -慢型和快 -慢型 AVNRT(P<0 .0 1)。 10 0例慢 -快型AVNRT中 ,5 8例女性较 42例男性年轻 (4 2 .0± 12 .9比 49.6± 11.8,P<0 .0 1) ,分别有 11例和 10例心内电生理检查时 DAVNP阴性 ,而 TEAP存在 DAVNP。结论　 DAVNP是慢 -快型 AVNRT的发生基础 ,而慢 -慢型和快 -慢型 AVNRT与 DAVNP的相关性较差。     

房室结功能曲线连续性房室结折返性心动过速患者的射频消融终点初探

目的　探讨房室结功能曲线连续性房室结折返性心动过速 (AVNRT)患者的射频消融终点。方法　在AVNRT患者中 ,对心房 A1 A2 和 A1 A2 A3程序刺激房室结功能曲线均呈连续性者为 组 ,A1 A2 刺激房室结功能曲线呈连续性而 A1 A2 A3刺激呈不连续性者为 a组 ,房室结功能曲线均呈不连续性者为 b组。行慢径区域消融后 ,对组间的电生理参数进行比较。结果　 组非典型 AVNRT的诱发率高于 组 (2 7.3 % vs5 .6% ,P<0 .0 5 )。在 I组和 a组 ,消融后最长 A2 H2 间期 (A2 H2 m ax)均比消融前有所缩短 ,但无显著性差异 (P>0 .0 5 ) ,而 b组则显著缩短 (3 76± 73 ms vs2 0 6± 5 6ms,P<0 .0 1)。消融后 组、 a组和 b组的最长 A3H3间期 (A3H3m ax)均比消融前显著缩短 (2 74± 71ms vs 196± 45 ms,P<0 .0 5 ;3 62± 91m s vs 2 2 6± 72 m s,P<0 .0 1;3 85± 88ms vs 2 19± 61ms,P<0 .0 1)。结论　非典型 AVNRT与房室结功能曲线的连续性有关。对于房室结功能曲线连续性的 AVNRT患者 ,消融后 A3H3max的缩短可作为消融终点的指标之一     

射频消融治疗房室结折返性心动过速不同终点的疗效观察

目的　评价射频消融治疗房室结折返性心动过速 ( AVNRT)的不同终点对远期复发的影响。方法　对 1 0 4例 AVNRT患者进行慢径消融 ,比较慢径传导消失组和慢径传导残留组 AVNRT复发率。结果　射频消融术后慢径传导消失 5 8例 ,慢径传导残留 4 6例 ,术后 1 8± 9个月随访期内 ,慢径传导消失组复发 2例 ( 3 .4 % ) ,慢径传导残留组复发 2例 ( 4.3 % ) ,两组无显著差别 ( P>0 .0 5 )。结论　射频消融术后慢径传导残留并不增加 AVNRT复发的危险性     

快速心房起搏时SV间期与SS间期的比值在房室结折返性心动过速慢径消融中的应用

评价快速心房起搏时最快 1∶1房室传导的SV间期 (SV间期 )与 1∶1房室传导的最短S1S1间期 (SS间期 )的比值 (SV/SS)在房室结折返性心动过速 (AVNRT)慢径消融中的应用 ,将AVNRT分为房室结功能曲线连续组 (Ⅰ组 ,10例 )及房室结功能曲线不连续组 (Ⅱ组 ,17例 )测量心房分级递增刺激时的SS间期与SV间期及SV/SS ,并进行消融前、后和组间比较。结果显示 ,两组消融后SV间期较消融前明显缩短 (Ⅰ组 :2 2 1.0± 2 2 .3vs 35 7.0± 43.7ms;Ⅱ组 :2 0 2 .1± 30 .6vs 379.4± 44 .2ms,P均 <0 .0 5 ) ;消融前后SS间期无明显变化 (Ⅰ组 :310 .0± 40 .6vs 30 8.0± 36 .8ms;Ⅱ组 :332 .9± 48.1vs 336 .5± 6 2 .3ms) ;两组中所有患者消融前SV/SS比值均 >1,而消融后SV/SS比值均 <1。结论 :SV/SS可作为慢径消融成功终点的辅助观察指标之一 ,尤其对于房室结传导曲线呈连续性者 ,使用此方法可简便地观察消融终点 ,增加消融的目的性。     

The Elusive Extracellular AV Nodal Potential: Studies from the Canine Heart, Ex Vivo

Various forms of extracellular recordings from the AV node (AVN) have been reported. However, lack of consistent validation have precluded the use of such recordings in experimental and clinical studies. In 14 Langendorff perfused dog hearts, the triangle of Koch (TOK) was exposed and an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted under the endocardium so that the bipolar pairs recorded electrograms from the apex to the base of the TOK. All recording were filtered between 0.05 and 250 Hz, except for a His bundle (Hb) recording (30–250 Hz) made from another bipolar electrode catheter placed in the aortic root. Transmembrane action potentials (AP) were recorded close to the sites of extracellular electrograms. Pin electrodes at the periphery of the bath were arranged to register two ECG leads from the volume conductor. During recovery of electrical activity 11 of 14 preparations developed a junctional rhythm that initially manifested only an AV nodal extracellular and corresponding intracellular AV nodal potentials followed gradually by conduction to the Hb and ventricles but no retrograde atrial activation; 3 preparations initially produced Hb rhythms based on extracellular and transmembrane AP recordings from the AVN and Hb. The amplitude and duration of the AVN extracellular potentials (average: 97 ± 26 V and 92 ± 25 msec, respectively) during AVN rhythms, significantly differed from those during atrial pacing (262 ± 185 V and 78 ± 26 msec, p < 0.05). Histologic sections of the sites underlying the electrodes recording AVN potentials showed AVN tissue throughout. We conclude that extracellular AV nodal potentials are independent waveforms with specific qualitative and quantitative characteristics that distinguish them from adjacent atrial, transitional, Hb or ventricular potentials.     

Case Report: Type I Second-Degree AV Block Masquerading as Type II Block

This report describes a patient with type I second-degree atrioventricular block and sequences consistent with type II block according to widely accepted criteria. The electrocardiograms illustrate the importance of deductive reasoning and the clinical context in the diagnostic evaluation of perplexing forms of second-degree AV block.     

Spontaneous transition of 2:1 atrioventricular block to 1:1 atrioventricular conduction during atrioventricular nodal reentrant tachycardia: evidence supporting the intra-Hisian or infra-Hisian area as the site of block

INTRODUCTION: The incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction during AV nodal reentrant tachycardia has not been well reported. Among previous studies, controversy also existed about the site of the 2:1 AV block during AV nodal reentrant tachycardia. METHODS AND RESULTS: In patients with 2:1 AV block during AV nodal reentrant tachycardia, the incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction and change of electrophysiologic properties during spontaneous transition were analyzed. Among the 20 patients with 2:1 AV block during AV nodal reentrant tachycardia, a His-bundle potential was absent in blocked beats during 2:1 AV block in 8 patients, and the maximal amplitude of the His-bundle potential in the blocked beats was the same as that in the conducted beats in 4 patients and was significantly smaller than that in the conducted beats in 8 patients (0.49 +/- 0.25 mV vs 0.16 +/- 0.07 mV, P = 0.007). Spontaneous transition of 2:1 AV block to 1:1 AV conduction occurred in 15 (75%) of 20 patients with 2:1 AV block during AV nodal reentrant tachycardia. Spontaneous transition of 2:1 AV block to 1:1 AV conduction was associated with transient right and/or left bundle branch block. The 1:1 AV conduction with transient bundle branch block was associated with significant His-ventricular (HV) interval prolongation (66 +/- 19 ms) compared with 2:1 AV block (44 +/- 6 ms, P < 0.01) and 1:1 AV conduction without bundle branch block (43 +/- 6 ms, P < 0.01). CONCLUSION: The 2:1 AV block during AV nodal reentrant tachycardia is functional; the level of block is demonstrated to be within or below the His bundle in a majority of patients with 2:1 AV block during AV nodal reentrant tachycardia, and a minority are possibly high in the junction between the AV node and His bundle.     

Simultaneous dual fast and slow pathway conduction upon induction of typical atrioventricular nodal reentrant tachycardia: electrophysiologic characteristics in a series of patients

INTRODUCTION: Simultaneous dual atrioventricular nodal conduction (SDNC) through slow (SP) and fast pathway (FP) is a rare phenomenon observed upon the induction of atrioventricular nodal reciprocating tachycardia (AVNRT). The aim of this study is to report the electrophysiological features of patients showing typical AVNRT induced through SDNC. METHODS AND RESULTS: Among 461 consecutive patients with typical AVNRT submitted to radiofrequency catheter ablation (RFCA), seven patients (1.5%) with SDNC at tachycardia onset (group I: 6 female; age 60-72 years, mean 65.2 +/- 3.8 years) and 118 age-matched controls (group II: 60 female; age 60-88 years, mean 68.4 +/- 6.8 years) were considered. Controls were further subdivided into two subgroups according to age: subgroup A (94 patients, age 60-75 years) and subgroup B (24 patients, age >75 years). The value of the following parameters was significantly higher in group I than in group II and in subgroup A: A-H interval [113 +/- 26 vs. 89 +/- 27 (P < 0.01) vs. 84 +/- 19 (P < 0.001)], ventriculoatrial conduction effective refractory period [355 +/- 85 vs. 293 +/- 87 (P < 0.05) vs. 281 +/- 82 (P < 0.05)], SP conduction time upon AVNRT induction [444 +/- 104 vs. 350 +/- 72 (P < 0.01); vs. 345 +/- 67 (P < 0.001)], AVNRT cycle length [484 +/- 103 vs. 396 +/- 71 ms (P < 0.05); vs. 384 +/- 69 (P < 0.05)], and rate of AVNRT induction from ventricle [71% vs. 10% (P = 0.001); vs. 6% (P = 0.001)]. Differences were mostly not significant between group I and subgroup B. SP location and RFCA success rate were similar in all groups. CONCLUSION: In a population of AVNRT patients, SDNC at AVNRT induction is infrequent and it prevails beyond the fifth decade of life and in females. SDNC is associated with peculiar AVN conduction features, which resemble the age-related modifications of AVN conduction.     

房室结折返性心动过速电生理机理初探

为观察房室结折返性心动过速(AVNRT)的电生理基础以指导治疗,对36例房室结双径路的电生理特点及其与AVNRT的关系进行分析,发现在AVNRT诱发组,快径路有效不应期和功能不应期分别为315±42ms和376±64ms,显著小于未诱发组的387±60ms和459±74ms,而慢径路传导时间/快径路有效不应期比值和慢快径路传导时间差,诱发组明显大于未诱发组(1.14±0.34比0.84±0.26,169±76ms比82±24ms)。提示上述指标对于判断双径路是否易于诱发AVNRT有一定的临床意义。     

Multiple Atrioventricular Nodal Pathways in Humans:

Multiple AV Nodal Pathways. Introduction : Multiple AV nodal pathway physiology can be demonstrated in certain patients with clinical AV reentrant tachycardia.
Methods and Results : Evidence suggesting multiple AV nodal pathway conduction was present in seven (two males; age range 15 to 75 years) of 78 patients (9%) who underwent electrophysiologic studies for AV nodal tachycardia. The presence of two discrete discontinuities in the AV nodal conduction curves suggested triple AV nodal pathway conduction. Detailed mapping of their retrograde atrial activation sequence was performed along the tricuspid annulus from the coronary sinus ostium to the His-bundle electrogram recording site. Three zones (anterior, middle, and posterior) correspond to the upper, middle, and lower third of the triangle of Koch, respectively. The fast pathway exits were determined as anterior (4/7) or middle (3/7), the intermediate pathway exits as middle (4/7) or posterior (3/7), and the slow pathway exits as middle (1/7) or posterior (6/7). Other evidence suggesting multiple AV nodal pathway conduction includes: (1) triple ventricular depolarizations from a single atrial impulse; (2) sequential dual ventricular echoes; (3) spontaneous transformation between the slow-fast and fast-slow forms of AV nodal reentrant tachycardia; and (4) persistent cycle length alternans during AV nodal reentrant tachycardia. In four patients, all three pathways were shown to be involved in AV nodal echoes or reentrant tachycardia.
Conclusion : Multiple AV nodal pathways are not uncommon and can be identified by careful electrophysiologic elucidation and mapping technique.     

Atrioventricular Nodal Reentry Tachycardia in Patients with Sinus Node Dysfunction: Electrophysiologic Characteristics, Clinical Presentation, and Results of Slow Pathway Ablation

AVNRT and Sinus Node Dysfunction. Introduction: Sinus node dysfunction (SND) is frequently associated with impaired AV conduction. This study investigated the electrophysiologic properties of dual AV nodal pathways in patients suffering from both SND and AV nodal reentrant tachycardia (AVNRT). Methods and Results: Two groups of patients with slow-fast AVNRT underwent invasive electrophysiologic testing and catheter ablation of the slow pathway. Group A comprised 10 patients with SND (age 70 ± 8 years), (Group B included 10 age-matched patients without SND (age 69 ± 7 years; P = NS) who served as controls. Patients of group A exhibited prolongation of the anterograde Wenckebach cycle lengths (WBCLs) of both the fast pathway (559 ± 96 vs 361 ± 38 msec; P < 0.01) and the slow pathway (409 ± 57 vs 339 ± 32 ms; P < 0.01). However, the delta between the WBCLs of the fast and the slow pathways was larger in patients of group A (150 ± 80 vs 22 ± 20 msec; P < 0.01). Retrograde fast pathway conduction was well preserved with no difference in WBCLs (356 ± 42 vs 330 ± 47 msec; P = NS). Cycle lengths of AVNRT were longer in group A (468 ± 46 vs 363 ± 37 msec; P < 0.01). Clinically, all patients of group A suffered from multiple episodes of AVNRT per week, which was not the case in any patient of group B (P < 0.01). Catheter ablation of the slow pathway eliminated AVNRT in all patients without complications. Conclusions: Patients with AVNRT and SND exhibit characteristic electrophysiologic alterations of both AV nodal pathways. Clinically, this results in significantly more frequent episodes of tachycardia. Slow pathway ablation appears to be safe and effective in these patients.