Nodal Conduction Research Articles

Differential right apical and left basal pacing: a new maneuver that rules out the presence of a left accessory pathway with retrograde conduction

Abstract Background Differential apex-base pacing or entrainment is a very useful maneuver in patients with concealed septal accessory pathways. This study evaluates for the first time the diagnostic value of differential right apical pacing (aRV) and basal left ventricular pacing (bLV) in patients with left accessory pathways before and after ablation. Purpose To determine the value of differential aRV and bLV pacing as a simple maneuver to assess the successful ablation of left accessory pathways. Methods Successive patients with preexcitation or concealed left accessory pathways were prospectively included. Baseline pre-ablation (PRE) 1:1 retrograde conduction was evaluated by the S-A interval during pacing at the aRV (PREaRV) and at the bLV (PREbLV) measured to the earliest atrial electrogram detected by a decapolar catheter placed in the coronary sinus. The S-A interval resulting from direct atrial capture during high outputpacing at the bLV at (PREdir) was also measured. The same S-A intervals, pacing at the same locations and measured to the same dipole in the coronary sinus were reassessed after ablation (POSaRV, POSbLV, POSdir) in order to compare the total values and their differences. Results 47 patients were included (age 31 yo [range 4 – 76 yo], 70% male sex, transeptal approach used in 62%). Ablation of the accessory pathway was successful in all patients. 5 patients could not be analyzed due to absence of 1:1 retrograde conduction before ablation, 27/43 (63%) patients had 1:1 retrograde nodal conduction after ablation. A significant prolongation of the S-A intervals were observed after ablation during pacing at the aRV (POSaRV – PREaRV = 43±38 ms, IC95% 27-59 ms, p<0,001) and from the bLV (POSbVI – PREbVI = 126±53 ms, IC95% 105-147 ms, p<0,001). As expected, the S-A interval during direct atrial capture from the bLV did not prolong (POSdir – PREdir = 2±10 ms, IC95% -2 – 6 ms, p=0,41). The difference PREaRV – PREbLV before ablation (difPRE) was 80±26 ms (IC95% 72-88 ms) and never overlapped with the difference POSaRV – POSbLV after ablation (-6 ±33 ms, IC95% -19 – 8 ms) (difPOS) except in one case of left posteroseptal accessory pathway. The δ value (difPRE – difPOS) was 83±40 ms (IC95% 67-100 ms, p<0,001). A difPOS value <20 ms discriminated all successful ablations of non posteroseptal accesory pathways. Conclusion The S-A values obtained during differential RV apical and LV basal pacing before and after ablation are valid to discriminate the efficacy of the procedure. The POSaVD – POSbVI value is always <20 ms after successful ablation and excludes retrograde conduction over any left non-posteroseptal accesory pathway. This same value is ≤0 ms in 72% of cases of successful ablation.Figure.

ECG-based estimation of respiration-induced autonomic modulation of AV nodal conduction during atrial fibrillation.

Introduction: Information about autonomic nervous system (ANS) activity may offer insights about atrial fibrillation (AF) progression and support personalized AF treatment but is not easily accessible from the ECG. In this study, we propose a new approach for ECG-based assessment of respiratory modulation in atrioventricular (AV) nodal refractory period and conduction delay. Methods: A 1-dimensional convolutional neural network (1D-CNN) was trained to estimate respiratory modulation of AV nodal conduction properties from 1-minute segments of RR series, respiration signals, and atrial fibrillatory rates (AFR) using synthetic data that replicates clinical ECG-derived data. The synthetic data were generated using a network model of the AV node and 4 million unique model parameter sets. The 1D-CNN was then used to analyze respiratory modulation in clinical deep breathing test data of 28 patients in AF, where an ECG-derived respiration signal was extracted using a novel approach based on periodic component analysis. Results: We demonstrated using synthetic data that the 1D-CNN can estimate the respiratory modulation from RR series alone with a Pearson sample correlation of r = 0.805 and that the addition of either respiration signal (r = 0.830), AFR (r = 0.837), or both (r = 0.855) improves the estimation. Discussion: Initial results from analysis of ECG data suggest that our proposed estimate of respiration-induced autonomic modulation, a resp, is reproducible and sufficiently sensitive to monitor changes and detect individual differences. However, further studies are needed to verify the reproducibility, sensitivity, and clinical significance of a resp.

Pharmacokinetics and Pharmacodynamics of Etripamil, an Intranasally Administered, Fast-Acting, Nondihydropyridine Calcium Channel Blocker.

Etripamil, a fast-acting nondihydropyridine L-type calcium channel blocker, is under investigation for potential self-administration for the acute treatment of supraventricular tachyarrhythmias in a medically unsupervised setting. We report detailed pharmacokinetics and pharmacodynamics of intranasally administered etripamil in healthy adults from 2 Phase 1, randomized, double-blind studies: Study MSP-2017-1096 (sequential dose-escalation, crossover study design, n = 64) and NODE-102 (single dose, 4-way crossover study, n = 24). Validated bioanalytical assays determined plasma concentrations of etripamil and its inactive metabolite. Noncompartmental pharmacokinetic parameters were calculated. Pharmacodynamic parameters were determined for PR interval, blood pressure, and heart rate. Etripamil was rapidly absorbed intranasally, with time to maximal plasma concentration of 5-8.5 minutes, corresponding to a rapid greater than 10% increase in mean maximum PR interval from baseline within 4-7 minutes of doses of 60mg or greater. Following peak plasma concentrations, systemic etripamil levels declined rapidly within the first 15 minutes following dosing and decreased more gradually thereafter. PR interval prolongation greater than 10% from baseline was generally sustained for about 45 minutes at doses of 60mg or greater. The mean terminal half-life ranged from about 1.5 hours with 60mg to about 2.5-3 hours for the 70- and 105-mg doses. Etripamil was generally well tolerated without symptomatic hypotension. Adverse events were primarily mild to moderate and related to the administration site; no serious adverse events or episodes of atrioventricular block occurred. Intranasal etripamil administration, at doses of 60mg or greater, produced rapidly occurring slowing of atrioventricular nodal conduction with a limited duration of effect without hemodynamic or electrocardiographic safety signals in healthy volunteers.

Atypical Wenckebach without grouped beating due to dual AV nodal conduction

A 31-year-old woman reported dizziness in the early postpartum period after receiving dexmedetomidine. The ECG was misinterpreted as complete heart block; however, more careful analysis revealed an atypical Wenckebach pattern with dual AV nodal conduction and termination of nonconducted P waves with junctional escape beats. The patient's rhythm returned to sinus after stopping dexmedetomidine.Atypical Wenckebach patterns account for greater than 50% of patients with Mobitz Type I AV block and can be misinterpreted as high-grade AV block. This case highlights the causes of atypical Wenckebach patterns and how careful analysis of intervals can help clinicians avoid misdiagnosis.

Pacing in Pediatric Patients with Postoperative Atrioventricular Block.

Surgery for congenital heart disease may compromise atrioventricular (AV) nodal conduction, potentially resulting in postoperative AV block. In the majority of cases, AV nodal function recovers during the early postoperative period and may only require short-term pacing support, typically provided via temporary epicardial wires. Permanent pacing is indicated when the postoperative AV block persists for more than 7 to 10days due to the risk of mortality if a pacemaker is not implanted. Although there is a subset of patients who may have late recovery of AV nodal function, those with continued postoperative AV block will need lifelong pacing therapy.

Abstract 18348: Causes and Predictors of 30-Day Readmissions Following Permanent Pacemaker Implantation in Patients With Cardiac Amyloidosis: From National Readmission Database (2016-2020)

Introduction: Cardiac amyloidosis (CA) is an infiltrative cardiomyopathy where local deposition of amyloid fibrils causes heart failure, arrhythmias, and conduction system abnormalities. Involvement of the AV nodal and infra-hisian conduction system increases the need for a permanent pacemaker (PPM). Studies have noted worse outcomes in patients with implantable-cardioverter defibrillator placement in amyloidosis, but a comparison with PPM is lacking. We sought to analyze readmissions in CA patients following PPM placement utilizing National Readmission Database (NRD). Methods: NRD (2016 to 2020) was queried to identify adults with a diagnosis of CA who underwent PPM implantation using ICD-10 CM and PCS codes. The primary outcome was a 30-day readmission rate. Secondary outcomes were in-hospital mortality, length of stay (LOS), total hospital charge (THC), and predictors of readmission. Multivariate/univariate logistic and linear regression analyses were used to analyze the outcomes and adjust for possible confounders. Results: A total of 1,027 encounters of CA who underwent PPM were identified, of which 975 were discharged alive. Within 30 days from discharge, 141 (14.5%) were readmitted. Those readmitted had a longer LOS and higher burden of comorbidities while were similar in age, sex, hospital characteristics, and household income status. Readmissions lead to an additional mean THC of $55,079 and a mean LOS of 6.3 days. The top five causes of readmissions were heart failure (23%), sepsis (6.6%), hypertensive heart disease (4%), bradycardia (3.5%), and acute kidney injury (3.2%). Figure-1 shows the forest plot of a multivariate analysis of independent factors associated with readmissions. Conclusions: Our findings show that up to 15% of patients with CA who undergo PPM implantation get readmitted with heart failure being the most common etiology. Optimizing comorbidities with PPM implantation in CA may provide better outcomes and reduce admissions.

Novel method to avoid serious injurious effects on the atrioventricular nodal (AVN) conduction during catheter ablation of the AVN slow pathway utilizing cryofreezing energy

BackgroundSlow pathway elimination of the atrioventricular node (AVN) is essential to treat AVN reentrant tachycardia (AVNRT). However, injury to the AVN conduction (IAVN) is one of the serious complications. Cryofreezing energy is expected to reduce the incidence of IAVN. This study aimed to investigate the usefulness of a novel method to avoid IAVN during cryoablation of AVNRT. MethodsA total of 157 patients (average age, 65.8 years; male, 71) suffering from AVNRT were included. Once the AVNRT terminated during cryo-ablation, then rapid atrial constant pacing (RACP) was performed during freezing at a rate lower 10 bpm than that inducing Wenchebach AV block in 74 (47.1 %) patients (Group A). The RACP rate was decreasingly reduced by 10 bpm in case of the occurrence of IAVN. When the RACP reached 100 bpm, the cryoablation was prematurely terminated. Group B patients (83 = 52.9 %) underwent cryoablation during sinus rhythm. All patients were allocated in a randomized fashion. We compared the severity of the IAVN between Groups A and B. ResultsThere were no significant differences at 12 months regarding the freedom from the AVNRT between Groups A and B. However, the duration of the IAVN was significantly longer in Group B than A (p = 0.02). There were no significant differences regarding the distance between the His recording sites and successful ablation sites between Groups A and B. No permanent IAVN requiring pacemaker implantation was provoked in either group. ConclusionRACP was useful to avoid sustained and serious IAVN during cryoablation of AVNRT.

Atrioventricular Conduction: Physiology and Autonomic Influences.

Atrioventricular (AV) nodal conduction is decremental and very prone to alterations in autonomic tone. Conduction through the His-Purkinje system (HPS) is via fast channel tissue and typically not that dependent on autonomic perturbations. Applying these principles, when the sinus rate is stable and then heart block suddenly occurs preceded by even a subtle slowing of heart rate, it typically is caused by increased vagal tone, and block occurs in the AV node. Heart block with activity strongly suggests block in the HPS. Enhanced sympathetic tone and reduced vagal tone can facilitate induction of both AV and atrioventricular node reentry.

The Case Files

The Case Files

Incidence and outcome of arrhythmias and electrical disease in patients with Trisomy 18.

Patients with Trisomy 18 have a high incidence of cardiac anomalies and are associated with early death. Because of early mortality, electrical system disease and arrhythmia has been difficult to delineate and the incidence remain unknown. We sought to describe the association and clinical outcomes of electrical system disease and cardiac tachy-arrhythmias in patients with Trisomy 18. This was a retrospective, single institutional study. All patients with Trisomy 18 were included in the study. Patient characteristics, congenital heart disease (CHD), conduction system and clinical tachy-arrhythmia data were collected on all patients. Outcomes including cardiac surgical interventions, electrical system interventions and death were collected until the time of study. Patients with tachy-arrhythmias/electrical system involvement were compared to those without to identify potential associated variables. A total of 54 patients with Trisomy 18 were included in analysis. The majority of patients was female and had associated CHD. AV nodal conduction system abnormalities with either first or second degree AV block were common (15%) as was QTc prolongation (37%). Tachy-arrhythmias were common with 22% of patients having at least one form of tachy-arrhythmia and associated with concomitant conduction system disease (p = 0.002). Tachy-arrhythmias were typically treatable with monitoring or medication with eventual resolution without need for procedural intervention. Although early death was common, there were no causes of death associated with tachy-arrhythmia or conduction system disease. In conclusion, patients with Trisomy 18 have a high incidence of conduction system abnormalities and burden of clinical tachy-arrhythmias. Although frequent, electrical system disease did not affect patient outcome or difficultly of care delivery.

FDG-PET/CT and rest myocardial perfusion imaging to predict high-degree atrioventricular block recovery in cardiac sarcoidosis.

High-degree atrioventricular block (AVB) recovery in CS has been shown to be highly variable despite immunosuppressive treatment, with no reliable tool available to predict odds of reversibility. This study sought to evaluate the potential of combined fluorodeoxyglucose (FDG) positron emission tomography (PET)/computed tomography (CT) and resting myocardial perfusion imaging (rMPI) to predict reversibility of newly diagnosed high-grade AVB in cardiac sarcoidosis (CS). We performed a single-center, retrospective analysis of patients with CS presenting with high-grade AVB who underwent combined FDG-PET/CT and rMPI. The 2016 JCS and the 2014 HRS diagnostic criteria were used for the diagnosis of CS. Patients with a history of coronary artery disease or prior immunosuppressive treatment were excluded. Patients were divided into AVB recovery and non-recovery subgroups. CS disease staging was based on FDG-PET and rMPI findings: (Stage 0) normal FDG-PET and rMPI (Stage 1) positive FDG-PET and normal rMPI (Stage 2) positive FDG-PET with perfusion deficits on rMPI (Stage 3) normal FDG-PET with perfusion deficits on rMPI. Twenty-seven patients, including 13 demonstrating AVB recovery, were identified. Eleven out of fourteen (78.6%) patients presenting with stage 1 CS demonstrated AVB recovery. Stage 1 CS was significantly more present in the recovery group compared to the non-recovery group (84.6% vs 21.4%, P = .002). Eleven presented with stage 2 CS, with only 2 (18.2%) recovering AV nodal conduction. Stage 2 CS presented more frequently in the non-recovery group (64.3% vs 15.4%, P = .020). Combined FDG-PET and rMPI employed to stage CS disease presenting with high-degree AVB appears to have good performance for predicting likelihood of recovery.

Pathophysiology and treatment of adults with arrhythmias in the emergency department, part 2: Ventricular and bradyarrhythmias.

In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. This is the second article in a 2-part series reviewing the pathophysiology and treatment considerations for arrhythmia. Part 1 of the series discussed aspects related to treating atrial arrhythmias. Here in part 2, the pathophysiology of ventricular arrhythmias and bradyarrhythmias and current evidence on treatment approaches are reviewed. Ventricular arrhythmias can arise suddenly and are a common cause of sudden cardiac death. Several antiarrhythmics may be effective in management of ventricular arrhythmias, but there is robust evidence to support the use of only a few of these agents, and that evidence was largely derived from trials involving patients with out-of-hospital cardiac arrest. Bradyarrhythmias range from asymptomatic mild prolongation of nodal conduction to severe conduction delays and impending cardiac arrest. Vasopressors, chronotropes, and pacing strategies require careful attention and titration to minimize adverse effects and patient harm. Ventricular arrhythmias and bradyarrhythmias can be consequential and require acute intervention. As experts in pharmacotherapy, acute care pharmacists can participate in providing high-level intervention by aiding in diagnostic workup and medication selection.

PO-01-067 ATRIO-VENTRICULAR DELAY AFTER DELIVERY OF PULSED FIELD ABLATION OF THE PULMONARY VEINS

Pulsed field ablation (PFA) has been introduced as a new ablation modality for PV isolation. While PFA appears to have increased safety through a lack of thermal injury leading to lower risks of collateral damage to bystander anatomical structures, PFA is known to cause sinus bradycardia, hypotension, and atrial fibrillation, probably mediated by high electrical field induced autonomic stimulation. However, the effect on atrioventricular (AV) nodal conduction is unknown. To measure AV delay immediately after PFA. 412 PFA deliveries recorded in 12 patients were analyzed using a novel electrophysiology recording system (ECGenius System, CathVison, Denmark). Each pulmonary vein was treated with a minimum of eight pulses of energy with a 20 electrodes pentaspline catheter. Energy was delivered in two anatomical positions with the catheter able to achieve two delivery shapes. Ten seconds of electrogram information was recoded pre and post every delivery and the PR interval was manually measured, with prolongations of 10 ms or more post ablation considered significant (Figure 1). Recovery of AV conduction was measured from the end of the energy delivery pulse to the first beat conducted with a delay of less than 10 ms from the measured pre-delivery baseline. The study enrolled 12 patients (4 female) with a mean age of 63.3 years (SD = 13.2). In total, 412 lesions were delivered. Two patients presented and were treated in an atrial arrhythmia and three patients had no measurable change in AV conduction. However, seven patients had 49 measurable delays in AV conduction after PFA energy delivery ranging from 10 ms to 214 ms with a mean delay of 36.2 ms (SD = 34.4 ms). Eight measured intervals exceeded 200 ms post delivery. Recovery from AV delay took an average of 5.17 sec (SD = 4.2 sec) with the longest recovery time being 25 sec. Table 1. shows delay and recovery by vein. This report details the observation of the occurrence of AV-delay after the delivery of PFA. The incidence of this phenomenon was 58.3% of patients in the study. Pulsed field ablation appears to have a transient effect on the intrinsic cardiac autonomic nervous system manifested in changes to atrioventricular node response.

Effectiveness of the repurposed drug isotretinoin in an experimental murine model of Chagas disease

Benznidazole and nifurtimox are the drugs currently used for the treatment of Chagas disease, however its side effects may affect patient adherence. In the search for new alternative therapies, we previously identified isotretinoin (ISO), an FDA-approved drug widely used for the treatment of severe acne through a drug repurposing strategy. ISO shows a strong activity against Trypanosoma cruzi parasites in the nanomolar range, and its mechanism of action is through the inhibition of T. cruzi polyamine and amino acid transporters from the Amino Acid/Auxin Permeases (AAAP) family. In this work, a murine model of chronic Chagas disease (C57BL/6 J mice), intraperitoneally infected with T. cruzi Nicaragua isolate (DTU TcI), were treated with different oral administrations of ISO: daily doses of 5 mg/kg/day for 30 days and weekly doses of 10 mg/kg during 13 weeks. The efficacy of the treatments was evaluated by monitoring blood parasitemia by qPCR, anti-T. cruzi antibodies by ELISA, and cardiac abnormalities by electrocardiography. No parasites were detected in blood after any of the ISO treatments. The electrocardiographic study of the untreated chronic mice showed a significant decrease in heart rate, while in the treated mice this negative chronotropic effect was not observed. Atrioventricular nodal conduction time in untreated mice was significantly longer than in treated animals. Mice treated even with ISO 10 mg/kg dose every 7 days, showed a significant reduction in anti-T. cruzi IgG levels. In conclusion, the intermittent administration of ISO 10 mg/kg would improve myocardial compromise during the chronic stage.

Syncope After Transcatheter Aortic Valve Implantation: Pace or Not?

Syncope After Transcatheter Aortic Valve Implantation: Pace or Not?

Right ventricular cardiac resynchronization therapy in patients with right ventricular conduction delay and heart failure

Right ventricular cardiac resynchronization therapy in patients with right ventricular conduction delay and heart failure

Cardiovascular safety pharmacology of ivermectin assessed using the isoflurane-anesthetized beagle dogs: ICH S7B follow-up study.

Antiparasitic ivermectin has been reported to induce cardiovascular adverse events, including orthostatic hypotension, tachycardia and cardiopulmonary arrest, of which the underlying pathophysiology remains unknown. Since its drug repurposing as an antiviral agent is underway at higher doses than those for antiparasitic, we evaluated the cardiovascular safety pharmacology of ivermectin using isoflurane-anesthetized beagle dogs (n=4). Ivermectin in doses of 0.1 followed by 1 mg/kg was intravenously infused over 10 min with an interval of 20 min, attaining peak plasma concentrations of 0.94 ± 0.04 and 8.82 ± 1.25 μg/mL, which were 29-31 and 276-288 times higher than those observed after its antiparasitic oral dose of 12 mg/body, respectively. The latter peak concentration was > 2 times greater than those inhibiting proliferation of dengue virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and hepatitis B virus in vitro. Ivermectin decreased heart rate without altering mean blood pressure, suggesting that ivermectin does not cause hypotension or tachycardia directly. Ivermectin hardly altered atrioventricular nodal or intraventricular conduction, indicating a lack of inhibitory action on Ca2+ or Na+ channel in vivo. Ivermectin prolonged QT interval/QTcV in a dose-related manner and tended to slow the repolarization speed in a reverse frequency-dependent manner, supporting previously described its IKr inhibition, which would explain Tpeak-Tend prolongation and heart-rate reduction in this study. Meanwhile, ivermectin did not significantly prolong J-Tpeakc or terminal repolarization period, indicating torsadogenic potential of ivermectin leading to the onset of cardiopulmonary arrest would be small. Thus, ivermectin has a broad range of cardiovascular safety profiles, which will help facilitate its drug repurposing.

His-bundle pacing and atrioventricular nodal ablation for noncontrolled atrial arrhythmia: A technical challenge with major clinical benefits

His-bundle pacing (HBP) is an appealing alternative to right ventricular pacing in patients referred for permanent ventricular pacing and atrioventricular nodal ablation (AVNA) because it preserves physiological ventricular activation. Only limited data regarding HBP combined with AVNA are available in the literature. The purpose of this study was to provide further evidence on the feasibility and efficacy of this therapeutic approach in patients with uncontrolled atrial arrhythmia. We prospectively included all patients who had undergone AVNA after HBP in 3 different hospitals between 2017 and2022. AVNA following HBP lead implantation was performed in 75 patients. Complete atrioventricular (AV) block was obtained in 58 patients (77%), and significant modulation of AV nodal conduction (heart rate <60 bpm) was obtained in 12 patients (16%). AVNA failure was observed in 5 patients (7%). Recording of an atrial signal by the HBP lead was more frequently observed in patients with AVNA modulation/failure than in patients with complete AV block (11/17 vs 5/58; P <.001). No lead dislodgment occurred during the AVNA procedures. Acute His-bundle (HB) capture threshold increase >1 V occurred in 11 patients (15%), with return to baseline value on day 1 in 9 patients. New York Heart Association functional class and left ventricular ejection fraction significantly improved from baseline to last follow-up (3.0 ± 0.7 vs 1.6 ± 0.5; P <.001; and 47% ± 14% vs 60% ± 9%; P <.0001, respectively). AVNA combined with HBP for noncontrolled atrial arrhythmia was feasible and clinically efficient. Implanting the HB lead on the ventricular aspect of the tricuspid annulus avoiding atrial signal recording can facilitate AVNA.

A clue to the triples from an echo.

A clue to the triples from an echo.

112 A CASE OF INCESSANT SLOW-FAST AVNRT TREATED WITH HIS BUNDLE PACING

Abstract Introduction Slow-fast AVNRT can rarely present as incessant SVT, particularly in patients with increased HV interval. We describe a case of incessant typical AVNRT, treated without transcatheter ablation. Case Presentation An 83-year-old man, with history of PAF, was admitted to our ICU complaining of dyspnea, dizziness and amaurosis. His ECG at presentation depicted sinus bradycardia, first degree AVB (PQ=400 ms) and RBBB (Fig 1A). After betablocker wash-out period, we decided to perform CSP using HBP to ensure AV synchrony and restore physiological pacing. During wash-out period, an incessant regular wide complex tachycardia with RBBB morphology and ventricular rate of 110 bpm occurred: the tracing showed a P wave immediately after the QRS, with RP &amp;lt; PR (Fig 1B). The tachycardia was incessant also in the EP lab. By means of 2 pacing leads (RV lead in the apical septum and RA lead in right appendage) and one diagnostic decapolar catheter (Inquiry, 2-2-2 Abbott) in His region, all connected to the polygraph, we performed an EPS. HV interval in sinus rhythm was 60 ms, AH 340 ms. The electrograms during tachycardia showed HVA sequence and 1:1 VA association, VA&amp;lt; 70 ms, cycle length 520 ms. Pacing from RV lead, we performed the ventricular overdrive pacing maneuver obtaining a VAV response; PPI-TCL was 280 ms and SA-VA difference was 205 ms (Fig 2A). We also noted a VA linking response to atrial overdrive pacing, and AHA response at the end of maneuver excluding JT (Fig 2B). In addition, pacing by the His catheter during tachycardia, we interrupted the arrythmia: the V signal after the last paced beat was not followed by retro-conducted A signal (Fig 2C). Finally, by administrating adenosine 12 mg the tachycardia interrupted with A as last signal recorded (Fig 2D). All these findings were consistent with an incessant typical AVNRT. We chose to treat AVRNT with sequential atrial-His pacing, placing a third lead in His region and programming the device in DDD 70-120, with selective His bundle capture, not correcting the RBBB (Fig 1C, D). Discussion In patients with poor anterograde AV nodal conduction, also slow-fast AVNRT can present as incessant tachycardia. In fact, a shorter sinus cycle length or atrial extrasystole could initiate sufficient delay in anterograde conduction to allow for recovery in conduction in the retrograde direction led to a persistent tachycardia. This case highlights the value of performing EPS diagnostic maneuvers also during PM implantations in order to personalize therapy and programming.