Ventricular Extrastimuli Research Articles

Editorial to “Atypical atrial resetting with ventricular extrastimulus during tachycardia: What is the mechanism?”

Editorial to “Atypical atrial resetting with ventricular extrastimulus during tachycardia: What is the mechanism?”

Prognostic value of non-invasive programmed ventricular stimulation after VT ablation to predict VT recurrences.

The prognostic value of (non)-invasive programmed ventricular stimulation (NIPS) to predict recurrences of ventricular tachycardia (VT) is under discussion. Optimal endpoints of VT ablation are not well defined, and optimal timepoint of NIPS is unknown. The goal of this study was to evaluate the ability of programmed ventricular stimulation at the end of the VT ablation procedure (PVS) and NIPS after VT ablation to identify patients at high risk for VT recurrence. Between January 2016 and February 2022, consecutive patients with VT and structural heart disease undergoing first VT ablation and consecutive NIPS were included. In total, 138 patients were included. All patients underwent NIPS through their implanted ICDs after a median of 3 (1-5) days after ablation (at least 2 drive cycle lengths (500 and 400ms) and up to four right ventricular extrastimuli until refractoriness). Clinical VT was defined by comparison with 12-lead electrocardiograms and stored ICD electrograms from spontaneous VT episodes. Patients were followed for a median of 37 (13-61) months. Of the 138 patients, 104 were non-inducible (75%), 27 were inducible for non-clinical VTs (20%), and 7 for clinical VT (5%). In 107 patients (78%), concordant results of PVS and NIPS were observed. After 37 ± 20months, the recurrence rate for any ventricular arrhythmia was 40% (normal NIPS 29% vs. inducible VT during NIPS 66%; log-rank p = 0.001) and for clinical VT was 3% (normal NIPS 1% vs. inducible VT during NIPS 9%; log-rank p = 0.045). Positive predictive value (PPV) and negative predictive value (NPV) of NIPS were higher compared to PVS (PPV: 65% vs. 46% and NPV: 68% vs. 61%). NIPS revealed the highest NPV among patients with ICM and LVEF > 35%. Patients with inducible VT during NIPS had the highest VT recurrences and overall mortality. Patients with both negative PVS and NIPS had the lowest any VT recurrence rates with 32%. Early re-ablation of patients with recurrent VTs during index hospitalization was feasible but did not reveal better long-term VT-free survival. In patients after VT ablation and structural heart disease, NIPS is superior to post-ablation PVS to stratify the risk of VT recurrences. The PPV and NPV of NIPS at day 3 were superior compared to PVS at the end of the procedure to predict recurrent VT, especially in patients with ICM.

Atypical atrial resetting with ventricular extrastimulus during tachycardia: What is the mechanism?

This atypical atrial resetting with ventricular extrastimulus delivered during supraventricular tachycardia is characterized by no capture of local ventricular deflection contralateral to the earliest atrial site and is a finding unmasking the presence of a nodoventricular pathway, the ventricular insertion of which is located apically, away from the mitral annulus.

Prevalence and characteristics of atrioventricular nodal reentrant tachycardia with a bystander concealed nodoventricular/nodofascicular pathway

BackgroundThe concealed nodoventricular/nodofascicular (NV/NF) pathway is mostly a bystander, retrograde bypass tract connecting the right ventricle/right bundle branch (RBB) and slow pathway that is observed in patients with atrioventricular nodal reentrant tachycardia (AVNRT). However, its prevalence and characteristics in response to pacing maneuvers have not been fully evaluated. ObjectiveThis study investigated the prevalence and characteristics of AVNRT with a bystander NV/NF pathway. MethodsWe retrospectively reviewed 153 consecutive patients undergoing catheter ablation of AVNRT. After exclusion of 52 patients with inadequate electrophysiologic data, 101 patients composed the study population. ResultsThree patients (3.0%) had bystander concealed NV/NF pathways, all of which were connected to the slow pathway. The tachycardia was typical slow pathway/fast pathway AVNRT in 2 patients and atypical fast pathway/slow pathway AVNRT in 1 patient. In all cases, His-refractory ventricular extra-stimuli (VES) reset the AVNRTs with delay through the NV/NF pathways. Ventricular overdrive pacing (VOP) in the early phase also reset the AVNRT with delay. Earlier VES and middle phase of VOP did not reset the tachycardia, and further earlier VES and late phase of VOP reset the tachycardia with advance through the RBB-His conduction. ConclusionA bystander NV/NF pathway was not rare in patients with AVNRT. The VES and VOP for the AVNRTs with the bystander NV/NF pathways were characterized by the 2-phase resetting phenomenon: initial transient resetting with delay through the NV/NF pathway, and late resetting with advance through the RBB-His conduction.

Improving functional substrate delineation for ablation of ventricular tachycardia using high-density electroanatomic mapping and double ventricular extra stimuli protocol

Abstract Background A partial delineation of targets for ventricular tachycardia (VT) ablation may contribute to a suboptimal success rate. Abnormal electrograms (EGMs) with low-voltage near-field components might be concealed within high-amplitude far-field signals. Our hypothesis posited that acquiring functional mapping after double ventricular extrastimuli (S3 protocol) could reveal relevant areas of functional substrate overlooked during sinus or S1 mapping. Purpose To assess the benefit and feasibility of functional substrate mapping using a full ventricle S3 protocol and to evaluate its colocalization with conducting channels (CCs) identified in late gadolinium enhancement cardiac magnetic resonance (LGE-CMR). Methods (Figure 1) - An S3 mapping protocol with a drive train of S1 followed by S2 (effective refractory period (ERP) +30ms) and S3 (ERP+50ms) from the RV apex was conducted in 40 consecutive patients undergoing scar-related VT ablation. Deceleration zones (DZs) and areas of late potentials (LPs) were identified for all maps (S1, S2, and S3). Pre-procedural non-invasive substrate assessment was performed with LGE-CMR and post-processing using a commercially available system with automated CC identification. Results The S3 protocol was completed in 34 of the 40 procedures (85.0%). Repeated induction of ventricular arrhythmias prevented the full S3 protocol in 5 patients (15.0%). Functional substrate identified during S3 activation mapping was significantly more extensive than that identified using S2 and S1, including a higher number of DZs (2.94, 2.47, and 1.82, respectively; p<0.01) and a wider area of LPs (44.1cm2, 38.2cm2, and 29.4cm2, respectively; p<0.001). The percentage of CCs unmasked by DZs and LPs using S3 maps was significantly higher than the ones using S2 and S1 maps(78%, 65%, and 48%; p<0.001, and 88%, 81%, and 68%; p<0.01, repectively). After VT ablation based on an S3 protocol, 77.9% of patients have been VT free during a median follow-up of 13.6 months. Conclusions (Graphical abstract -Figure 2) - This novel substrate-based protocol for assessing functional substrate is feasible in most patients, enables better identification of ablation targets, and has the potential to improve patient prognosis post-ablation.Methods - The S3 protocolConclusion - Graphical abstract

Intracardiac electrophysiology to characterize susceptibility to ventricular arrhythmias in murine models.

Introduction: Sudden cardiac death (SCD) and ventricular fibrillation are rare but severe complications of many cardiovascular diseases and represent a major health issue worldwide. Although the primary causes are often acute or chronic coronary diseases, genetic conditions, such as inherited channelopathies or non-ischemic cardiomyopathies are leading causes of SCD among the young. However, relevant experimental models to study the underlying mechanisms of arrhythmias and develop new therapies are still needed. The number of genetically engineered mouse models with cardiac phenotype is growing, making electrophysiological studies in mice essential tools to study arrhythmogenicity and arrhythmia mechanisms and to test novel treatments. Recently, intracardiac catheterization via the jugular vein was described to induce and record ventricular arrhythmias in living anesthetized mice. Several strategies have been reported, developed in healthy wild-type animals and based on aggressive right ventricular stimulation. Methods: Here, we report a protocol based on programmed electrical stimulation (PES) performed in clinical practice in patients with cardiac rhythm disorders, adapted to two transgenic mice models of arrhythmia - Brugada syndrome and cardiolaminopathy. Results: We show that this progressive protocol, based on a limited number of right ventricular extrastimuli, enables to reveal different rhythmic phenotypes between control and diseased mice. In this study, we provide detailed information on PES in mice, including catheter positioning, stimulation protocols, intracardiac and surface ECG interpretation and we reveal a higher susceptibility of two mouse lines to experience triggered ventricular arrhythmias, when compared to control mice. Discussion: Overall, this technique allows to characterize arrhythmias and provides results in phenotyping 2 arrhythmogenic-disease murine models.

Assotiation of testosterone levels and oxidative stress activity with 10-year survival in men with cardiac resynchronization therapy

Aim. To investigate the association of testosterone levels (TES) and oxidative stress activity with 10-year survival in men with cardiac resynchronization therapy (CRT).Methods. 86 men with CRT (59.0±9.8 years; 66.3% ischemic cardiomyopathy) were divided into 4 groups: Gr.1 (n=19) TES<median level (16.4nmol/l) + myeloperoxidase (MPO) < median level (32.5 ng/mL); Gr.2 (n=18) TES<median level + MPO>median level; Gr.3 (n=23) TES> medians + MPO < median level; Gr.4 (n=26) TES > median level + MPO > median level. Echocardiography parameters, incidence of ventricular extrasystole, TES in plasma, estradiol, progesterone, dehydroepiandrosterone sulfate, norepinephrine, MPO, NT-proBNP, matrix metalloproteinase, tissue inhibitor of metalloproteinase were assessed. Prognostic level of NT-proBNP was assessed by ROC analysis; 10-year survival was measured by Kaplan-Meier method, factors associated with it were evaluated using Cox regression.Results. The majority of patients were NYHA II and NYHA III for Gr. 3 and Gr.4 respectively (р3-4=0,010). At baseline: there was no difference in echocardiography parameters, levels of NT-proBNP, MPO, steroids, matrix metalloproteinase between groups; tissue inhibitor of metalloproteinase was higher in Gr.2 and Gr.4; the highest norepinephrine levels was in Gr.4. Follow-up: reverse cardiac remodeling was associated with NT-proBNP decreasing and was registered in Gr.4 and Gr. 3. The level of MPO was decreased in Gr.3, Gr.4., and was the highest in Gr.4. The level of estradiol was increased in Gr.1; There were no difference in hormone levels in Gr.2. TES, dehydroepiandrosterone sulfate was increased, but progesterone was decreased in Gr.3 and in Gr.4. The norepinephrine`s levels were increased in all groups. The number of ventricular extrastimuli was increased in Gr.4. Predictive level of NT-proBNP was 756.0 pg/ml (AUC=0.685; p=0.003; sensitivity: 64%, specificity: 68%). The 10-year survival rate was 15.4%; 33.5%; 76.3%; 24.4% for Gr. 1-4 respectively (Log Rank test: Gr.1-2=0.378; Gr.1-3<0.001; Gr.1-4=0.070; Gr.2-3=0.009; Gr.2-4=0.772; Gr.3-4=0.010). The survivance was higher in patients with the best CRT response time (p=0.004), the level of NT-proBNP>756.0 pg/ml (p=0.001) in Gr.1, Gr.2; the best CRT response time (p=0.001), left ventricular ejection fraction (p=0.046), MPO>median (p=0.041), amiodarone administration (0.008) in Gr. 3, Gr. 4.Conclusion. CRT modulates steroidogenesis. Increase of TES and dehydroepiandrosterone sulfate with lower oxidative stress activity is associated with greater reverse cardiac remodeling and better 10-year survival rate. The higher level of TES and simultaneously MPO more than 32.5 pg/ml were related to less reverse cardiac remodeling, higher rate of amiodarone administration by 5.2 times, increasment of ventricular arrhythmias rate and higher relative risk of death by 4.2 times. Relationship between 10-year survival rate and period of best CRT response indicates less physiological nature of forceful modulating effects of CRT.

The benefit of a double ventricular extra stimuli protocol to improve functional substrate mapping during ablation of ventricular tachycardia. – The S3-VT-FREE project

The benefit of a double ventricular extra stimuli protocol to improve functional substrate mapping during ablation of ventricular tachycardia. – The S3-VT-FREE project

Pseudo-slow-fast atrioventricular nodal reentrant tachycardia: Is the fast pathway a criminal or innocent bystander?

The intracardiac electrograms are shown during scanned single premature ventricular extrastimuli with a decreasing coupling interval in a very short RP tachycardia. What is the diagnosis and is the fast pathway essential for sustaining the tachycardia?

The benefit of a double ventricular extra stimuli protocol to improve functional substrate mapping during ablation of ventricular tachycardia. - The S3-VT-FREE project

Abstract Introduction Ablation of ventricular tachycardia (VT) based on substrate-based mapping has been proposed to itemize areas of interest identifying areas of low-voltage, late potentials (LPs), and deceleration zones (DZs). However, partial delineation of targets for ablation is likely responsible for a suboptimal long-term success rate. The abnormal electrograms (EGMs), featuring low-voltage near-field components may be hidden within the high-amplitude far-field signal. We hypothesized that the acquisition of functional mapping after double ventricular extrastimuli (S3 protocol) would uncover relevant areas of functional substrate that could be missed during sinus or S1 map. We aim to evaluate the potential benefit and the feasibility of functional substrate mapping using an S3 protocol for VT ablation and to assess its colocalization with detected corridors using late gadolinium enhancement magnetic resonance imaging (LGE-MRI). Methods We included consecutively 29 patients with structural cardiomypathy who underwent a VT ablation. The S3 protocol included: (1) assessment of the ventricular effective refractory period (ERP), (2) pacing protocol from the apex of the right ventricle with S1 x 6 (cycle length: 600ms) followed by S2 (ERP+30ms) and S3 (ERP+50ms). Electroanatomical mapping was acquired with the EnsiteX system (Abbott, IL) using HD Grid catheter and omnipolar signals. ILAMs were used to identify deceleration zones and areas of late potentials were identified for all maps. A non-invasive substrate assessment was done with LGE-MRI and post-processing with a commercially available system (ADAS3D, Spain) with automated identification of corridors. Results The S3 protocol was completed in 25 of the 29 procedures (86.2%). The repeated induction of ventricular arrhythmias did not allow for full protocol of the S3 protocol in 4 patients (13.8%). The functional substrate identified during the S3 activation mapping was significantly more extensive than the one identified using S1 and S2 activation mappings (p<0.05) (Table). The S3 protocol unmasked a higher number of DZs (p<0.01), a wider area of LPs (p<0.01), and a longer duration of the DZs (p=0.01). All DZ maps were compared with preprocedural cardiac magnetic resonance. The number of DZs matching with conduction corridors identified by LGE-MRI was higher in the activation mapping of S3 compared with the S1 and S2 ones (p=0.02). After VT ablation based on an S3 protocol, 88% of patients have been VT free during a median follow-up of 9 months. Conclusions This novel substrate-based protocol to assess the ventricular functional substrate is feasible in the majority of patients (86.2%) and allows for a better identification of targets for ablation and could facilitate VT ablation, and improve the prognosis of the patients after ablation.

Abstract 17250: It's the Journey, Not the Destination: Demonstration of an Uncommon Variation of Para-Hisian Pacing

A 21 year-old college athlete presented with palpitations during exercise. ECG and transthoracic echo were normal. He underwent electrophysiology study. With catheter placement, the patient had atrial fibrillation without preexcitation. On isoproterenol, spontaneous salvos of supraventricular tachycardia (SVT) occurred. Coronary sinus activation was concentric. SVT never sustained, limiting diagnostic maneuvers. In SVT, the ventriculoatrial (VA) time was 145 msec, and there was no decrement of VA conduction with ventricular extrastimuli. Para-Hisian pacing (PHP) was performed. At high output, local myocardial + Purkinje (LM+P) capture was observed, with a VA time of 130 msec; at lower output, selective Purkinje (SP) capture was observed, with a narrower QRS (Figure 1A), and paradoxically longer VA time (160 msec) (Figure 1B). The diagnosis of a retrograde conducting-only accessory pathway (AP) was made, mapped with ventricular pacing, and ablated on the posteroseptum. SVT was no longer inducible. Discussion: PHP is employed to identify presence of a septal retrograde conducting AP based on findings of equal VA times with LM and LM+P capture. Here, the traditional findings of PHP (LM and LM+P capture) were absent because LM capture did not occur, and a third, distinct manner of activating the ventricle (via SP capture) produced unexpected results. In the presence of a retrograde conducting AP, the VA time with narrow-QRS by way of SP capture (sequential activation of the Purkinje system then myocardial conduction) was paradoxically longer than that of wider-QRS LM+P capture (concurrent Purkinje and myocardial conduction), because the path of VA conduction via the AP is “closer” to the site of first ventricular activation. The comparison of SP to LM+P capture may in and of itself declare the presence of an AP; however, LM, LM+P, and SP capture together may be useful to identify a second concealed AP providing incremental diagnostic information to conventional PHP.

Clinical profile and electrophysiological characteristics of atypical atrioventricular nodal reentrant tachycardia: A decade's experience

ObjectiveTo assess the clinical features and inducibility characteristics of atypical atrioventricular nodal reentrant tachycardia (AVNRT) and compare it with typical AVNRT. BackgroundAVNRT is the commonest form of paroxysmal supraventricular tachycardia. The mechanism of AVNRT is very varied. Several classification systems evolved with better understanding but a simplified approach of classification into typical and atypical AVNRT is justifiable and clinically more relevant. In our study, we have assessed the epidemiological profile of atypical AVNRT in a single institute over 10 years and analysed pertinent electrophysiological characteristics. MethodIn this retrospective observational single center study we analysed data of all AVNRT cases from January 2011 to June 2021. In our study we classified atypical AVNRT and typical AVNRT based on the HA interval; HA≤70 ms in the His bundle region during tachycardia was considered as typical AVNRT. Other parameters were also analysed during tachycardia, such as: induction by atrial or ventricular pacing, AH/HA ratio, tachycardia cycle length and site of the earliest atrial activation. The demographic profile of the patients were also compared between 2 groups. ResultsAtypical AVNRT was found in 75/1431 patients (5.2%) of all cases of AVNRT. The age of patients with atypical AVNRT was 52.4 ± 15.2 years (range 9–82 years) while that for typical AVNRT it was 48.2 ± 15.7 years (2–89 years), p = 0.023. There was no gender difference. Atypical AVNRT was induced by only ventricular extrastimuli (VES) in 17/75 (22.6%) while in typical AVNRT this was seen in only 12/1356 patients (0.9%, p < 0.001). Induction of atypical AVNRT was seen by both atrial extrastimuli (AES) and VES in 17/75 patients (22.6%) while in typical AVNRT this was seen in 64/1356 patients (4.8%, p < 0.001). Atypical AVNRT was induced by only AES in 40/75 patients (53.3%) while in typical AVNRT this was seen in 1280/1356 patients (94.3%, p < 0.001). An AH >200 ms during tachycardia was seen in all patients with typical AVNRT and in only 31/75 patients (41.3%) of atypical AVNRT (p < 0.00001). An interesting finding in atypical AVNRT was the earliest atrial activation at the His bundle region in 10/75 (13.3%) patients. ConclusionAtypical AVNRT prevalence depends on the way it is classified; this was 5.2% of all AVNRT cases in our study. Typical AVNRT was seen more frequently in comparatively younger age group and was more often induced by AES. Atypical AVNRT was much more commonly induced by only VES compared to typical AVNRT. It was not so unusual in atypical AVNRT to find the earliest atrial activation in the His bundle region.

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.

Ventricular tachycardia substrate ablation in patients with slightly depressed left ventricular ejection fraction. Predictors of VT-free survival in a prospective multicentre registry

Abstract Funding Acknowledgements Type of funding sources: None. Background There is no consensus about the need for ICD implantation in patients with slightly depressed left ventricle ejection fraction (LVEF) after catheter ablation for hemodynamically tolerated ventricular tachycardia (VT). Purpose This study aims to investigate predictors of mortality VT-free survival in this population. Methods We evaluated predictors of VT-free survival in patients with LVEF&amp;gt;40% from a prospective multicenter register of patients undergoing VT substrate ablation for hemodynamically tolerated VT. Decision to protect with ICD implantation at hospital discharge was performed according to the judgment of the treating cardiologist. The patients included in the study were followed every six months. Ventricular arrhythmia-free survival was the primary endpoint. Any episode of sustained VT (&amp;gt; 30 s) or appropriate ICD therapy was considered VT recurrence. Results One-hundred thirty-two patients [67±13 years, 91% male, 50±8% mean LVEF, 85 (65%) with ischemic heart disease] with a LVEF&amp;gt;40% were identified. Twenty-one (16%) of them were non-inducible at the end of the procedure and were discharged without ICD implantation as they were considered to have a low risk of recurrences. After a mean follow-up of 26±23 months, 32 (24%) patients had VT recurrences. A complete arrhythmogenic substrate elimination [HR: 0.34 (0.16-0.7), p&amp;lt;0.01] and the use multiple ventricular extrastimuli for hidden slow conduction (HSC) identification and ablation [HR: 0.51 (0.27-1.1), p=0.09] were related with VT-free survival (Figure 1). 53 (40%) patients fulfilled both criteria, having a 8% recurrence rate during the follow-up. Compared with the clinical decision making of ICD implantation at hospital discharge, the use of these two variables better identify patients at risk for VT recurrences, with a net reclassification improvement of 23% (Figure 2). Conclusions VT recurrence after VT substrate ablation in patients with slightly depressed LVEF remains high. However, complete substrate elimination and HSC analysis and ablation are related with higher VT-free survival and identify a subgroup of patients in whom ICD might be not beneficial.

PO-03-224 ELECTROPHYSIOLOGY STUDY WITH VENTRICULAR STIMULATION DOES NOT ADEQUATELY RISK STRATIFY PATIENTS WITH MYOTONIC DYSTROPHY

Myotonic dystrophy (MD) types 1 and 2 frequently are associated with progressive conduction disease. Furthermore, patients are at risk ventricular arrhythmias (VAs), although prediction of this remains difficult. The 2021 HRS Guidelines give a IIb recommendation to the use of electrophysiology study (EPS) with ventricular stimulation (v-stim) to risk stratify patients for VAs. The utility of EPS in predicting the development of VAs, however, has not been explored in this patient population. To examine the natural history of MD patients with positive and negative v-stim during EPS. Patients with a history of MD undergoing EPS with associated v-stim from 2007 to present were retrospectively identified. EPS included measurement of baseline conduction intervals. Ventricular stimulation was performed from two sites, most commonly the right ventricular apex and the right ventricular outflow tract, with delivery of up to three ventricular extra-stimuli with a drive cycle length of 600 ms and 400 ms. V-stim was deemed positive when sustained monomorphic ventricular tachycardia (VT) was present or required intervention (pace termination or cardioversion) due to hemodynamic compromise. From 2007-2022, 26 consecutive patients with confirmed type 1 or type 2 myotonic dystrophy presented for EPS with v-stim. Mean age was 51 +/- 12.6 years and mean LV ejection fraction of 63 +/- 9.4%. Eight (31%) v-stim protocols utilized Isoproterenol. Four v-stim protocols were positive for sustained or hemodynamically significant VT, one of which was induced with 600 doubles, the others with triple extra-stimuli. 22 of 26 subjects received a device implant, with 18 receiving pacemakers (PPM) and 4 intracardiac defibrillators (ICD). All four of the patients with positive v-stims underwent ICD implant. After a mean of 5.7 years of follow up, 7 patients with pacemakers had sustained VT, 6 of whom had negative v-stims. Of the 4 patients with positive v-stims, only 1 developed sustained VT in follow-up. In this single center, observational study, v-stim in patients with myotonic dystrophy was not useful in predicting the subsequent development of clinical VAs as a vast majority of MD patients who developed VAs had negative v-stims. Given the changing ventricular substrate in patients with MD, implantation of a dual chamber ICD should be considered without performing an EP study with ventricular stimulation.

Short RP tachycardia with Concentric atrial activation: What is the mechanism?

A 50-year old man with a structurally normal heart presented with recurrent palpitations for six months. This was in spite of a recent radiofrequency ablation at another center for a presumed diagnosis of atrio-ventricular nodal reentrant tachycardia (AVNRT). Interestingly, his first radiofrequency ablation for a tachyarrhythmia was over a decade ago, but records were unavailable. The 12 lead Electrocardiogram (ECG) revealed a short RP tachycardia at rate of 170 bpm. There was no preexcitation during sinus rhythm. Baseline intervals were normal during the ensuing electrophysiology study (EPS). The catheter positions with the annotations His (His bundle), CS (coronary sinus; proximal bipole 9-10 at CS ostium and distal bipole 1-2) and RV (right ventricle apex) are self-explanatory. A regular narrow complex tachycardia with rate related right bundle branch block (CL 280-340 ms, shortest VA 90 ms, and AH 165 ms) was reproducibly induced with a single atrial extra stimulus test (AEST) (Figure 1a). The response to maneuvers performed during tachycardia are denoted: i.e. right ventricular overdrive pacing (VOP) (Figure 1b), His refractory ventricular extra stimulus (HRVES) from the RV (Figure 1c), as well the left ventricular (LV) apex via the radiofrequency ablation catheter (RF 1-2, Figure 1d). What can be deciphered as the mechanism of this tachycardia? This article is protected by copyright. All rights reserved.

Repetitive multiform narrow complex tachycardia

A 73-year-old man presented to the emergency department with palpitations. After experiencing transient exertional palpitations and dyspnea a few months earlier, investigation revealed moderate left ventricular dysfunction and extensive coronary artery disease with evidence of prior inferior infarction. He underwent bypass grafting and remained symptom free with normalization of his ejection fraction until the current presentation. Figure 1 demonstrates his presenting rhythm that did not respond to adenosine but terminated with intravenous diltiazem. What is the most likely mechanism of the tachycardia? Figure 1 shows a regular narrow complex tachycardia with 3 distinct alternating QRS morphologies: (1) right bundle branch block (RBBB), V1 R 120 ms, V4 precordial transition, left superior axis; (2) RBBB, V1 rsRʹ 100 ms, positive precordial concordance, left superior axis; and (3) RBBB, V1 R 100 ms, positive precordial concordance, left superior axis. The RBBB and left superior axis of all 3 morphologies suggest that the ventricles are activated via the left posterior fascicle, or at the very least, there is early engagement of this fascicle. While supraventricular tachycardia with aberrant conduction is theoretically possible, varying ventricular morphologies in this fashion, lack of termination with adenosine, and the relatively narrow QRS duration (<130 ms) would make this less likely. Together with the response to diltiazem, the overall evidence suggests ventricular tachycardia involving the left posterior fascicle. The classic form of idiopathic fascicular ventricular tachycardia involves the left posterior fascicle, in which there is slow antegrade conduction along abnormal Purkinje fibers in the mid-septum (resulting in P1 potentials) and conduction over the left posterior fascicle (resulting in P2 potentials).1Nogami A. Naito S. Tada H. et al.Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia.J Am Coll Cardiol. 2000; 36: 811-823Crossref PubMed Scopus (218) Google Scholar In any individual patient, variable relationships of the abnormal Purkinje fiber to the left posterior fascicle can result in a more basal or apical site of breakout to the left ventricle; these differences can often be suggested on the surface electrocardiogram by the width of the QRS complex and the precordial transition.2Liu Q. Shehata M. Jiang R. et al.Macroreentrant loop in ventricular tachycardia from the left posterior fascicle: new implications for mapping and ablation.Circ Arrhythm Electrophysiol. 2016; 9e004272Crossref Scopus (7) Google Scholar,3Ma W. Lu F. Shehata M. et al.Catheter ablation of idiopathic left posterior fascicular ventricular tachycardia: predicting the site of origin via mapping and electrocardiography.Circ Arrhythm Electrophysiol. 2017; 10e005240Crossref PubMed Scopus (1) Google Scholar Sung et al4Sung R.K. Kim A.M. Tseng Z.H. et al.Diagnosis and ablation of multiform fascicular tachycardia.J Cardiovasc Electrophysiol. 2013; 24: 297-304Crossref PubMed Scopus (29) Google Scholar described multiform fascicular QRS complexes due to alternate conduction over the left anterior fascicle and the left posterior fascicle from the septal fascicle, but the QRS forms described in the present report are different. Idiopathic fascicular ventricular tachycardia typically occurs in patients with structurally normal hearts, which was not the case in the present report. However, abnormal Purkinje fibers have also been implicated in a minority of patients with ischemic ventricular tachycardia and extension of inferoposterior scar to the left posterior fascicle.5Bogun F. Good E. Reich S. et al.Role of Purkinje fibers in post-infarction ventricular tachycardia.J Am Coll Cardiol. 2006; 48: 2500-2507Crossref PubMed Scopus (121) Google Scholar In this case, it was hypothesized that different QRS morphologies were due to varying sites of left ventricular breakout (Figure 2). The patient underwent electrophysiology study, where multiple episodes of ventricular tachycardia were able to be induced with ventricular extrastimuli similar to those seen on presentation. Ablation of the left posterior fascicle was undertaken, with subsequent noninducibility and no further episodes after 12 months of follow-up.

The Value of Programmed Ventricular Extrastimuli From the Right Ventricular Basal Septum During Supraventricular Tachycardia

BackgroundThe difference between the right ventricular (RV) apical stimulus–atrial electrogram (SA) interval during resetting of supraventricular tachycardia (SVT) versus the ventriculoatrial (VA) interval during SVT (ΔSA-VAapex) is an established technique for discerning SVT mechanisms but is limited by a significant diagnostic overlap. ObjectivesThis study hypothesized that the difference between the RV SA interval during resetting of SVTs versus the VA interval during SVTs (ΔSA-VA) would yield a more robust differentiation of atrioventricular nodal re-entrant tachycardia (AVNRT) from atrioventricular reciprocating tachycardia (AVRT) when using the RV basal septal stimulation (ΔSA-VAbase) as compared to the RV apical stimulation (ΔSA-VAapex). Moreover, it was predicted that the ΔSA-VAbase might distinguish septal from free wall accessory pathways (APs) effectively. MethodsIn this prospective study, 105 patients with AVNRTs (age 48 ± 20 years, 44% male) and 130 with AVRTs (age 26 ± 18 years, 54% male) underwent programmed ventricular extrastimuli delivered from both the RV basal septum and RV apex. The ΔSA-VA values were compared between the 2 sites. ResultsThe ΔSA-VAbase was shorter than the ΔSA-VAapex during AVRT (44 ± 30 ms vs 58 ± 29 ms; P < 0.001), and the opposite occurred during AVNRT (133 ± 31 ms vs 125 ± 25 ms; P = 0.03). A ΔSA-VAbase of ≧85 milliseconds had a sensitivity of 97% and specificity of 96% for identifying AVNRT. Furthermore, a ΔSA-VAbase of 45-85 milliseconds identified AVRT with left free wall APs (sensitivity 86%, specificity 95%), 20-45 milliseconds for posterior septal APs (sensitivity 72%, specificity 96%), and <20 milliseconds for right free wall or anterior/mid septal APs (sensitivity 86%, specificity 98%). ConclusionsThe ΔSA-VAbase during programmed ventricular extrastimuli produced a robust differentiation between AVNRT and AVRT regardless of the AP location with ≧85 milliseconds as an excellent cutoff point. This straightforward technique further allowed localizing 4 general AP sites.

Electrophysiological characteristics and catheter ablation of atypical fast-slow atrioventricular nodal reentrant tachycardia using an inferolateral left atrial slow pathway

Abstract Background Understandings of subtypes of atypical atrioventricular nodal reentrant tachycardia (AVNRT) using variants of slow pathway (SP) are still growing. Inferolateral (inf-lat-) left atrial (LA) SP is a rare variant extending into an inf-lat-LA along the mitral annulus (MA). Purpose To characterize an unknown subtype of atypical fast-slow (F/S-) AVNRT using an inf-lat-LA-SP as a retrograde limb (inf-lat-LA-F/S-AVNRT). Methods This Japanese multicenter retrospective study enrolled 4 patients of inf-lat-LA-F/S-AVNRT that was characterized by the earliest site of atrial activation during tachycardia (EAA) between 3 and 6 o'clock along the MA. The diagnosis was made by an exclusion of AV reentrant tachycardia (AVRT) and atrial tachycardia (AT) according to the standard criteria and was confirmed by successful elimination of tachycardia and the inf-lat-LA-SP. Results Surface ECG during tachycardia revealed long RP appearance except one who had short RP due to a short conduction time across the inf-lat-LA-SP. During tachycardia, far-field LA activation preceding near-field activation of coronary sinus (CS) musculature was visible in the CS recording in 2. Retrograde conduction via the inf-lat-LA-SP with a decremental delay was consistently reproducible with ventricular stimulation in 2, 1 of whom had double atrial response, while it was always masked by the presence of a retrograde conduction via the fast pathway in 1 and a retrograde block at the lower common pathway in 1. An injection of a small dose of ATP transiently interrupted a retrograde conduction over the inf-lat-LA-SP, suggesting its ATP-sensitivity. Exclusion of AVRT was made by no resetting of tachycardia with left ventricular extrastimulus in 2 and VA dissociation during overdrive pacing of tachycardia in remaining 2. Exclusion of AT was made by V-A-V response after ventricular entrainment in 1 and termination without atrial capture by ventricular pacing in 2. Ablation of the right-sided SP was unsuccessful to eliminate the tachycardia, but ablation at or near the EAA by transseptal approach was successful to cure the tachycardia, associated with an elimination of a retrograde conduction over the inf-lat-LA-SP following a development of an accelerated junction rhythm in all. Low-frequency potentials preceding local atrial activation, consistent with a retrograde activation via the inf-lat-LA-SP were detected along the MA medial to the EAA in 1. Conclusions Differential diagnosis of tachycardia with the EAA in the inf-lat-LA and especially long RP appearance should include inf-lat-LA-F/S-AVNRT. Presumed arrhythmogenic substrate of the inf-lat-LA-SP seemed to be consistent with the remnant of embryogenic AV ring tissue in the electropharmacological and locational characteristics. Successful elimination of this AVNRT can be obtained by ablation of the inf-lat-LA-SP, but not of the right-sided SP. Funding Acknowledgement Type of funding sources: None.

A narrow QRS complex tachycardia: What is the mechanism?

A 45-year-old man complained of recurrent episodes of palpitations. Twelve-lead electrocardiograms revealed a long RP and regular narrow QRS complex tachycardia. The baseline atrio-His and His-ventricular intervals were 130 and 55 ms, respectively. A narrow QRS complex tachycardia with a cycle length of 407 ms was reproducibly induced by a single atrial or ventricular extrastimulus. During the tachycardia, the atrial activation sequence with earliest activation in the proximal coronary sinus was identical to the retrograde atrial activation sequence during right ventricular pacing.