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Parahisian pacing (PHP) is a useful maneuver during electrophysiology study of supraventricular tachycardia (SVT) especially when the tachycardia is non-sustained. Various responses during PHP can differentiate between the routes of VA conduction (VAC). In a case of WPW syndrome with orthodromic re-entrant tachycardia, we encountered various responses which one must be cognizant about to avoid erroneous conclusions. Along with para-hisian capture and only ventricular capture, simultaneous atrial capture (SAC) and pure His capture were also noted. Moreover, during pure-His capture underlying distal antegrade right bundle branch block (RBBB) was encountered making it an intriguing case.

A 60 years male patient underwent permanent pacemaker [DDDR -with dual chamber pacing (D) with dual chamber sensing (D) with dual mode of response (D) with rate responsive pacing(R) -St Jude's medical (Abbott- Endurity 2160)] implantation for complete heart block (CHB). After 4 months patient was admitted for congestive heart failure. 12 Lead electrocardiograms (ECG) was suggestive of tachycardia at 130 beats per minute (regular rhythm), with ventricular complexes preceded by pacing spikes and maintenance of 1:1 atrio-ventricular relationship. Echocardiography showed global hypokinesia of left ventricular (LV) myocardium with reduced LV ejection fraction. LV dysfunction and heart failure were attributed to tachy-cardiomyopathy. Pacemaker telemetry data demonstrated that the tachycardia was likely to be pacemaker-mediated endless loop tachycardia (ELT). ELT in this case was perpetuated secondary to shortening of post ventricular atrial refractory period (PVARP), intact retrograde ventriculo-atrial (VA) conduction and addition of antiarrhythmic drugs prolonging retrograde VA conduction. Rate response (Dynamic) PVARP was reprogrammed allowing PVARP extension. Following this ELT was terminated. LV ejection fraction was normalized on subsequent follow up visit after seven days.

Ventriculoatrial (VA) conduction is a critical component in many arrhythmias, has a diagnostic value in electrophysiology study (EPS), and is implicated in pacemaker-mediated arrhythmias. This study sought to characterize retrograde conduction during EPS and to utilize it as a diagnostic tool in patients without AV block. Patients with intact AV conduction undergoing EPS were included in this study to systematically evaluate baseline VA conduction. If absent, parahisian pacing was used to determine the level of block (nodal or infranodal). Recovery of VA conduction with increased sympathetic activity was assessed with isoproterenol infusion. Baseline characteristics and electrophysiological data were collected and analyzed. Among the 801 patients studied, VA conduction was present in 98% (81% at baseline and 17% after isoproterenol infusion). Parahisian pacing demonstrated that the block was at the AV node level among 150 patients with VA dissociation at baseline. Among patients presenting with supraventricular tachycardia (SVT), 98.7% with atrioventricular nodal reentrant tachycardia (AVNRT) had VA conduction at baseline versus 82.7% presenting with other SVT (atrial fibrillation excluded), P < 0.001. Thus, the absence of VA conduction at baseline during an EPS for SVT carries a negative predictive value (NPV) of 96.9% for AVNRT. VA conduction is present in most patients (98%) with intact AV conduction. The level of VA dissociation when present at baseline is always at the level of the AV node. Patients with SVT presenting for EPS that lacked VA conduction at baseline were unlikely to have AVNRT.

A 64‐year‐old female underwent catheter ablation of long R‐P' tachycardia. Ventricular pacing exhibited retrograde conduction with an identical atrial activation sequence as during tachycardia because of an accessory pathway (AP) with a long VA conduction. A radiofrequency application within the posterior coronary sinus (CS) could achieve a change of activation pattern from distal‐to‐proximal to proximal‐to‐distal within CS proximal to the ablation site, caused by conduction block of CS musculature (CSM) at the proximal site. This phenomenon could explain that this AP was connected between the CSM and the left ventricle, in site far away from the discrete connection between the left atrium and CSM.

Case A 40-year-old gentleman underwent electrophysiology study for WPW syndrome with recurrent orthodromic atrioventricular reentrant tachycardia (AVRT). He had a right anterior accessory pathway (AP) which was ablated closer to the septum anterior to His catheter, ablation-distal (ABL) not recording any His signal during and after ablation (Appendix 1ABC). During the study, parahisian pacing (PHP) was performed before and after ablation as a routine protocol to determine the route of VA conduction (VAC). During the study 4 catheters were used: one quadripolar catheter for His region, One roving ablation catheter [for RV pacing/ mapping (MAP)/ablation], 2 decapolar catheters for coronary sinus (CS) and right atrium (RA). During PHP, both the His and MAP/ABL catheters were placed at His region. The CS catheter could not be placed fully deep inside, hence CS-12 was located near middle CS whereas the CS-34 was 2-3 cm inside proximal CS (Appendix 1BC). The decapolar catheter, placed in RA, was on the atrial aspect of tricuspid annulus, with RA-5 bipole near high right atrium (HRA). Pacing was performed at 600 ms cycle length (PCL) as her sinus CL was 700-750 ms. Starting at 20 mA current @ 2 ms pulse width and keeping the PCL and catheter position fixed, the current output was gradually reduced in a stepwise manner when various responses were noted. What are the responses observed in Fig.1 and Fig. 2?

We report the case of a 31-year-old man with Uhl’s anomaly. Echocardiography revealed severely enlarged nonfunctioning right ventricle and unusual findings of the premature opening of the pulmonary valve along with substantial forward flow during late-diastole, indicating that pulmonary circulation was largely dependent on compensatory right atrial contraction. Moreover, right-to-left shunt through the patent foramen ovale (PFO) achieved systemic circulation at the expense of severe hypoxia. During accelerated idioventricular rhythm (AIVR) accompanied by ventriculo-atrial (VA) conduction, hypoxemia deteriorated further because of an increased right-to-left shunt through the PFO. We report the case of an adult with Uhl’s anomaly whose hemodynamics was largely dependent on the ventricularized right atrium and PFO. Although the unique hemodynamics contributed to his survival into adulthood, detrimental aspects manifested themselves during AIVR with VA conduction like a “double-edged sword.”

We describe a case of a 65-year-old gentleman with nonischemic cardiomyopathy and left bundle branch block who underwent cardiac resynchronization therapy device. After becoming a responder initially, he experienced significant clinical worsening on follow-up. Device interrogation revealed several long episodes of inappropriate automatic mode switch (AMS) entry due to far-field R wave oversensing resulting in loss of atrioventricular synchrony. Moreover, pacing in VVI mode with consistent VA conduction taking place during the AMS episodes was also found to be detrimental, which helped in sustaining the episodes and produced pacemaker syndrome like phenomenon. Attempts made to resolve the issue by prolonging the post-ventricular atrial blanking period was unsuccessful, hence we adjusted the atrial channel sensitivity to troubleshoot the problem.

Pacemaker-mediated arrhythmia (PMA) is a broad term used to describe the abnormal rhythms in which the pacing system contributes importantly to. There are a variety of arrhythmias caused by or related to a pacing system. But in this chapter, we focus on only those arrhythmias mediated by a dual (atrial and ventricular) pacing system in patients with intact retrograde VA conduction. We have re-classified these arrhythmias into three types: (1) repetitive reentrant ventriculoatrial synchrony (RRVAS), (2) repetitive non-reentrant ventriculoatrial synchrony (RNRVAS), and (3) repetitive non-reentrant ventriculoatrial 1:2 synchrony (RNRVA1:2S). Although these three types of pacemaker-mediated arrhythmias share a common feature in that there is retrograde VA conduction, their clinical manifestations, mechanisms, and pacemaker programming features are distinctively different. In this chapter, we have discussed each of these arrhythmias using clinical cases, ECG tracings, and schematic diagrams.

The heart is a vital organ that relies on the orchestrated propagation of electrical stimuli to coordinate each heartbeat. Abnormalities in the heart’s electrical behaviour can be managed with a cardiac pacemaker. Recently, the closed-loop testing of pacemakers with an emulation (real-time simulation) of the heart has been proposed. This enables developers to interrogate their pacemaker design without having to engage in costly or lengthy clinical trials. Many high-fidelity heart models have been developed, but are too computationally intensive to be simulated in real-time. Heart models, designed specifically for the closed-loop testing of pacemaker logic, are too abstract to be useful for the testing of pacemaker implementations. In the context of pacemaker testing, compared to high-fidelity heart models, this article presents a more computationally efficient heart model that generates realistic piecewise continuous electrical signals. The heart model is composed of cardiac cells that are connected by paths. Our heart model is based on the Stony Brook cardiac cell model and the UPenn path model, and improves them by stabilising the activation behaviour of the cells and by capturing the piecewise continuous behaviour of electrical propagation. We provide simulation results that show our ability to faithfully model a range of arrhythmias, such as VA conduction, heart blocks, and long Q-T syndrome. Moreover, re-entrant circuits (that cause arrhythmia) can be faithfully modelled, which only the discrete-event UPenn heart model is also able to achieve.

Background Coexistence of idiopathic left fascicular ventricular tachycardia (ILFVT) and atrioventricular nodal reentrant tachycardia (AVNRT) has been rarely reported. Objectives The study aimed at elucidating the prevalence of coexisted AVNRT in patients with ILFVT during longitudinal follow-up. The electrophysiological properties and clinical predictors of coexisted ILFVT and AVNRT were investigated. Methods From 1999 to 2017, a total of 108 patients (age: 33.7 ± 14.3, 84 male) with ILFVT from one tertiary center were consecutively enrolled. The prevalence of coexisted arrhythmias was explored during a longitudinal follow-up and the electrophysiological parameters from the index procedure were compared. Results During a mean follow-up period of 106.8 ± 69.5 months, 21 of 108 patients (19.4%) had coexisted AVNRT. The electrophysiological study demonstrated patients with coexisted ILFVT and AVNRT were characterized by more antegrade dual AV node conduction (52.4% vs. 19.5%, P = 0.002; 9.5%), shorter antegrade slow pathway effective refractory period (285.1 ± 34.1 ms vs. 329.2 ± 69.2 ms, P = 0.034), longer retrograde fast pathway effective refractory period (368.9 ± 56.7 ms vs. 312.5 ± 95.2, P = 0.036), and less VA dissociation (19.0% vs. 60.9%, P = 0.001) than those without a coexisted AVNRT. Multivariate logistic analysis showed that presence of antegrade dual AV nodal physiology and retrograde VA conduction could predict a coexisted AVNRT in patients with ILFVT (P = 0.005, OR: 4.80, 95% CI: 1.65-14.37 and P = 0.002, OR: 0.14, 95% CI: 0.04-0.49, respectively). Conclusion There was a high prevalence of coexisted AVNRT in patients with ILFVT during longitudinal follow-up. The presence of antegrade dual AV nodal physiology and retrograde VA conduction can predict the coexisted AVNRT in patients with ILFVT.

Intact retrograde ventriculoatrial (VA) conduction in the presence of complete atrioventricular (AV) heart block has been well-documented in the past. We sought to describe the prevalence and clinical significance of intact VA conduction accompanied by complete antegrade AV block in patients with implanted cardiac rhythm management (CRM) devices. During routine follow-up of CRM devices in our device clinic, 42 patients were found to be in a state of complete heart block. All patients presented in sinus rhythm. The patients' underlying rhythms were tested with the inhibition of pacing and documented AV dissociation. Subsequently, retrograde VA conduction was tested with ventricular pacing. In the 42 patients with complete heart block as the underlying rhythm, five patients demonstrated retrograde VA conduction. In conclusion, the prevalence of intact of VA conduction was 11.9% in our study. The implications of this phenomenon can have noteworthy clinical significance. The occurrence of pacemaker-mediated tachycardia and repetitive nonreentrant VA synchrony are discussed herein. All patients, even those with a device indication of complete heart block, should be tested for retrograde conduction at implantation and during routine follow-up.

Radiofrequency (RF) ablation of the slow pathway (SP) in atrioventricular nodal reentry tachycardia (AVNRT) is occasionally complicated with atrioventricular block (AVB) often predicted by junctional beats (JB) with loss of ventriculo-atrial (VA) conduction.We analyzed retrospectively 153 patients undergoing ablation of SP for typical AVNRT. Patients were divided into two age groups: 127 ≤ 70 years and 26 70 years. We analyzed the interval between the atrial electrogram in the His-bundle position and the distal ablation catheter [A(H)-A(RFd)] and between the distal ablation catheter and the proximal coronary sinus catheter [A(RFd)-A(CS)] before RF applications with and without JB. We evaluated if these intervals can be used as predictors of JB incidence and also of JB with loss of VA conduction. We also assessed if age influences the risk of loss of VA conduction.The A(H)-A(RFd) and A(RFd)-A(CS) intervals were significantly shorter in RF applications causing JB than those without JB (33 ± 11 ms vs 39 ± 9 ms, P 0.001, 14 ± 9 ms vs 20 ± 7 ms, P 0.001, respectively). The A(H)-A(RFd) and A(RFd)-A(CS) intervals were also significantly shorter in RFs causing JB with VA block than those with VA conduction (29 ± 11 ms vs 35 ± 11 ms, P 0.001, 8 ± 8 ms vs 17 ± 8 ms, P 0.001, respectively). Patients 70 years had shorter intervals (36 ± 11 ms vs 29 ± 8 ms, P = 0.012, 17 ± 8 ms vs 13 ± 7 ms, P = 0.027, respectively), while VA block was more common in this age group.The A(H)-A(RFd) and A(RFd)-A(CS) intervals can be used as markers for predicting JB occurrence as well as impending AVB. JB with loss of VA conduction occur more often in older patients possibly due to a higher position of SP.

Objectives This study sought to evaluate the utility of ventriculoatrial (VA) conduction patterns in response to adenosine in predicting inducibility of orthodromic reciprocating tachycardia (ORT). Background Adenosine is known to consistently block atrioventricular (AV) nodal conduction. We hypothesized that persistent VA conduction despite administration of adenosine would have a high predictive value for identifying the presence of a retrograde accessory pathway (AP) and associated ORT. Methods A total of 168 patients undergoing electrophysiological study for supraventricular tachycardia (SVT) had assessment of VA conduction during ventricular pacing and adenosine administration. Standard pacing maneuvers were then used for induction and diagnosis of the SVT mechanism. Results Absence of VA block to adenosine (doses up to 24 mg) had 88% sensitivity and 91% specificity for identifying ORT (positive predictive value 76%, negative predictive value 96%). Four patients with adenosine-induced VA block and inducible ORT had decremental APs. Adenosine caused VA block in 6 patients with eccentric VA activation due to atypical AV nodal conduction, and concentric VA conduction persisted in all 12 patients with a septal AP. Adenosine unmasked free-wall APs in 10 patients by blocking AV nodal conduction, shifting VA activation from concentric to eccentric. Conclusions The response of VA conduction to adenosine is a highly sensitive and specific method for detecting retrograde AP conduction and inducible ORT. Adenosine-induced VA block rules out inducible ORT due to a nondecremental AP. In cases of VA fusion, adenosine-induced block of AV nodal conduction can delineate the location of the AP atrial insertion site.

Background Atrioventricular reciprocating tachycardia (AVRT) utilizing a concealed accessory pathway is common. It is well appreciated that some patients may have multiple accessory pathways with separate atrial and ventricular insertion sites. Methods We present three cases of AVRT utilizing concealed pathways with evidence that each utilizing a single ventricular insertion and two discrete atrial insertion sites. Results In case one, two discrete atrial insertion sites were mapped in two separate procedures, and only during the second ablation was the Kent potential identified. Ablation of the Kent potential at this site remote from the two atrial insertion sites resulted in the termination of the retrograde conduction in both pathways. Case two presented with supraventricular tachycardia (SVT) with alternating eccentric atrial activation patterns without alteration in the tachycardia cycle length. The two distinct atrial insertion sites during orthodromic AVRT and ventricular pacing were targeted and each of the two atrial insertion sites were successfully mapped and ablated. In case three, retrograde decremental conduction utilizing both atrial insertion sites was identified prior to ablation. After mapping and ablation of the first discrete atrial insertion site, tachycardia persisted utilizing the second atrial insertion site. Only after ablation of the second atrial insertion site was SVT noninducible, and VA conduction was no longer present. Conclusions Concealed retrograde accessory pathways with discrete atrial insertion sites may have a common ventricular insertion site. Identification and ablation of the ventricular insertion site or the separate discrete atrial insertion sites result in successful treatment.

Pacemakers are devices that are used worldwide for bradyarrhythmias. They are robust devices that function properly from implantation to depletion of battery. Rarely malfunctions appear, one of them being pacemaker-mediated tachycardia in patients implanted with double-chamber devices when retrograde ventriculoatrial conduction is present. Retrograde ventriculoatrial conduction can be present in up to 50–70% of normal patients. In patients with a normal heart, usually it does not manifest clinically. Even in the case of an advanced AV block, retrograde VA conduction can still be present. Patients implanted with a cardiac device like pacemakers or defibrillators can exhibit ventriculoatrial conduction: 14% of patients with complete AV block and up to 80% of patients with sinus node disease. In patients with double-chamber pacemakers or double-chamber defibrillators, using an atrial sensing mode can serve as a second AV pathway and support reentry: antegrade pathway through the pacemaker and retrograde pathway through the AV node.

Similar to endless loop tachycardia (ELT), repetitive nonreentrant ventriculoatrial synchrony (RNRVAS) is a ventriculoatrial (VA) synchrony pacemaker-mediated arrhythmia. RNRVAS was first described in 1990 and can only occur in the presence of retrograde VA conduction and dual-chamber or cardiac resynchronization devices with tracking (P-synchronous ventricular pacing such as DDD, DDDR) or nontracking pacing modes that allow AV-sequential pacing (DDI, DDIR). RNRVAS is promoted by (1) high lower rate limit or any feature that allows rapid pacing, (2) long AV intervals, or (3) long postventricular atrial refractory period (PVARP). In contrast to ELT, RNRVAS is a less well-recognized form of pacemaker-mediated arrhythmia; thus, unlike ELT, there are no specific device algorithms to prevent, recognize, and terminate RNRVAS. However, RNRVAS has been recently shown to occur frequently. We present a series of cases, some of which were found fortuitously. Owing to its clinical implications, we propose that algorithms should be developed to prevent, identify, and terminate RNRVAS.

Background Identification of a possible ventriculoatrial (VA) dissociation in wide QRS complex tachycardias is one of the most reliable criteria for differentiation of tachycardia origin. The Lewis lead has been proposed for detection of atrial activity during ventricular tachycardias. Hypothesis A modified Lewis-lead-ECG will be superior to the standard-lead ECG for detection of ventriculoatrial conduction during ventricular tachycardia. Methods Forty-seven patients underwent electrophysiological study, stimulated with a fixed cycle length of 400 ms in the ventricle. During stimulation, a standard-lead ECG and a modified Lewis-lead ECG were recorded. Simultaneously, VA conduction was documented by intracardiac electrograms. Surface ECGs were presented to 6 blinded examiners for VA conduction assessment. Results Type of VA conduction was correctly diagnosed in significantly more ECGs in the Lewis-lead ECG group (mean, 35.0 [75%]) than in the standard-lead ECG group (mean, 29.2 [62%]; P = 0.045). Ventriculoatrial dissociation also was significantly more often correctly diagnosed in the Lewis-lead ECG group (mean, 17.7 [71%]) than in the standard-lead ECG group (mean, 12.7 [49%]; P = 0.014). Interobserver agreement was moderate in both groups (κ = 0.45 and κ = 0.49, respectively). Conclusions Compared with standard-lead ECG, modified Lewis-lead ECG is associated with significantly improved detection of VA conduction type during fast ventricular pacing and thus may help improve ECG diagnosis.

A cardiac resynchronization therapy defibrillator (CRT-D) (Medtronic Inc. Protecta XT) was implanted in a 67-year-old man who had cardiac sarcoidosis with extremely low cardiac function. He had ventricular tachycardia which was controlled by catheter ablation, medication and pacing. The programmed mode was DDI, lower rate was 90 beats/minute, paced AV delay was 150 ms, and the noncompetitive atrial pacing (NCAP) function was programmed as 300 ms.After his admission for pneumonia and heart failure, we changed his DDI mode to a DDD mode because he had atrial tachycardia, which led to inadequate bi-ventricular pacing. After a while, there were cycle lengths which were longer than his device setting and alternately varied. We were able to avoid this phenomenon with AV delay of 120 ms and NCAP of 200 ms.NCAP is an algorithm which creates a gap above a certain period after the detection of an atrial signal during the postventricular atrial refractory period of the pacemaker. This is to prevent atrial tachycardia and repetitive non-reentrant ventriculoatrial (VA) synchrony in the presence of retrograde VA conduction. But in this case, NCAP algorithm induced much lower rate than the programmed basic lower rate. This situation produced some arrhythmias and exacerbated symptoms of heart failure. This had to be paid attention to, especially when the device was programmed at high basic heart rate.

Ventriculo-atrial (VA) conduction can have negative consequences for patients with implanted pacemakers and defibrillators. There is concern whether impaired VA conduction could recover during stressful situations. Although the influence of isoproterenol and atropine are well established, the effect of adrenaline has not been studied systematically. The objective of this study was to determine if adrenaline can facilitate recovery of VA conduction in patients implanted with pacemakers.A prospective study was conducted on 61 consecutive patients during a 4-month period (April-July 2014). The presence of VA conduction was assessed during the pacemaker implantation procedure. In case of an impaired VA conduction, adrenaline infusio was used as a stress surrogate to test conduction recovery.The indications for pacemaker implantation were: sinus node dysfunction in 18 patients, atrioventricular (AV) block in 40 patients, binodal dysfunction (sinus node+ AV node) in two patients and other (carotid sinus syndrome) in one patient. In the basal state, 15/61 (24.6%) presented spontaneous VA conduction and 46/61 (75.4%) had no VA conduction. After administration of adrenaline, there was VA conduction recovery in 5/46 (10.9%) patients.Adrenaline infusion produced recovery of VA conduction in 10.9% of patients with absent VA conduction in a basal state. Recovery of VA conduction during physiological or pathological stresses could be responsible for the pacemaker syndrome, PMT episodes, or certain implantable cardiac defibrillator detection issues.

Background The purpose of this study was to assess the relationship between changes in sinus node cycle length (SNCL) during ventricular fibrillation (VF) and the peripheral changes in blood pressure (BP) and sympathetic nerve activity (SNA) in human subjects. We hypothesized that patients with no SNCL shortening during VF have a vasovagal-like response with a greater decrease in BP and SNA when compared to patients with SNCL shortening. Methods SNCL, BP, and SNA recordings were attempted in 24 patients undergoing the implantation of a dual-chamber implantable defibrillator. Changes were measured during the first 5 seconds of VF and compared with the 5 seconds prior to VF induction. Results SNCL shortened during VF in nine patients (mean%∆SNCL = –12 ± 8%) and remained unchanged or lengthened in seven patients (mean%∆SNCL = 7 ± 7%). Eight patients had ventriculoatrial (VA) conduction prohibiting assessment of SNCL changes. In patients with SNCL shortening, the %∆MBP (mean BP) was –47 ± 6% compared to –58 ± 8% in patients with no SNCL shortening (P < 0.01). In patients with VA conduction, the %∆MBP was –54 ± 3%. SNA recordings were successfully obtained in four patients. When compared to baseline, SNA increased by 34 ± 30% in two patients with SNCL shortening, decreased by 25% in one patient with SNCL lengthening, and by 90% in the fourth patient with VA conduction. Conclusions We have shown that patients with no SNCL shortening have a significantly greater decrease in MBP during VF when compared to patients with SNCL shortening. The underlying mechanism appears to be reflex mediated with a vasovagal-like response in patients with no SNCL shortening.

An 81-year-old woman who had undergone dual chamber pacemaker implantation for sick sinus syndrome was referred to our hospital with drug-refractory common atrioventricular (AV) nodal reentrant tachycardia. Ventricular pacing (Vp) following premature atrial contraction (PAC) with a long AV interval induced ventriculoatrial (VA) conduction, which allowed the tachycardia to be initiated. The sensed AV interval was shortened to 80 ms, allowing Vp during the refractory period of VA conduction. Postventricular atrial refractory period was shortened to 180 ms to sense PACs with short coupling interval. After reprogramming, the suppression of the tachycardia by blocking VA conduction following Vp was confirmed.

BACKGROUND Concealed left-sided accessory pathways (CLAP) are a cause of supraventricular tachycardia (SVT) in the young. Most are mapped with right ventricular (RV) apical/outflow pacing. Rarely, alternative means of mapping are required. We review our experience from three pediatric electrophysiology (EP) centers with a rare form of "hidden" CLAP. METHODS All patients

Background: The prevalence of ventriculo-atrial (VA) conduction varies from 20% to 90%, depending on the population studied (Militianu et al., 1997; Inoue et al., 1985; Kazmierczak et al., 1993; Ciemniewski et al., 1990; Hayes and Furman, 1983; Westveer et al., 1984). This wide range is mostly based on studies done in patients with implanted devices or impaired atrioventricular conduction. However, the prevalence of VA conduction in structurally normal heart has not been well documented till date. Objective: To study the prevalence and identify predictors of retrograde conduction via the His-Purkinje system and AV node in structurally normal hearts. Methods: We included 54 consecutive adults without structural heart disease who underwent electrophysiological (EP) study for various tachycardias. The basic parameters including PR, AH and HV intervals, atrioventricular Wenckebach point (AVWP) and anterograde effective refractory period (ERP) of atrioventricular node (AVNERP), were measured after ablation. The VA conduction was assessed basally and if absent, after isoprenaline. The VA Wenckebach point (VAWP) and retrograde ERP(VAERP) were recorded in patients showing VA conduction. Results: The mean age was 37.1 ± 12.6years. Twenty five (46%) of the patients were men. VA conduction was present in 30 (55%) patients at baseline. Of the remaining 24 patients, 18 (34%) showed VA conduction after isoprenaline. Only 6 (11%) patients failed to reveal VA conduction even after adequate response to isoprenaline. Amongst all clinical and EP variables analysed, only the HV interval was shorter (p

A 91-year-old woman received a dual-chamber pacemaker for sick sinus syndrome and intermittently abnormal atrioventricular (AV) conduction. The pacemaker was set in DDI mode with a 350-ms AV delay to preserve intrinsic ventricular activity. She complained of palpitation during AV sequential pacing. The electrocardiogram showed a 2:1 AV rhythm from 1:1 ventriculoatrial (VA) conduction during ventricular pacing in DDI mode with a long AV interval. After reprogramming of the pacemaker in DDD mode with a 250-ms AV interval and additional 100-ms prolongation of the AV interval by the ventricular intrinsic preference function, VA conduction disappeared and the patient's symptom were alleviated without increasing unnecessary right ventricular pacing.

Introduction. Pacemaker syndrome consists of the symptoms and signs present in the single chamber (VVI) pacemaker patient with electrode placed in the right ventricular apex. It is caused by inadequate timing of atrial and ventricular contractions. Pacemaker syndrome without a pacemaker (or pseudopacemaker syndrome) refers to occurrence of symptoms in the presence of marked first-degree atrioventricular (AV) block, when P wave is too close to the preceding QRS complex producing the same haemodynamic disturbance as artificial pacemaker cardiac stimulation with retrograde VA conduction. Case Outline. We present the patient with acute inferior myocardial infarction due to late bare metal stent thrombosis, treated with primary pectutaneous coronary intervention. Hospital course was complicated by complete heart block which was treated with temporary pacing. During the stand-by mode of temporary pacing, sinus rhythm with marked first-degree AV block (PQ interval 480 ms) was observed while the patients re-experienced the symptoms that were present prior to pacemaker implantation. Temporary pacing was continued for the next 24 hours when spontaneous shorteninig of PQ interval (250-270 ms) was noticed; since the patient was asymptomatic during the stand-by mode, the pacemaker electrodes were removed and the patient discharged 11 days after admission. Conclusion. Conduction disturbances, such as the varying degrees of AV blocks, are relatively common in acute inferior myocardial infarction. The first degree AV blok is usually asymptomatic and does not require treatment, unless when it is associated with pseudopacemaker syndrome. In that case, temporary pacing provides haemodynamic stability until conduction system recovers.

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.

The atrioventricular (AV) node allows ante- and retrograde conduction between atria and ventricles. It is commonly assumed that these AV nodal conduction properties go hand in hand. However, ante- and retrograde AV conduction can be completely independent from each other in individual patients. We report about a patient with permanent AV block III degrees requiring implantation of a pacemaker. As soon as a dual-chamber device was connected to the implanted leads, a tachycardia started at the maximum tracking rate, which was subsequently reprogrammed from 120 to 170 bpm. Non-invasive electrophysiologic testing showed that this patient demonstrated 1:1 ventriculoatrial (VA) conduction up to 170 bpm leading to endless loop tachycardia (ELT) while the antegrade AV block III degrees persisted. This case impressively illustrates that one has to take into account that patients with antegrade AV block III degrees may still have a high VA conduction capacity leading to ELT. Dual-chamber devices therefore have to be programmed accordingly, activating dedicated reactions after ventricular premature beats and automatic ELT detection and termination algorithms.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common regular supraventricular tachycardia. Slow pathway (SP) modification has evolved as the first-line treatment,1,2 with acute success rates of 95% to 98%. A sensitive sign for success of the procedure is observation of accelerated junctional rhythm (JR) during ablation.3 The serious complication of AV block (AVB) can occur, and affects ≈1% to 2.3% of patients during or after catheter ablation procedures.2,4 Some studies have demonstrated that loss of VA conduction during radiofrequency application predicts impending AVB during ablation.5,6 From this illustrative series of cases assembled from 4 large tertiary care centers during a period of 3 years, we analyze some possible reasons for occurrence of AVB, and suggest methods to prevent this complication during SP modification procedures. Editor’s Perspective see p 745 A 58-year-old woman with a history of paroxysmal supraventricular tachycardia was refractory to medical therapy and referred for ablation. The baseline AH and HV intervals were 80 and 50 ms, respectively. Atrial pacing at 600 ms demonstrated fast pathway conduction and jump to SP conduction with a single echo beat (Figure 1A, left). A narrow QRS tachycardia with the same retrograde conduction sequence was induced during isoproterenol infusion, by atrial programmed stimulation (Figure 1A, right), which was diagnosed as AVNRT with cycle length (CL) of 380 ms, AH of 280 ms, HV of 50 ms, and VA of 50ms. No further pacing maneuvers were performed during tachycardia and SP modification was performed guided by fluoroscopy with a power setting of 30 W, temperature 60°C and total duration of 35 s. During radiofrequency delivery, JR with 1:1 retrograde conduction was observed during radiofrequency application with a CL between 500 and 600 ms, and 4 beats of sinus rhythm with …

Antidromic Tachycardia in Patients with an Atriofascicular Fiber. Background: The typical and most common tachycardia in patients with atriofascicular pathways is a macro reentrant tachycardia, with anterograde conduction over the decrementally conducting bypass tract and retrograde conduction over the right bundle branch-His-AV node axis resulting in a short V-right bundle branch and short V-H interval. Objectives: To report on changes in rate and QRS configuration when right bundle branch block (RBBB) develops spontaneously during antidromic tachycardia using an atriofascicular fiber. Methods: Three of 25 patients with an antidromic circus movement tachycardia using a right-sided atriofascicular pathway showed episodes of right bundle branch block (RBBB) during ventriculo-atrial conduction. Effect of retrograde RBBB on tachycardia rate and QRS configuration was studied using intracardiac and extracardiac recordings. Results: All 3 patients showed prolongation of their V-A interval when retrograde RBBB occurred during tachycardia, resulting in a longer tachycardia cycle length. The VA time increase ranged from 85 to 100 msec, with a mean 346 ± 5 msec. Two of the 3 patients also showed a change in QRS configuration due to a more leftward shift of the frontal plane QRS axis. Conclusion: Rate changes in antidromic tachycardia in patients with atriofascicular fibers can be based on a shift in VA conduction from one bundle branch to the other. This may be accompanied by changes in the frontal plane QRS axis because of a change in ventricular activation sequence.

What to do when a person without any cardiac complaint shows a Wolff-Parkinson-White (WPW) pattern on the ECG has been an important question for more than 2 decades. Recent articles by Pappone et al1–3 make it necessary to revisit that question. Epidemiological data indicate that 0.1% to 0.3% of the general population have ECG findings suggesting that during sinus rhythm, in addition to AV conduction over the AV node His pathway, there is also AV conduction over an accessory AV pathway (AP).4 This means that each year ≈4 new cases are found in a population of 100 000. It is also known that there is a 4-fold increase of this finding in family members of WPW patients.5 The WPW patient is often symptomatic because of cardiac arrhythmias. When arrhythmias are present, the disorder is called the WPW syndrome. The 2 most common types of arrhythmia in the WPW syndrome are (1) a circus movement tachycardia (CMT), also called an AV reentrant tachycardia, in which AV conduction goes by way of the normal AV conduction system and VA conduction over the AP and (2) atrial fibrillation (AF).6 AF can be a life-threatening arrhythmia in the WPW syndrome if the AV AP has a short anterograde refractory period (RP), allowing many atrial impulses to be conducted to the ventricle. That will result in very high ventricular rates with possible deterioration into ventricular fibrillation (VF) and sudden death.7,8 A CMT that in general is well tolerated by the patient when additional heart disease is absent may deteriorate into AF, and the ventricular rate and risk for VF will depend on the anterograde RP of the AP. Therefore, the most important question in the asymptomatic WPW patient in whom the typical ECG accidentally is recorded is whether he or …

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.

Septal Pre-Excitation in Pace Prevention of Atrial Fibrillation. Background: Pre-excitation of the intra-atrial septum (IAS) by pacing at the ostium of the coronary sinus (CSO) can prevent atrial fibrillation (AF) in caseof single atrial premature beats (APBs). We investigated whether pre-excitation of IAS, either by pacing at CSO or at the right ventricle in the presence of retrograde conduction (RV), can prevent atrial tachyarrhythmia triggered by single and multiple APBs. AF vulnerability was compared to pacing at the right atrium (RA) and sinus rhythm (SR). Methods: Seventeen patients, age 52 ′ 21 years, who exhibited retrograde VA conduction and reproducible induction of atrial tachyarrhythmia during an electrophysiological procedure, were studied. Both during SR and pacing (S1-S1:600 ms) at RA, CSO, and right ventricle (RV), single (A1-S2:200 ms) and multiple premature stimuli (A1-S2-S3-S4:200-180-180 ms) were delivered at RA (4 x diastolic threshold). Results: During pacing at RA, single and multiple APBs invariably induced runs of atrial tachyarrhythmia (mean duration 34 ′ 67 sec and 37 ′ 69 sec, range 1 sec to 20 min). During preventive pacing at CSO and RV, single APBs (A1-S2:200 ms) did not induce atrial arrhythmia (0 ′ 0 sec, 0 ′ 0 sec, P < 0.05 vs pacing at RA). In contrast, when multiple APBs were applied, pacing at CSO or RV failed to prevent initiation of AF (mean duration 36 ′ 63 sec, 38 ′ 65 sec, NS). Also during SR, single APBs did not induce AF (0 ′ 0 sec, P < 0.05 vs pacing at RA) whereas multiple APBs invariably induced AF (39 ′ 74 sec, NS). Conclusions: Compared to pacing at RA, pre-excitation of IAS either by pacing at CSO or at RV with retrograde conduction can prevent initiation of paroxysms of atrial tachyarrhythmia triggered by single but not by multiple right APBs. These findings imply that the potential benefit of choosing an optimal pacing site in patients requiring atrial-based pacing is limited. Moreover, in the absence of bradycardia, no specific pacing site offers incremental benefit over the natural "protective" effect of sinus rhythm.

Objectives: The incidence and the physiologic roles for direct fast pathway-His bundle connections were examined in 102 rabbit hearts. Methods: Extracellular bipolar and intracellular microelectrode recordings were made from the superfused rabbit AV junction. Results: In 13 of 27 preparations demonstrating anterior extensions of the fast pathway, the retrograde HA ERP and 2:1 block cycle length were shortened (128 ± 12 and 145 ± 5 msec, respectively) versus the remaining 89 preparations (178 ± 15 and 185 ± 10 msec, respectively, p < 0.01). The former values were similar to the ERP and 2:1 block cycle length of fast pathway transitional cells (128 ± 23 and 141 ± 4 msec, respectively), suggestive of a direct fast pathway-His bundle connection. A deflection recorded between the A and H potentials of the His bundle electrogram could be dissociated from both atrial and His bundle activation. Intracellular microelectrode recordings and light microscopy confirmed the deflection to be an accessory pathway consisting of an anterior extension of fast pathway transitional cells connecting the atrium and His bundle. Transection along the AV groove anterior to the compact AV node (N = 5) increased the retrograde ERP and Wenckebach block cycle length by severing the AH connection, or transection of the penetrating bundle (N = 4) produced antegrade AH block without altering rapid retrograde conduction. Conclusions: Fast pathway-His bundle connections were present in 13 of 102 rabbit hearts, providing an anatomic and physiologic basis for rapid retrograde VA conduction and a possible retrograde pathway for sustained AV nodal reentrant tachycardia.

Heart rate turbulence (HRT) has been described as a predictor of high-risk patients with cardiac diseases. The purpose of this study is to determine how the degree of prematurity of a ventricular premature beat (VPB%) and retrograde ventriculoatrial (VA) conduction of VPBs affect HRT. We studied 30 patients without organic heart disease. We calculated turbulent slope (TS) and turbulent onset (TO) from VPBs induced by programmed stimulation from the right ventricular apex. TS was inversely and TO was positively correlated to VPB%. Without retrograde VA conduction of VPBs, TS was inversely and TO was positively correlated to VPB%. In VPBs with retrograde VA conduction, there were no significant correlations between TO and TS with VPB%. In conclusion, TS and TO calculated from VPBs with different degrees of prematurity varied widely. Both VPB% and characteristics of retrograde VA conduction may affect HRT.

Focal junctional tachycardia (FJT) is characterized by a rapid often irregular narrow complex tachycardia with episodes of atrioventricular (AV) dissociation. This uncommon arrhythmia is most likely due to abnormal automaticity or triggered activity. The patients are often quite symptomatic and if left untreated may develop heart failure particularly if their tachycardia is incessant. In patients refractory to medical management, the role of radiofrequency ablation involves either (1) selective ablation of the tachycardia focus while preserving AV conduction or as a last resort (2) AV junction ablation followed by pacemaker implantation. The clinician should first assess whether ventriculoatrial (VA) conduction is present or absent during tachycardia. If present, radiofrequency ablation should be applied at the site of earliest retrograde atrial activation. In the absence of VA conduction and hence an atrial target site, sequential lesions should be applied in the posterior septum (slow pathway region) followed by lesions applied in midseptum and anteroseptum respectively if tachycardia persists. To further minimize the risk of AV nodal block, some authors delivered radiofrequency energy during atrial overdrive pacing to assess AV conduction during ablation. Others recommended mapping the perinodal region and applying radiofrequency ablation at the site where catheter manipulation resulted in tachycardia termination. Using this ablative approach, the risk of AV block is around 5-10%.

Pacemaker syndrome is the development of fatigue and dyspnea in patients with ventricular pacing caused by VA conduction and the resultant atrial contraction against a closed AV valve. First-degree AV block with a very prolonged PR interval has also been reported to present with symptoms of pacemaker syndrome and has sometimes been described as pseudopacemaker syndrome or pacemaker-like syndrome.1 We report a case of pacemaker-like syndrome who presented with florid heart failure and alternans that were abolished with AV pacing. A 65-year-old woman presented with few months history of dyspnoea on exertion gradually progressing to New York Heart Association class IV. She was admitted twice at the emergency department over a period of a …

This report describes the occurrence of a repetitive nonreentrant ventriculoatrial (VA) synchronous rhythm precipitated by the noncompetitive atrial pacing algorithm of a Medtronic DDDR pacemaker. This algorithm delivers an atrial stimulus 300ms after the detection of an atrial signal in the postventricular atrial refractory period of the pacemaker. In our patient, the atrial stimulus released by the algorithm was ineffectual because it encountered prolonged refractoriness of the atrial myocardium. This situation produced a repetitive nonreentrant VAl synchronous rhythm in the setting of retrograde VA conduction.

Background: Pacemaker marker annotations facilitate the interpretation of device behavior in addition to ECG recordings. However, they are only available in conjunction with a programmer. We studied the diagnostic value of a prototype Telemetry Holter Decoder (THD), providing continuous marker annotations on a conventional Holter. Methods: The study included 20 patients with VDD or DDDR pacemakers. A 24-hour Holter was performed using the THD. Marker annotations are transmitted from the pacemaker to the THD, which transforms them into analog signals, which are recorded on one of the Holter channels. Results: During a total recording time of 458 hours, high quality marker annotations were retrieved for every patient. Artefacts disturbed the recordings during 184 min (0.67%). The THD provided information not discernible on the ECG: intermittent atrial undersensing during sinus rhythm (1096 times). Atrial tachycardias, not visible on the ECG, were detected in 2 patients. The activation of tachycardia response algorithms was clearly annotated in 11,516 events. A total of 8875 PVC's occurred, 57.8% of which were classified incorrectly in the event counters as conducted or fusion beats. Atrial far-field sensing or VA conduction was demonstrated 4294 times. Electromagnetic interferences, not visible on the ECG, could be seen three times. Conclusion: Recording of continuous high-quality marker annotation on a conventional Holter is feasible. The THD provides important information on device behavior, even in patients assumed to have regular device function, and shows to be clearly superior to ECG interpretation alone. Such data can be used for improved programming, troubleshooting and for the validation of new algorithms. A.N.E. 2002;7(1):22–28