房室结折返性性心动过速时房室非同步兴奋的电生理机制

１３例房室结折返性心动过速（ＡＶＮＲＴ），其心动过速的表现为房室非同步兴奋，其中房室２：１传导１１例，房室分离２例。房室非同步现象说明心房和心室并非ＡＶＮＲＴ折返环路的必须部分。心房参与心动过速取决于结周心房组织的不应期，心室参与心动过速取决于希浦系统的不应期，由于心房组织的不应期通常较短，而希浦系统的不应期相对较长，因此非同步现象以房室阻滞或分离多见，室房阻滞或分离少见。正确识别ＡＶＮＲＴ时房室     

长RP间期阵发性室上性心动过速的电生理鉴别方法

阵发性室上性心动过速包括房室结折返性心动过速、房室折返性心动过速及房性心动过速等多种类型。目前临床上常用的鉴别方法包括心动过速时应用心室起搏拖带、希氏束不应期/非不应期的心室期前刺激及心房不同部位起搏的方法,窦性心律下应用希氏束旁起搏、心室不同部位/频率刺激等方法。心室起搏拖带可观察多个指标,为临床最常用的鉴别方法之一...     

第3讲 阵发性室上性心动过速的鉴别诊断

阵发性室上性心动过速（paroxysmal supraventricular tachycardia,PSVT）简称室上速,异位激动点在希氏束以上,心动过速形成时心室不是必须参与成分,大多数心电图表现为QRS波群形态正常、RR间期规则的快速心律。多数室上速由折返机制引起,折返可发生在窦房结、房室结、心房,分别称为窦房折返性心动过速、房室结内折返性心动过速（AVNRT）、心房折返性心动过速。     

aVL导联终末部切迹在室上性心动过速中的鉴别诊断价值

房室结折返性心动过速（atrioventricular nodal reentrant tachycardia,AVNRT）为临床最常见的室上性心动过速,AVNRT时（本研究指慢快型）心房和心室一般为同时激动或心房激动略晚于心室,     

房室结折返性心动过速的治疗（附102例报告）

折返性心动过速的发生须具备的条件是(1)有二条传导速度不等的冲动传导道路，如房室速和房室旁道；房室结功能性纵行分离既快通道和慢通道以及窦房结和心房交界处。(2)二条通路中一条呈单向阻滞。(3)另一条传导缓慢，以致有足够的时间折返并再次应激。折返发生在窦房结和心房交接处和心房内部引起窦性或房性心动过速；发生在房室结内，由功能性纵行分离引起的双径通路导致房室结折返心动过速；而预激症者的旁路所构成折返环则引起往返性心动过速。     

房室结双径路消融中特殊电生理现象分析与处理

目的 :分析房室结折返性心动过速 (AVNRT)慢径路消融中特殊电生理现象及处理体会。方法 :慢径路消融前常规行心内电生理检查。结果 :有特殊电生理现象者 8例 ,其中 3例患者AVNRT开始时表现为房室 2 :1传导 ,阻滞点在希氏束以上部位 ;3例患者房室结功能曲线呈连续性 ;1例为慢 -慢型AVNRT ;1例心内电生理检查未能诱发出AVNRT。所有患者慢径消融均成功。结论 :术前应行详细的心内电生理检查和仔细鉴别 ,其消融方法与典型AVNRT相同     

起源于冠状静脉窦口的右侧旁路合并房室结双径路的诊断与鉴别

目的探讨复杂多径路心动过速时的应用拖带和程序S2刺激进行诊断和鉴别分析。 方法回顾性分析1例间歇性预激波患者频发室上性心动过速,经心脏电生理检查行右心室拖带刺激和心室程序S2刺激,测量最后一跳刺激信号到自身心房波间期减去心动过速下心室到心房的间期(SA-VA)和起搏后间期(PPI)－心动过速周长(TCC),并行常规射频导管消融术治疗。 结果术中心室分级刺激S1S1：350 ms诱发右侧旁路参与的房室折返性心动过速,TCL为372 ms, PPI为395 ms,继续行心房S1S2：500/310 ms刺激,"跳跃"诱发同前一样的室房波不融合心动过速。再次行心房S1S1：280 ms刺激,可反复诱发慢快型房室结折返性心动过速。在旁路参与的心动过速下给予心室程序S2刺激,测量PPI为385.1 ms, TCL为360.1 ms,PPI－TCL≤20 ms,证实为右侧旁路参与的房室折返性心动过速,同时存在慢快型房室结折返性行心动过速,给予常规射频导管消融成功径路和旁路。术后随访12个月未有心动过速发作。 结论通过右心室心室拖带刺激,以及测量SA-VA间期和PPI-TCL间期可以用来鉴别典型房室结折返性心动过速与间隔房室旁路。     

房室结双径路消融中特殊电生理现象分析与处理

目的：分析房室结折返性心动过速（AVNRT）慢径路消融中特殊电生理现象及处理体会。方法：慢径路消融前常规行心内电生理检查。结果：有特殊电生理现象者8例，其中3例患者AVNRT开始时表现为房室2：1传导，阻滞点在希氏束以上部位；3例患者房室结功能曲线呈连续性；1例为慢-慢型AVNRT；1例心内电生理检查未能诱发出AVNRT。所有患者慢径消融均成功，结论：术前应行详细的心内电生理检查和仔细鉴别，其消融方法与典型AVNRT相同。     

房室结折返性心动过速慢径路消融过程中交界心律的电生理特征

目的:分析房室结折返性心动过速行慢径路消融过程中,出现交界心律时心房激动特征以及希氏束波到高位右心房的传导时间.方法:行慢径路消融的房室结折返性心动过速患者100例,分别测量心动过速时希氏束波到高位右心房的传导时问(HAT),以及交界心律出现时希氏束波到高位右心房的传导时间(HAJ).结果:在慢快型和慢中型折返性心动过速慢径路消融过程中,交界心律出现时逆传心房激动顺序与心动过速相比仅有微小的变化.交界性心律时逆传HA间期短于心动过速时的HA间期(P<0.05),在快慢型折返性心动过速慢径路消融过程中,交界心律出现时没有逆传心房激动.结论:在慢快型和慢中型折返性心动过速慢径路消融过程中,交界心律通过快径路和中间径路逆传;在快慢型折返性心动过速慢径路消融过程中,交界心律逆传阻滞.     

射频消融治疗房室结双径路的迟发效应1例

报道1例房室结双径路合并室上性心动过速 (SVT)患者射频消融手术失败后发生迟发效应而成功的病例. 患者,女性,42岁,反复发作SVT 10年.食管电生理检查诊断为房室结折返性心动过速(AVNRT),行心内电生理检查及射频消融术.心内电生理检查过程中,导管操作、分级递增刺激及程序刺激均可诱发SVT .并可见A-H跳跃、His递减传导等房室结传导特征,确诊为AVNRT.后位法行慢径消融,以时间滴定法共放电11次,其间有多次交界区心律出现,后因仪器故障中断手术,术毕时,程序刺激仍可诱发SVT.3天后再次手术时,电生理检查:170次/min心房刺激房室呈文氏传导,心室刺激、异丙肾上腺素刺激后再次行心房、心室刺激均未诱发室上速,无A-H跳跃.     

Analysis of Atrioventricular Nodal Reentrant Tachycardia with Variable Ventriculoatrial Block: Characteristics of the Upper Common Pathway

Background: The precise nature of the upper turnaround part of atrioventricular nodal reentrant tachycardia (AVNRT) is not entirely understood.
Methods: In nine patients with AVNRT accompanied by variable ventriculoatrial (VA) conduction block, we examined the electrophysiologic characteristics of its upper common pathway.
Results: Tachycardia was induced by atrial burst and/or extrastimulus followed by atrial-His jump, and the earliest atrial electrogram was observed at the His bundle site in all patients. Twelve incidents of VA block: Wenckebach VA block (n = 7), 2:1 VA block (n = 4), and intermittent (n = 1) were observed. In two of seven Wenckebach VA block, the retrograde earliest atrial activation site shifted from the His bundle site to coronary sinus ostium just before VA block. Prolongation of His-His interval occurred during VA block in 11 of 12 incidents. After isoproterenol administration, 1:1 VA conduction resumed in all patients. Catheter ablation at the right inferoparaseptum eliminated antegrade slow pathway conduction and rendered AVNRT noninducible in all patients.
Conclusion: Selective elimination of the slow pathway conduction at the inferoparaseptal right atrium may suggest that the subatrial tissue linking the retrograde fast and antegrade slow pathways forms the upper common pathway in AVNRT with VA block.     

"V-H-A Pattern" as a criterion for the differential diagnosis of atypical AV nodal reentrant tachycardia from AV reciprocating tachycardia

BACKGROUND: During ventricular extrastimulation, His bundle potential (H) following ventricular (V) and followed by atrial potentials (A), i.e., V-H-A, is observed in the His bundle electrogram when ventriculo-atrial (VA) conduction occurs via the normal conduction system. We examined the diagnostic value of V-H-A for atypical form of atrioventricular nodal reentrant tachycardia (AVNRT), which showed the earliest atrial activation site at the posterior paraseptal region during the tachycardia. METHODS: We prospectively examined the response of VA conduction to ventricular extrastimulation during basic drive pacing performed during sinus rhythm in 16 patients with atypical AVNRT masquerading atrioventricular reciprocating tachycardia (AVRT) utilizing a posterior paraseptal accessory pathway and 21 with AVRT utilizing a posterior paraseptal accessory pathway. Long RP' tachycardia with RP'/RR > 0.5 was excluded. The incidences of V-H-A and dual AV nodal physiology (DP) were compared between atypical AVNRT and AVRT. RESULTS: V-H-A was demonstrated in all the 16 patients (100%) in atypical AVNRT and in only 1 of the 21 (5%) in AVRT (P < 0.001). DP was demonstrated in 10 patients (63%) in atypical AVNRT and in 4 (19%) in AVRT (P < 0.05). The sensitivity of V-H-A for atypical AVNRT was higher than that of DP (P < 0.05). Positive and negative predictive values were 94% and 100%, respectively, for V-H-A and 71% and 74%, respectively, for DP. CONCLUSIONS: The appearance of V-H-A during ventricular extrastimulation is a simple criterion for differentiating atypical AVNRT masquerading AVRT from AVRT utilizing a posterior paraseptal accessory pathway.     

Inducible atrioventricular nodal reentrant echo behind organic 2:1 infra-hisian block during sinus rhythm

A 77-year-old male patient with an intermittent 2:1 infra-Hisian block during sinus rhythm was presented with dizziness and near-syncope. During electrophysiological (EP) study, dual atrioventricular (AV) nodal pathways and retrograde fast pathway were easily induced by atrial and ventricular programmed stimulation, respectively. A typical slow-fast AV nodal reentrant echo beat also could be demonstrated by single atrial extrastimulation. Atrioventricular nodal reentrant tachycardia (AVNRT) can occasionally exhibit 2:1 AV block. Conversely, AV nodal reentry property had been rarely reported behind 2:1 infra-Hisian block. The EP presentation from this case may support the notion that tissues below the His are not part of the reentrant circuit of AVNRT.     

Specificity of Retrograde Conduction in Screening for Atrioventricular Nodal Reentrant Tachycardia

Baseline AV conduction properties (antegrade and retrograde) are often used to assess the presence of dual AV nodal physiology or concealed AV accessory pathways. Although retrograde conduction (RET) is assumed to be a prerequisite for AV nodal reentrant tachycardia (AVNRT), its prevalence during baseline measurements has not been evaluated. We reviewed all cases of AVNRT referred for radiofrequency ablation to determine the prevalence of RET at baseline evaluation and after isoproterenol infusion. Results: Seventy-three patients with AVNRT underwent full electrophysiological evaluation. Sixty-six patients had manifest RET and inducible AVNRT during baseline atrial and ventricular stimulation. Seven patients initially demonstrated complete RET block despite antegrade evidence of dual AV nodal physiology. In 3 of these 7 patients AVNRT was inducible at baseline despite the absence of RET. In the other four patients isoproterenol infusion was required for induction of AVNRT, however only 3 of these 4 patients developed RET. One of these remaining patients had persistent VA block after isoproterenol. Conclusions: The induction of AVNRT in the absence of RET suggests that this is not an obligatory feature of this arrhythmia. Therefore, baseline AV conduction properties are unreliable in assessing the presence of AVNRT and isoproterenol infusions should be used routinely to expose RET and reentrant tachycardia.     

Age Related Changes in Dual AV Nodal Physiology

Dual atrioventricular nodal (DAVN) physiology has been reported in up to 63% of pediatric patients with anatomically normal hearts, yet atrioventricular nodal reentrant tachycardia (AVNRT) accounts for only 13%–16% of supraventicular tachycardia (SVT) in childhood. The incidence of AVNRT increases with age and becomes the most common form of SVT by adolescence. We investigated the age related electrophysiological responses to programmed atrial and ventricular stimulation in 14 pediatric patients who underwent intracardiac electro-physiological study prior to radiofrequency catheter ablation for AVNRT and who exhibited DAVN physiology. Single atrial and ventricular extrastimuli were placed following drive trains with cycle lengths of 400–700 ms and 350–500 ms, respectively. Six children (mean age 8.2 years, range 5.2–11.5 years) were compared to eight adolescents (mean age 16.6 years, range 13.3–20.7 years). Adolescents were found to have a significantly longer fast pathway effective refractory period (ERP) (median 375 vs 270 ms, P = 0.03), slow pathway ERP (median 270 vs 218 ms, P = 0.04), atrio-Hisian (AH) during AVNRT (median 300 vs 225 ms, P = 0.007), and AVNRT cycle length (median 350 vs 290ms, P = 0.03). There was a strong trend for the AH measured at the fast pathway ERP to be longer in adolescents than in children (median 258 vs 198 ms, P = 0.055). The AH at the fast pathway ERP was more strongly correlated with baseline cycle length than with age (r = 0.7, P = 0.01 vs r = 0.5, P = 0.7). There was no significant difference in the retrograde VA conduction between adolescents and children. These results demonstrate an age related difference in AV nodal response to programmed atrial stimuli in pediatric patients with DAVN physiology and AVNRT. These differences are consistent with mechanisms that may explain the increased incidence of AVNRT in adolescents compared to children.     

Demonstration of Right and Left Atrial Dissociation by Atrial Rapid Pacing or Extrastimulation During Fast-Slow (Uncommon) Form of Atrioventricular Nodal Reentrant Tachycardia

Some recent works suggest that extranodal atrial fibers may form part of the reenlry circuit in the atrioventricular (AV) nodal reentrant tachycardia (AVNRT). This hypothesis is based on the fact that the perinodal dissection successfully abolished AVNRT while preserving intact AV conduction. Apart from the surgical success, the electrophysiological evidence supporting this hypothesis has not been demonstrated, especially in the uncommon (fast-slow) form of AVNRT. We present some electrophysiological evidence suggesting atrial participation in eight patients with the fast-slow form of AVNRT. During the tachycardia, rapid pacing or extrastimulation was done from the orifice of the coronary sinus (CS) and the right atrium (RA), while recording the electrograms of the CS and the low septal RA. In seven patients, right and left atrial dissociation was demonstrated during pacing from the RA, while in the remaining one this was demonstrated from the CS. The interatrial dissociation will be unlikely if the intranodal reentry circuit connects with the atria via a single upper common pathway. This suggests that the upper turnaround of the reentry circuit involves atrial tissue and that the extranodal accessory pathway with long conduction times may form the ascending limb of the circuit (atrionodal reentry). Alternatively, the reentry circuit is entirely intranodal and two or more connecting pathways are present between the atria and the circuit.     

Role of Specialized Conducting Fibers in the Genesis of "AV Nodal" Re-entry Tachycardia

Recent reports have suggested that an accessory bypass tract connecting the His bundle to the atrium (His-atrial fiber) may form the retrograde limb of "AV nodal" re-entry tachycardia (AVNRT). We studied 12 patients with AVNRT in whom the presence of an accessory atrioventricular fiber (Kent fiber) was excluded. We investigated the possibility of a His-atrial (H-A) fiber by examining the nature of retrograde conduction and by assessing the necessity of the atrium as a part of the re-entry pathway. Retrograde conduction through the A V node had characteristics similar to retrograde conduction over a Kent bundle; that is, retrograde conduction times were short and did not vary. With echo beats (Ae) evoked during antegrade refractory period determination early premature beats resulted in prolongation of the AH interval with no change in HA_e interval. During AVNRT the A'H':H'A' ratios ranged from 2.0–8.0 (mean 4.0 ± 1.8) and with changes in tachycardia cycle length the H'A interval remained constant. During retrograde refractory period determination, delay occurred below the AV node without change in the H-A interval. Estimations of retrograde conduction times by all 3 methods were not significantly different (p > 0.2). The pattern of retrograde conduction suggests anatomical or functional specialized fibers as the retrograde limb of the tachycardia. The necessity of the atria as a part of the re-entry circuit was assessed by the introduction of atrial premature beats (APBs) in the region of the atrial septum during AVNRT in 10 patients. APBs pre-excited the atria by 40–140 ms without changing the cycle length of the tachycardia, providing strong evidence against the participation of an extranodal His-atrial fiber in AVNRT, In conclusion, retrograde conduction during AVNRT appears to take place over a functional or anatomical specialized fiber within the AV node and not over an extranodal H-A fiber.     

Effects of An Acute Increase in Atrial Pressure on Atrial Refractoriness in Humans

Contraction-excitation feedback has been studied extensively in mammalian ventricles. In contrast, little is known about contraction-excitation feedback in mammalian atria. The objective of this study was to investigate the effect of acute alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness. Twenty patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory periods (ARP) were measured during AV pacing at a cycle length of 500 msec and an AV interval of 120 msec. Acute increases in atrial pressure were induced by pacing the atrium and ventricle simultaneously for the final two beats of the drive train. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval of the final two beats of the drive train was shortened from 120 msec to 0 msec, the peak right atrial pressure increased from 7 ± 3 mmHg to 15 ± 5 mmHg (P < 0.001). The increase in atrial pressure associated with simultaneous pacing of the atrium and ventricle resulted in shortening of the atrial ERP and ARP by 7.3 ± 5.2 and 6.2 ± 3.5 msec, respectively (P < 0.0011). Similar results were obtained during autonomic blockade. These findings confirm the presence of contraction-excitation feedback in normal human atria.     

Diagnostic Approach to Narrow Complex Tachycardia with VA Block

Narrow complex tachycardia with VA block is rare. The differential diagnosis usually consists of (1) junctional tachycardia (JT) with retrograde block: (2) AV nodal reentrant tachycardia (AVNRT) with proximal common pathway block; and finally (3) nodofascicular tachycardia using the His-Purkinje system for antegrade conduction and a nodofascicular pathway for retrograde conduction. Analysis of tachycardia onset and termination, the effect of bundle branch block on tachycardia cycle length, and the response to atrial and ventricular premature depolarization must be carefully done. Making the correct diagnosis is crucial as the success rate in eliminating the tachycardia will depend on tachycardia mechanism.     

Adenosine Induced Intraatrial Block

Adenosine, an endogenous nucleoside with potent negative chronotropic and dromotropic effects on the sinus and AV nodes, is thought to have little if any antiarrhythmic effect on normal atrial tissue. However, there may be an electrophysiological basis for an adenosine effect on atrial tissue with atypical conduction properties. We examined the electrophysiological effects of adenosine in a patient with decremental atrial conduction properties. During incremental pacing from the high right atrium there was gradual prolongation of the intraatrial interval between the high right atrium and the low septal atrium, from 180 to 280 msec, until 2:1 intraatrial block occurred at a pacing cycie length of 280 msec. Adenosine (6 mg IV) resulted in transient intraatrial block followed by prolonged intraatrial conduction during high right atrial pacing at a cycle length of 400 msec. Thus, similar to its effects on the AV node and decremental AV accessory pathways, adenosine may also slow and abolish conduction in decremental atrial issue, an effect that is likeiy attributed to adenosine induced hyperpolarizing K⁺ current in partially depolarized atrial tissue.