Retrograde Conduction Research Articles

Abstract 13903: Pacemaker Mediated Arrhythmia Following AV Synchronous Leadless Pacemaker Implantation

Background: Leadless pacemakers have gained popularity in providing permanent pacing in select patient populations. Pacemaker mediated tachycardia and arrhythmias have been well described in patients with dual chamber pacemakers, but up to this point not in leadless pacing. Case Description: A 91-year-old female with symptomatic bradycardia and 2:1 AV block underwent implantation of a Micra AV pacemaker programmed VDD 60-100 bpm. Five months later, she presented with decompensated heart failure with a heart rate of 88 bpm and a newly reduced left ventricular ejection fraction of 30%. Device interrogation showed 95% ventricular pacing, with 91% AV synchrony. The Micra was found to be tracking an atrial rhythm between 80-100 bpm more than 80% of the time (Figure 1A). RV pacing induced cardiomyopathy was suspected and she underwent placement of a bi-ventricular pacemaker. During implant, a short VA time was noted and changes in the V-V cycle length predicted changes in the A-A cycle length (Figure 1B). Micra ventricular pacing was held resulting in an AV paced rhythm from the CRT system and a drop in rate to 60 bpm (Figure 1C). These results indicate that the Micra pacemaker was tracking the atrial mechanical contraction (AM) from a retrograde conducted P-wave resulting in elevated heart rates from a pacemaker-driven arrhythmia. Discussion: In patients with poor AV conduction, intact VA conduction, and SA node dysfunction, Micra AV may create pacemaker mediated arrhythmia by tracking the AM of the retrograde conducted P-wave. Careful patient selection to avoid Micra AV placement in patients with SA node dysfunction, and close attention to the rate histogram on device interrogation may prevent development and facilitate recognition of this unique cause of pacemaker-mediated arrhythmia.

Landiolol, an intravenous β1-selective blocker, is useful for dissociating a fusion of atrial activation via accessory pathway and atrioventricular node.

During ventricular pacing, a fusion of atrial activation may occur owing to the simultaneous retrograde conduction of the atrioventricular (AV) node and accessory pathway (AP), potentially leading to an inaccurate mapping of the atrial AP insertion site. We tested the hypothesis that landiolol, an ultra-short-acting intravenous β1-blocker, could dissociate a fusion of atrial activation. We conducted a prospective before-and-after study to investigate the effect of landiolol on retrograde conduction via the AV node and AP. We enrolled 21 consecutive patients with orthodromic AV reciprocating tachycardia who underwent electrophysiological studies at our hospital between January 1, 2018, and August 31, 2020. Six patients exhibited a fusion of atrial activation. After landiolol administration (10 μg/kg/min), the effective refractory period was unchanged in AP (280 [240-290] ms vs. 280 [245-295] ms, p = .91), whereas that of the AV node was prolonged (275 [215-380] ms vs. 332 [278-445] ms, p = .03). The Wenckebach pacing rate via retrograde AV node decreased after landiolol administration (180 [140-200] beats per minute [bpm] vs. 140 [120-180] bpm, p = .02). Thus, landiolol decreased the minimum ventricular pacing rate required to dissociate a fusion of atrial activation (180 [160-200] bpm vs. 140 [128-155] bpm, p = .007). Radiofrequency catheter ablation under landiolol administration successfully eliminated AP in all patients during ventricular pacing without complications or recurrence. Landiolol inhibited the AV node without affecting the AP and helped dissociate a fusion of atrial activation at a lower ventricular pacing rate.

Retrograde ventriculoatrial jump-What is the mechanism?

During ventricular extra stimuli(VES) protocol a VA jump was noted. In upper panel with VES @ 500/270 ms (Fig A) the His signal appeared after the A-EGM, ruling out pure nodal VA conduction and confirming presence of an accessory pathway (AP). The H signal was delayed due to probable retrograde RBBB. The atrium was already depolarised via AP and the VA traversing via left bundle-His-node got blocked with a H signal. In the lower panel with VES of 500/260 ms the retrograde AP conduction reached the effective refractory period and pure nodal VA conduction took place along with retrograde RBBB. The retrograde VA jump was hence due to a jump from AP to AV node.

PO-04-057 ATRIAL FIBRILLATION CURED BY PACEMAKER REPROGRAMMING

Atrial fibrillation (AF) is commonly detected by remote monitoring of implanted devices. A common question is whether to start anticoagulation in patients with detected AF at risk of stroke. However, the cause of AF is rarely able to be diagnosed or corrected. Repetitive non-reentrant ventriculoatrial synchrony (RNRVAS) is a pacemaker mediated arrhythmia that can occur in patients with intact ventriculoatrial (VA) conduction. Ventricular pacing with retrograde atrial activation that falls within the PVARP is followed by atrial pacing, often delivered while the atrium is refractory. Retrograde atrial activation from the next ventricular paced beat facilitates a repetitive (but non-reentrant) process. Atrial arrhythmias may occasionally result. To highlight the importance of recognizing and correcting RNRVAS as a cause of device-mediated arrhythmia. NA A 68-year-old man with hypertension and sinus node dysfunction underwent dual chamber pacemaker implant (Abbott Assurity). Device interrogation 5-years later showed repetitive episodes of AF that might warrant anticoagulation. Device tracings revealed RNRVAS: retrograde atrial activation falling in PVARP, followed by competitive sensor driven atrial pacing with non-capture, until a captured atrial event initiated AF (Figure, red arrow). Anticoagulation was deferred in favor of device reprogramming, including: 1) reduction in the lower rate; 2) reduction in paced AV delay; and 3) disabling of rate-response. The patient had no further AF episodes. RNRVAS is largely benign but may facilitate initiation of AF or other supraventricular arrhythmias that lead to symptoms or inappropriate therapy. Both RNRVAS and device-triggered AF may be underrecognized. Current devices do not have automatic diagnostic or treatment algorithms. Therefore, it is important to be aware of RNRVAS triggered AF in patients with a dual-chamber device and newly diagnosed AF. RNRVAS tends to occur with a long programmed AV delay (such as is often used to avoid ventricular pacing) and a relatively fast lower rate. Reprogramming to shorten the AV delay, decrease the lower rate or decrease the PVARP are the primary methods of correction. Awareness of pacemaker triggered AF may help avoid inappropriate initiation of anticoagulation or other therapies.

PO-05-226 ORTHODROMIC RECIPROCATING TACHYCARDIA RELYING ON ABERRANT CONDUCTION: NEED FOR A LAGER CIRCUIT

Aberrant conduction during orthodromic reciprocating tachycardia (ORT) can prolong the ventriculo-atrial conduction time, which is found essential for the reentry in certain situations. To investigate the prevalence and different mechanism of aberrancy-dependent ORT. ORT cases relying on aberrancy from 220 cases in our center were searched using the following criteria: (1) Multiple episodes of ORT with aberrant conduction in ECG ; (2) No baseline BBB during sinus rhythm; (3) Absence of narrow QRS form during tachycardia unless isoproterenol used; (4) Restoration of bundle branch conduction giving rise to tachycardia termination or circuit alteration. ECGs and intracardiac tracings during study were carefully examined. 3 patients from 220 patients (1.4%) with ORT showed the phenomenon of dependence on aberrancy. Clinical tachycardia episodes of the patients were short in time. All accessory pathways (APs) were located at anterolateral regions of atrioventricular annulus. None of them had baseline bundle branch block. Creating functional bundle branch block was necessary to induce the tachycardias. In the first patient with ORT and left bundle branch block (LBBB), a late-delivered premature ventricular contraction (PVC) was able to advance the next A and reset the tachycardia, which was diagnostic for ORT with aberrancy. Meanwhile, left bundle branch conduction was restored which narrowed the next QRS complex. Tachycardia was then terminated by the advanced wavefront reaching the ventricular insertion site of AP which was refractory. In the second case, termination of the tachycardia was always preceded by a spontaneous LBBB restoration, with the V and subsequent A at MA advanced, suggesting anterograde block in the AV node. In the other case was, induction required both right BBB and slow pathway conduction. When isoproterenol was given, fast pathway recovered followed by BBB restoration, which made anterograde limb again switched to slow pathway. All pathways were successfully ablated during the procedure. All patients have been free of arrhythmias for at least 6 months. Extra transseptal time caused by aberrancy can be an integral part of ORT, which can explain the infrequent or late onset and unsustainable episodes of ORT in certain patients and is useful in understanding the circuit and localizing the pathway.

PO-04-109 OUTCOMES OF RADIOFREQUENCY CATHETER ABLATION OF DISTINCT ANTERO-SEPTAL ACCESSORY PATHWAYS BY CONVENTIONAL ELECTROPHYSIOLOGICAL MAPPING

Ablation of para-hisian accessory pathways (APs) is challenging because of their proximity to the conduction system. A high incidence of atrio-ventricular (AV) conduction injury (up to 50%) was observed for the ablation of true para-hisian APs. In this retrospective study, we report the outcomes of a large series of patients with antero-septal APs (including true para-hisian APs) who underwent radiofrequency catheter ablation (RFCA). Among 1676 consecutive patients undergoing RFCA of APs between January 2016 and September 2022 in our center, 276 patients with an isolated antero-septal AP were enrolled. Conventional intracardiac mapping and fluoroscopy were used in all procedures. All procedures were performed by an experienced operator with a standard 3.5 mm irrigated tip catheter. A para-hisian AP was confirmed when an His potential was recorded by the distal ablation catheter at the site of earliest atrial activation during orthodromic AVRT or after ablation of the manifest AP. APs were categorized as true para-hisian if a sharp high-amplitude His potential was recorded. Among the 276 patients (mean age 27±10 years; 150 males) with an antero-septal AP: 55 patients (20%) had a true para-hisian AP (Group 1); 89 patients (32%) had a not-sharp low-amplitude His potential (Group 2); 132 patients (48%) had no His potential recorded (Group 3). The three Groups showed no significant difference in clinical (age, sex, history of AF and AVRT, structural heart disease) and EPS variables (conduction properties of APs and inducibility of AVRT and AF). Inferior vena cava (n=260) and aortic retrograde (n=16, targeting the left basal septum) approaches were used. Procedural acute success (no evidence of residual preexcitation or abnormal retrograde conduction) was obtained in all patients. No patient experienced acute severe complications. RF ablation time was longer in Group 1 (135±41 sec vs 115±27 sec [Group 2] vs 92 sec ±18 sec [Group 3], p=0.03). Accelerated junctional rhythm during RFCA was more frequent in Group 1 (25% vs 14% [Group 2] vs 3% [Group 3], p=0.02). After a median follow-up of 40 (2-78) months no high-grade AV block was reported. 1 patient of Group 1 had a recurrent para-hisian AP and underwent a second successful RFCA. In this large series of antero-septal APs (including a high number of true para-hisian APs), electrophysiologically-guided RFCA was safe and highly effective.

PO-05-147 RIGHT ON Q: WIDE-COMPLEX TACHYCARDIA IN SETTING OF DEXTROPOSITION

Dextroposition is a rare cardiac malformation defined as rightward cardiac displacement with leftward apex, vs. dextrocardia, which is rightward base-axis orientation. We report the second known case of dextroposition with accessory pathway, presenting as preexcited atrial tachycardia. Abnormal anatomy complicates ECG localization and pathway ablation. N/A N/A A 50-year-old woman was admitted with respiratory distress due to EBV infection. Chest X-ray showed right-sided heart. A month later, she presented in wide-complex tachycardia, rate 205 bpm. She was cardioverted after minimal response to procainamide/adenosine. Post-cardioversion ECG showed short PR interval and preexcitation, confirming presence of accessory pathway. However, the wide-complex tachycardia had morphology identical to baseline, supporting preexcited atrial tachycardia over AVRT. Despite X-ray findings and reverse R-wave progression in precordial leads, presence of left axis deviation and initial negative deflection in aVR argued against dextrocardia. Moreover, aVR had negative T- and P-waves, findings associated with levocardia. Thus, dextroposition was suspected. Millstein and Arruda criteria suggested posteroseptal accessory pathway, but no data on their applicability in right-sided heart exist. EP study was performed. Eccentric VA conduction was noted. Earliest activation was at proximal coronary sinus. During isoproterenol infusion, patient went into atrial tachycardia, cycle length 420ms. Multiple AT foci were identified, including at right atrial appendage and tricuspid annulus. During ablation, patient developed atrial fibrillation with preexcited RR <250ms, confirming high-risk accessory pathway. Given numerous AT foci and high risk, it was decided to focus on pathway over tachycardia sites. Pathway was successfully ablated at ostia of coronary sinus and middle cardiac vein. One prior case of accessory pathway ablation in dextroposition has been reported. This patient had left lateral pathway and multiple congenital abnormalities including lung hypoplasia. While our patient was found to have multifocal atrial tachycardia, she had no clinical or radiographic lung disease. ECG changes in dextroposition are less predictable than in dextrocardia; they vary with cardiac rotation, axis position, and lead position. Comorbid accessory pathway is rare; ECG-anatomy relationship is ill-defined. Structural abnormalities pose individual challenges during electrophysiologic procedures.

Behavior of Retrograde Conduction Time at Supraventricular Tachycardia Induction and its Role in Differential Diagnosis

Background: Differential diagnosis between orthodromic reentrant tachycardia (ORT) and atypical nodal reentrant tachycardia (ANRT) can be challenging. Our hypothesis was that ANRT presents more variability in retrograde conduction time at tachycardia onset than ORT. Objectives: The objectives of this study were to assess retrograde conduction time variability at the start of tachycardia in ANRT and ORT, and postulate a new diagnostic tool to differentiate these two types of arrhythmias. Methods: The ventriculoatrial (VA) interval of the first beats after tachycardia induction was measured until stabilization. The difference between the maximum and minimum VA interval was defined as delta VA (ΔVA), and the number of beats needed for VA interval stabilization was also assessed. Atrial tachycardias were excluded. Results: In a total of 101 patients included in the study, ORT was diagnosed in 64 patients and ANRT in 37. ΔVA interval was 0 (interquartile range [IQR] 0-5) milliseconds (ms) in ORT vs. 40 (21-55) ms in ANRT (p &lt;0.001). The VA interval significantly stabilized earlier in ORT (1.5 [1-3] beats) than in ANRT (5 [4-7] beats) (p&lt;0.001). A ΔVA &lt;10 ms diagnosed ORT with 100% sensitivity, specificity, and positive and negative predictive values. Ventriculoatrial interval stabilization in less than 3 beats predicted ORT with good diagnostic accuracy. The results were similar considering only accessory septal pathways. Typical NRTs presented an intermediate variation. Conclusion: Presence of ΔVA &lt;10 ms is a simple criterion that accurately differentiates ORT from ANRT, independently of the accessory pathway localization.

The masquerade: What is the wide complex tachycardia?

A 19-year-old boy with rheumatic heart disease, post mitral valve replacement three years earlier, presented with recurrent episodes of palpitations. Sinus rhythm ECG showed left bundle branch block (LBBB). During symptoms, ECG showed regular wide complex tachycardia (WCT) at a rate of 140 beats per min (bpm) with QRS identical to sinus rhythm. Echocardiography revealed a dilated left ventricle with severely depressed systolic function. An electrophysiology study was performed. Four catheters - high right atrium, coronary sinus, right ventricle (RV), and multipolar catheter with close electrode spacing in the His region - were placed. The baseline His-Ventricle (HV) interval was 70 msec. Ventricular pacing showed central and decremental retrograde conduction. Clinical tachycardia at a rate of 140 bpm was initiated during atrial extra stimulus protocol with isoprenaline. The initiation and continuation of the tachycardia are shown (Figures1 and2). What is the best explanation for the arrhythmia seen? This article is protected by copyright. All rights reserved.

A compact multi-functional model of the rabbit atrioventricular node with dual pathways.

The atrioventricular node (AVN) is considered a "black box", and the functioning of its dual pathways remains controversial and not fully understood. In contrast to numerous clinical studies, there are only a few mathematical models of the node. In this paper, we present a compact, computationally lightweight multi-functional rabbit AVN model based on the Aliev-Panfilov two-variable cardiac cell model. The one-dimensional AVN model includes fast (FP) and slow (SP) pathways, primary pacemaking in the sinoatrial node, and subsidiary pacemaking in the SP. To obtain the direction-dependent conduction properties of the AVN, together with gradients of intercellular coupling and cell refractoriness, we implemented the asymmetry of coupling between model cells. We hypothesized that the asymmetry can reflect some effects related to the complexity of the real 3D structure of AVN. In addition, the model is accompanied by a visualization of electrical conduction in the AVN, revealing the interaction between SP and FP in the form of ladder diagrams. The AVN model demonstrates broad functionality, including normal sinus rhythm, AVN automaticity, filtering of high-rate atrial rhythms during atrial fibrillation and atrial flutter with Wenckebach periodicity, direction-dependent properties, and realistic anterograde and retrograde conduction curves in the control case and the cases of FP and SP ablation. To show the validity of the proposed model, we compare the simulation results with the available experimental data. Despite its simplicity, the proposed model can be used both as a stand-alone module and as a part of complex three-dimensional atrial or whole heart simulation systems, and can help to understand some puzzling functions of AVN.

Junctional Tachycardia

Junctional tachycardia (JT) is typically considered to have an automatic mechanism originating from the distal atrioventricular node. When there is 1:1 retrograde conduction via the fast pathway, JT would resemble the typical form of atrioventricular nodal re-entrant tachycardia (AVNRT). Atrial pacing maneuvers have been proposed to exclude AVNRT and suggest a diagnosis of JT. However, after excluding AVNRT, one should consider the possibility of an infra-atrial narrow QRS re-entrant tachycardia, which can exhibit features that resemble AVNRT as well as JT. Pacing maneuvers and mapping techniques should be performed to assess for infra-atrial re-entrant tachycardia before concluding that JT is the mechanism of a narrow QRS tachycardia. Distinguishing JT from typical AVNRT or infra-atrial re-entrant tachycardia has notable implications regarding the approach to ablation of the tachycardia. Ultimately, a contemporary review of the evidence on JT raises some questions as to the mechanism and source of what has traditionally been considered JT.

Syncope After Transcatheter Aortic Valve Implantation: Pace or Not?

Syncope After Transcatheter Aortic Valve Implantation: Pace or Not?

Pseudo repetitive non-reentrant ventriculoatrial synchrony: Current challenges.

We recently described a novel pacemaker-mediated arrhythmia in Abbott cardiac implantable electronic devices (CIED), called pseudo-RNRVAS, that mimics repetitive non-reentrant ventriculoatrial synchrony (RNRVAS), but can appear in patients with ventriculoatrial (VA) block. It is caused by sinus-p-waves, trapped in the post-ventricular atrial refractory period (PVARP), which mimic VA conduction. The p-waves are followed by atrial pacing during the myocardial refractory time, which can trigger atrial fibrillation (AF). Pseudo-RNRVAS and RNRVAS are probably more common than appreciated, but the recognition and differentiation of the two can be challenging because most CIEDs do not recognize and store them. We illustrate practical challenges in the assessment of Pseudo-RNRVAS and provide programming options that proved safe and effective for preventing Pseudo-RNRVAS and reducing the risk for typical RNRVAS. We illustrate in 10 patients the characteristics of Pseudo-RNRVAS and their treatment. The outcome regarding the recurrence of pseudo-RNRVAS after 6 months of follow-up was collected. Inappropriate atrial pacing during pseudo-RNRVAS resulted in AF in six patients. After shortening the PVARP in nine, inactivation/reduction of rate response in four, and reduction of the basic pacing rate in one patient, pseudo-RNRVAS was avoided in eight patients and reduced in one. In one patient AF became permanent. Pseudo-RNRVAS is a pacemaker-mediated arrhythmia that can appear in patients without VA conduction and may lead to AF. The suggested adjustments of pacing parameters were safe and effective in preventing the arrhythmia.

A supraventricular tachycardia and the response to parahisian pacing: What is the mechanism?

A 21-year-old man underwent an electrophysiological study because of a documented supraventricular tachycardia (SVT). Baseline atrial-His and His-ventricular intervals were normal, and programmed ventricular extrastimulation (VES) demonstrated decremental ventriculoatrial (VA) conduction with a concentric atrial activation sequence (Figure 1A ). An SVT was induced during programmed atrial stimulation with an identical atrial activation sequence as that during VES, but attempts at right ventricular (RV) entrainment consistently terminated the tachycardia (Figure 1B). The His-RV catheter was removed, and a mapping catheter was inserted instead to perform parahisian pacing. The response is shown in Figure 2A . Based on these electrophysiological findings, what is the mechanism of this tachycardia and the most appropriate interpretation of the parahisian pacing response? Figure 2A: Response to parahisian pacing. B: Recovery from the mechanical bump of the bypass tract (BT). From the third beat, the BT potential emerges, with shortening of the ventriculoatrial (VA) interval. Arrows indicate BT potentials. HA = His-atrial; SA = stimulus-atrial; other abbreviations as in Figure 1. View Large Image Figure Viewer Download Hi-res image

A clue to the triples from an echo.

A clue to the triples from an echo.

Potential triggering of repetitive nonreentrant ventriculoatrial synchrony by loss of atrial capture

Data on the factors that trigger repetitive nonreentrant ventriculoatrial synchrony (RNRVAS) are limited. We hypothesize that loss of atrial capture may trigger RNRVAS. We aimed to use an atrial threshold test to observe the development of RNRVAS upon loss of atrial capture in patients with implantable cardiac electronic devices (CIED). Patients with DDD mode CIEDs [177 patients, 67.5± 14.8 (70) years; 70 women] were included. Atrial threshold test was done in DDD mode at a rate at least 10 beats above the basal heart rate, with an AV delay of 300 ms (range 250-350). A multivariable logistic regression model was used to assess the independent predictors of RNRVAS. RNRVAS was observed in 69 of the 177 patients (39.0%) during atrial threshold test. In patients with VA conduction, incidence of RNRVAS increased to 76.7%. In univariate analysis, younger age (p= .038) and the presence of VA conduction (p< .001) were associated with an increased risk of RNRVAS, whereas complete AV block or any AV node conduction defect (p< .001) and the ventricular pacing ratio (p= .001) were inversely related to the risk of RNRVAS occurrence after loss of atrial capture. In multivariate analysis complete AV block (p= .009) and ventricular pacing ratio (p= .029) appeared as independent factors inversely related to the risk of RNRVAS development. In this study, we demonstrated that loss of atrial capture results in RNRVAS in one-third of patients with a CIED in DDD mode, and in three-fourths of those with VA conduction under certain predisposing CIED settings.

81 PITFALLS IN LATERAL ACCESSORY PATHWAY ABLATION: THE IMPORTANCE TO RECOGNIZE MITRAL ISTHMUS CONDUCTION BLOCK DURING REDO PROCEDURES

Abstract Introduction Inaccurate mapping and ablation of left-lateral concealed AP can result in mitral isthmus conduction block, mimicking concentric retrograde activation. AVRT recurrences are frequent because ablation leaves the conduction through the AP intact. Case Report A 50-years-old patient with history of previous ablations of concealed left-lateral AP underwent third redo procedure due to reoccurrence of SVT. Quadripolar catheters were placed in the His bundle and RV apex; a decapolar catheter was placed in the CS. Retrograde conduction during ventricular pacing was non decremental. CS activation was concentric during AVRT. Mitral anulus was mapped via transeptal approach, showing mitral isthmus block, justifying the “concentric” atrial activation appearance, due to a left counterclockwise activation circuit and short VA interval distally to the previous ablations site. Single RF application of 1.9 sec interrupted the AP conduction. Effective ablation was confirmed by failure to induce tachycardia and by induction of AV dissociation using adenosine during ventricular pacing. Conclusion Change of retrograde activation pattern during AVRT reoccurrences may be referred to iatrogenic atrial conduction block achieved during ablation, rather than to the presence of a concomitant misdiagnosed AP.

Could premature ventricular contractions lead to atrial remodeling?

Premature ventricular contraction (PVC) is a frequent kind of arrhythmia that affects around 1% of the general population. While PVC most frequently impairs ventricular function in structurally normal heart, retrograde ventriculo-atrial conduction can occur in people with PVC. These retrograde atrial activations may mimic pulmonary vein-derived atrial ectopies. As a result, PVC may raise the risk of atrial fibrillation (AF) by retrograde ventriculo-atrial conduction. The Four-Dimensional Automated Left Atrial Quantification (4D Auto LAQ) tool is a left atrial analytical approach that utilizes three-dimensional volume data to quantify the volume, as well as LA longitudinal and circumferential strains. The purpose of this study was to determine if clinical diagnosis of PVC is connected with abnormal LA function as determined by LA strain evaluation utilizing a 4D Auto LAQ compared to the healthy population. The 58 patients with frequent PVCs and 53 healthy volunteers as a control group were enrolled in the study. Imaging was performed using the GE Vivid E95 echocardiography equipment (GE Healthcare; Vingmed Ultrasound, Horten, Norway) equipped with an M5S probe (frequency range: 1.5-4.6 MHz) and a 4V probe (frequency range: 1.5-4.0 MHz). Images were imported into and were selected for analysis using the EchoPAC203 software (GE Healthcare). The analysis mode was selected, followed by the volume and 4D Auto LAQ submodes. Following that, the sample point was positioned in the center of the mitral orifice in each of the three planes. The review function was used to acquire the LA parameters measured by 4D Auto LAQ, including volume and strain parameters. The maximum left atrial volume (LAVmax) and minimal left atrial volume (LAVmin) were significantly higher in the patient group (38.91 ± 9.72 vs. 46.31 ± 10.22, 17.75 ± 4.52 vs. 23.10 ± 7.13, respectively, all p values <.001). On the other hand left atrial reservoir longitudinal strain (LASr), conduit longitudinal strain (LAScd), contraction longitudinal strain (LASct), reservoir circumferential strain (LASr-c), conduit circumferential strain (LAScd-c), and contraction circumferential strain (LASct-c) were significantly lower in patient group (26.64 ± 5.64 vs.19.16 ± 4.58, -19.53 ± 3.72 vs. -11.28 ± 3.47, -10.34 ± 1.56 vs. -4.59 ± 1.49, 30.72 ± 4.04 vs. 19.31 ± 2.60, -19.91 ± 1.78 vs. -13.38 ± 2.85, -15.89 ± 6.37 vs. -9.24 ± 1.63, respectively, all p values <.001). The present study found that premature ventricular complexes can lead to atrial remodeling as well as ventricular remodeling in patients with PVC and 4D LAQ technology can quantitatively examine left atrial function and determine these alterations early.

Abstract 13613: Prevalence of Atrial Fibrillation and Procedure-Outcome in Patients Undergoing Catheter Ablation for Premature Ventricular Contractions

Introduction: Atrial fibrillation (AF) and premature ventricular contractions (PVC) are common arrhythmias encountered in clinical practice. Theoretically, retrograde atrial conduction can occur in the presence of PVC, causing atrial ectopy. However, the clinical significance of this association is not defined yet. Hypothesis: We investigated the prevalence of AF in patients with PVC and its impact on PVC ablation. Methods:: Consecutive patients undergoing PVC ablation at our institution between 2016 and 2019 were included in this analysis. Patients with structural heart disease, hyperthyroidism, malignancy, alcoholism and advanced renal or hepatic disease were excluded. For all patients, 12-lead ECG was used to diagnose AF and assess PVC morphology. During the index procedure, all PVC morphologies were targeted for ablation. Patients were followed up with remote monitoring as well as ICD interrogations and office visits every 6 months for 2 years. Detection of any PVC in the electrogram was considered as recurrence. Results: A total of 394 patients undergoing PVC ablation were included of which 96 (24%) had the documented evidence of AF. Baseline characteristics of the study population without (group 1, n=298) versus with AF (group 2, n=96) is provided in table 1. Clinical parameters were comparable between the groups except age, which was higher in group 2. PVCs with multiple (≥2) morphology were detected at the index procedure in 41 (13.7%) and 58 (60.4%) patients in group 1 and 2 respectively (p &lt;0.001). At 2 years of follow-up, recurrence rate following PVC-ablation was significantly higher in group 2 compared to group 1 (17 (18%) vs 27 (9%), p=0.026). Conclusions: In this consecutive series, AF was documented in 1/4 th of the population undergoing PVC ablation and presence of AF was associated with lower procedural success at long term, which could be attributed to older age and significantly higher prevalence of multiple morphology’ PVCs in the group 2 population.

Pacemaker-Mediated Tachycardia Interpolated Into Ventricular Tachycardia

In a 77-year-old patient with a history of inferior myocardial infarction and dual-chamber pacemaker (Effecta DR, Biotronik) implanted for carotid sinus syndrome, a routine Holter electrocardiogram recorded 3 consecutive tachycardias: irregular monomorphic ventricular tachycardia (VT), pacemaker-mediated tachycardia (PMT), and reoccurred VT (re-VT) of the same morphology as the initial one, but regular and faster than the PMT (Fig. 1).The pacemaker settings were as follows: DDD mode; pacing rate, 50 to 130 bpm; programmed atrioventricular delay, paced 145 ms and sensed 105 ms; and postventricular atrial refractory period (PVARP), 250 ms and 400 ms following premature ventricular contraction.What was the most likely mechanism of this arrhythmia?B) PMT was triggered by atrial premature beat and terminated by the re-VT (Fig. 2) Concerning the mode of the PMT initiation, the VT could not trigger PMT because its retrograde P wave (in Fig. 2, stars denote retrograde P waves; those of the VT and re-VT are marked below and those of the PMT above the middle electrocardiographic channel) occurred during the PVARP (gray horizontal marks in the ladder diagram). Given that the interrogation showed no pacemaker malfunctions and that the electrocardiogram showed no artifacts, an atrial ectopic beat (with isoelectric P wave) is the only likely trigger for PMT.Concerning the mode of PMT termination, the episode was too short to activate the device's PMT termination algorithm. Furthermore, the retrograde P wave from the last PMT beat, which appeared after 344 ms, indicates that retrograde conduction has been prolonged, but without occurrence of a block that would have stopped the PMT. Thus, the re-VT is what terminated the PMT by the first impulse following fusion (f2 in Fig. 2), which depolarized ventricles before the possible onset of the next paced beat. Retrograde conduction prolongation (by 24 ms) and programmed atrioventricular delay prolongation (by 50 ms, for Biotronik's PMT status confirmation) during the last PMT cycle provided a time for the onset of the re-VT and thus indirectly participated in the PMT termination.Based on the constant cycle length (382 ms) of the re-VT during the prolongation of ventriculoatrial conduction (from 170 to 240 ms), the re-VT was most probably microreentrant. Different retrograde conduction times of the VT (160 ms) and PMT (315 ms) might suggest the existence of a dual retrograde conduction with separate pathways for each of the 2 tachycardias, but any evidence for such speculation is lacking. In any case, this case illustrates the complexity of possible interactions between spontaneous and device-mediated arrhythmias.