Atrioventricular Node Research Articles

Comparative utility of omnipolar and bipolar electroanatomic mapping methods to detect and localize dual nodal substrate in patients with atrioventricular nodal reentrant tachycardia.

Catheter-based slow pathway modification (SPM) for atrioventricular nodal reentrant tachycardia (AVNRT) is traditionally performed at empiric sites using anatomical landmarks and test ablation feedback within the triangle of Koch (TK). While studies have described more tailored techniques such as bipolar low voltage bridge (LVB) and wavefront collision identification, few have systematically compared the diagnostic yields of each and none have investigated whether omnipolar mapping technology provides incremental benefit. The objective of this study was to compare the utility of omnipolar andbipolar-derived qualitative and quantitative measurements in identifying and localizing dual AVN substrate in patients with versus without AVNRT. A retrospective case-control study of consecutive patients with paroxysmal supraventricular tachycardia undergoing electrophysiology study with both omnipolar and bipolar mapping from 2022-2023. Thirteen AVNRT cases (median age 16.1 years, 512 TK points) were compared to nine non-AVNRT controls (median age 15.7 years, 332 TK points). Among qualitative variables, an omnipolar activation vector pivot, defined as a ≥45 degree change in activation direction within the TK, had the highest positive (81%) and negative predictive values (100%) for identifying AVNRT cases and had a median distance of 1 mm from SPM sites. Among quantitative variables, the optimal discriminatory performance for successful SPM sites was observed using bipolar voltage restricted to a peak frequency >340 Hz (c statistic 0.75). Omnipolar vector pivot analysis represents an automated, annotation-independent qualitative technique that is sensitive and specific for AVNRT substrate and co-localizes with successful SPM sites. Bipolar voltage quantitatively describes SP anisotropy better than omnipolar voltage, and the addition of peak frequency signal analysis further optimizes the selection of SPM sites.

Editorial to predictors of the need for atrioventricular nodal ablation following redo ablation for atrial fibrillation

Editorial to predictors of the need for atrioventricular nodal ablation following redo ablation for atrial fibrillation

A surgical resection case of myxoma arising from the posterior wall of the left atrium complicated with complete atrioventricular block

An 80-year-old female was referred to our institution due to transient right upper limb weakness. Transthoracic and transesophageal echocardiography revealed a tumor in the left atrium. The tumor was attached to the posterior wall of the left atrium near the atrioventricular node. Intraoperative pathological examination revealed that the tumor was a myxoma, and complete resection was successfully performed. However, she experienced persistent complete atrioventricular block postoperatively and required pacemaker implantation.

Targeting confluent areas of slow conduction and electrogram fragmentation for atrioventricular node re-entrant tachycardia ablation.

Targeting confluent areas of slow conduction and electrogram fragmentation for atrioventricular node re-entrant tachycardia ablation.

Severe Hyperkalemia: Electrocardiographic Tips for Early Recognition Based on a Case Report

Background: Rapid correction of severe hyperkalemia is mandatory to survival due to its induction of fatal cardiac arrhythmias. The electrocardiogram serves as the diagnostic tool that can provide insight into such fatal arrhythmias. We present two relevant alterations seen in an 84-year-old female patient with previous anterior myocardial infarction, angioplasty of the circumflex coronary artery, left ventricular ejection fraction of 35%, hypertension, dyslipidemia, paroxysmal atrial fibrillation, and diabetes. The Case: The patient had 4-days with asthenia, adynamia and dyspnea. Lung auscultation showed bilateral base rales with cardiomegaly and interstitial edema identified on chest x-ray. Lab work revealed severe metabolic acidosis, increased plasma urea, creatinine, and severe hyperkalemia (7.9 mEq/liter) considered secondary to acute renal failure. Treatment was initiated with 0.9% sodium chloride, bicarbonate, ASA diuretics and polarizing solution (insulin), resulting in a reduction of hyperkalemia to 6.1 mEq/liter. The patient suffered a cardiorespiratory arrest with recovery and needed intubation and dopamine for hemodynamic support but died 15 hours after admission. Conclusion: The electrocardiographic findings characteristic of severe hyperkalemia were: (i) regular rhythm (cycle length 920-950 ms) without discernible P-waves, which may have a junctional or ventricular origin and less probably could be a manifestation of sinoventricular conduction (preferential conduction from the sinus node to the AV node through specialized tracts without activation of the atrial cardiomyocytes), and (ii) sine wave morphology (markedly wide QRS, absence of ST-segment and broadly based T-waves). These electrocardiographic features, typical of hyperkalemia exceeding 7.0 mEq/liter, are harbingers of malignant arrhythmias and should prompt immediate therapy.

Impact of pulmonary vein isolation on the prognosis of patients with atrial fibrillation and heart failure with reduced ejection fraction: an updated systematic review and meta-analysis

Aim. The study aimed to conduct a systematic review and meta-analysis of randomized clinical trials (RCTs) to determine the effect of pulmonary vein isolation (PVI) on the prognosis of patients with atrial fibrillation (AF) and chronic heart failure with reduced ejection fraction (HFrEF).Material and methods. We searched PubMed (MEDLINE), Google Scholar, and the Cochrane Library databases for studies that compared PVI with a conservative rhythm/heart rate (HR) control strategy in patients with AF and HFrEF. The primary endpoint in the major RCTs examining the effect of PVI on the prognosis of patients with HFrEF was a composite endpoint of all-cause mortality or HF-related hospitalization. Hazard ratios (HRs) based on Cox regression analysis were used as the baseline survival rates for the meta-analysis. To determine the weighted mean differences in improvement in left ventricular ejection fraction (LVEF) in the PVI and non-PVI groups, a pooled analysis of the mean LVEF changes with standard deviations taking into account the number of subjects in the compared groups was performed.Results. For this systematic review, 11 studies were selected from 2216 publications, which included 2379 patients. Three RCTs (n=968) were subjected to meta-analysis on time-to-event outcomes. The average follow-up period was 34 months. According to the meta-analysis, PVI was associated with a significant reduction in the risk of composite endpoint (HR: 0,53; 95% confidence interval (CI): 0,33-0,85; p=0,009). In addition, PVI compared with drug rhythm/rate control was associated with a significant reduction in the all-cause mortality risk (HR: 0,55; 95% CI: 0,34-0,89; p=0,01). Finally, a meta-analysis of 10 RCTs (n=1516) found a significant improvement in LVEF compared with drug rhythm/HR control or atrioventricular node ablation with biventricular pacing. The weighted mean difference in the LVEF change over time after 6-12-month follow-up was 5,25% (95% CI: 4,03-6,47; p<0,001).Conclusion. PVI in patients with AF and HFrEF compared with drug rhythm/HR control is associated with a significant reduction in the risk of all-cause mortality and HF-related hospitalization and a greater improvement in LVEF compared with baseline.

A jump in the atrioventricular conduction curve is not caused by a switch from fast pathway to slow pathway conduction.

Background: A jump in the atrioventricular (AV) conduction curve is the current clinical criterion of dual-pathway electrophysiology. However, the assumption that a jump indicates a switch from fast pathway (FP) to slow pathway (SP) conduction remains unconfirmed. This study was carried out to investigate whether a jump indeed indicates a transition from FP to SP conduction, and if not, what the potential cause is. Methods: Eighty-one experimental records from rabbit AV nodal preparations containing the following data were analyzed: 1) had at least one AV conduction curve and 2) had recording of His electrogram alternans (a validated new index of dual-pathway conduction). Most cases also had intracellular action potential recordings from the AV nodal fibers. Results: Of the 81 preparations, 11 (13%) showed a jump in the AV conduction curve. The jumps always occurred after the FP to SP transition. The FP-SP transition occurred at prematurity at 196 ± 39ms versus the jump at 114 ± 13ms (p < 0.001). The beat with a jump showed an SP-FP pattern in seven and an SP-SP pattern in four preparations. The jumps were always associated with and most likely caused by the formation of intranodal/nodal-atrial reentry and its subsequent conduction, rather than a switch from FP to SP conduction. Conclusion: Contrary to what has been assumed, a transition from FP to SP conduction does not produce a jump in the AV conduction curve. A jump in the AV conduction curve is most likely caused by the formation of intranodal/nodal-atrial reentry and its subsequent conduction.

Nonpharmacologic rate control of postoperative atrial fibrillation in the canine sterile pericarditis model.

Postoperative atrial fibrillation (POAF) is common following open heart surgery, and is associated with significant morbidity. Medications used for ventricular rate control of POAF may not be effective in controlling rapid ventricular rates during the postoperative period because of increased sympathetic tone. The purpose of this study was to develop nonpharmacologic rate control of POAF by atrioventricular node (AVN) fat pad stimulation using clinically available temporary pacing wires in the canine sterile pericarditis model. We studied 10 sterile pericarditis dogs in the closed-chest state on postoperative days 1-3. The AVN fat pad stimulation (amplitude 2-15 mA; frequency 20 Hz; pulse width 0.03-0.2 ms) was performed during sustained POAF (>5 min). We measured ventricular rate and inefficient ventricular contractions during sustained POAF and compared it with and without AVN fat pad stimulation. Also, the parameters of AVN fat pad stimulation to achieve a rate control of POAF were measured over the postoperative days. Eleven episodes of sustained POAF were induced in 5/10 sterile pericarditis dogs in the closed-chest state on postoperative days 1-2. During POAF, the AVN fat pad stimulation decreased the ventricular rate from 178 ± 52 bpm to 100 ± 8 bpm in nine episodes. Nonpharmacologic rate control therapy successfully controlled the ventricular rate and eliminated inefficient ventricular contractions during POAF for the duration of the AVN fat pad stimulation. The AVN fat pad stimulation output remained relatively stable over the postoperative days. During sustained POAF, nonpharmacologic rate control by AVN fat pad stimulation effectively and safely controlled rapid ventricular rates throughout the postoperative period.

Upper common pathway analysis using late atrial premature depolarization in atrioventricular nodal reentry tachycardia

BackgroundAnatomic and electrophysiologic findings suggest that the actual circuit of atrioventricular nodal reentrant tachycardia (AVNRT) involves the perinodal atrium. However, occasional instances in which the atrium is dissociated from the AVNRT have led to the concept of an upper common pathway (UCP). ObjectiveWe aimed to assess the prevalence of UCP in AVNRT using a late atrial premature depolarization (LAPD) maneuver. MethodsPatients who were diagnosed with typical AVNRT by electrophysiologic studies were enrolled. For evaluation of the presence of UCP, an LAPD was given at the coronary sinus ostium (osCS) during AVNRT, and then pacing was repeated incrementally every 10 ms. Electrograms in the earliest retrograde atrial activation site (ERAS) near the proximal His were mapped and recorded during the pacing. Results were interpreted as follows: absence of UCP—an LAPD from the osCS can reset the tachycardia without depolarizing the ERAS; presence of UCP—an LAPD from the osCS can depolarize the ERAS without resetting the tachycardia; and indeterminate—an LAPD from the osCS either resets the ERAS and tachycardia simultaneously or does not reset both. ResultsThe LAPD maneuver was performed in 126 patients with AVNRT. It demonstrated an absence of UCP in 121 (96.0%) patients and the presence of UCP in 3 (2.4%) patients; the result was indeterminate in 2 (1.6%) patients. ConclusionThe LAPD maneuver revealed that the presence of UCP is indicated in only rare cases of AVNRT. In most AVNRT cases, the atrium is involved in the reentry circuit.

Cryoballoon cardioneuroablation: New electrophysiological insights

BackgroundCardioneuroablation(CNA) targeting ganglionated plexi has shown promise in treating vasovagal syncope. Only radiofrequency ablation has been used to achieve this goal thus far. ObjectiveWe investigated the utility of cryo-balloon ablation(CBA) of the pulmonary veins as a potential simplified approach to CNA. MethodsWe are reporting our observations of autonomic modulation in a series of 17 patients undergoing CBA for atrial fibrillation and our early experience using CBA of the PVs in 3 patients with malignant vagal syncope. ResultsIn 17 patients undergoing CBA of AF, sinus cycle length was recorded intra-procedurally after ablation of individual PVs. We demonstrated most pronounced shortening of the sinus cycle length after isolation of the right upper PV which was ablated last. There was reduced SNRT and AV nodal ERP after CBA. The elevation in resting heart rate by 6-7 beats/minute following CBA persisted during a follow-up of 12 months. We performed CBA of the PVs in 3 patients with recurrent vagal syncope mediated by sinus arrest (n=2) and AV block (n=1). In all patients, isolation of the right upper PV resulted in marked shortening of sinus cycle length. During a follow-up of 178±43 days (134-219 days) CNA resulted in abolition of pauses, bradycardia related symptoms and syncope in all patients. ConclusionCBA of the PVs (most importantly the right upper PV) may be a predictable anatomic CNA approach in patients with refractory vagal syncope due to sinus arrest and/or AV block and may deserve systematic investigation as a tool to perform CNA.

Predictors of the need for atrioventricular nodal ablation following redo ablation for atrial fibrillation

AbstractBackgroundPatients who have recurrent atrial fibrillation (AF) following redo catheter ablation may eventually be managed with a pace‐and‐ablate approach, involving pacemaker implant followed by atrioventricular nodal ablation (AVNA). We sought to determine which factors would predict subsequent AVNA in patients undergoing redo AF ablation.MethodsWe analyzed patients undergoing redo AF ablations between 2013 and 2019 at our institution. Follow‐up was censored on December 31, 2021. Patients with no available follow‐up data were excluded. Time‐to‐event analysis with Cox proportional hazard regression was used to compare those who underwent AVNA to those who did not.ResultsA total of 467 patients were included, of whom 39 (8.4%) underwent AVNA. After multivariable adjustment, female sex (aHR 4.68 [95% CI 2.30–9.50]; p &lt; 0.001), ischemic heart disease (aHR 2.99 [95% CI 1.25–7.16]; p = 0.014), presence of a preexisting pacemaker (aHR 3.25 [95% CI 1.10–9.60]; p = 0.033), and persistent AF (aHR 2.22 [95% CI 1.07–4.59]; p = 0.032) were associated with increased risk of subsequent AVNA requirement.ConclusionFemale sex, ischemic heart disease, and persistent AF may be useful clinical predictors of the requirement for subsequent AVNA and may be considered as part of shared clinical decision making.

Editorial to irrigated contact‐force sensing catheter may be beneficial for redo ablation of slow–fast atrioventricular nodal reentrant tachycardia in pediatric and adolescent patients

Editorial to irrigated contact‐force sensing catheter may be beneficial for redo ablation of slow–fast atrioventricular nodal reentrant tachycardia in pediatric and adolescent patients

The Upper Common Pathway in Atrioventricular Nodal Reentrant Tachycardia: A Comprehensive Review of Evidence and Current Perspectives.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia, and its diagnostic and therapeutic approaches have been well-established. Traditionally, AVNRT is understood to be an intranodal reentry having two bystander pathways; the upper common pathway (UCP) which connects to the atrium and the lower common pathway which connects to the ventricle. However, the existence of the UCP remains a subject of ongoing debate. The assertion of the UCP's presence is supported by electrophysiological evidence suggesting that the atrium is not essential for the perpetuation of AVNRT. Nonetheless, numerous anatomical studies have failed to identify any structure that could be conclusively designated as the UCP. The histological and electrophysiological characteristics of the slow and fast pathways, which are the core components of AVNRT, suggest the inclusion of atrial myocardium in the reentry circuit. While clear interpretation of these discrepancies remains elusive, potential explanations may be derived from existing evidence and recent research findings concerning the actual AVNRT circuit.

Modern physiological approach to inappropriate ICD shocks due to atrial fibrillation with very fast ventricular response. A case report

BackgroundFast-conducting atrial fibrillation misinterpreted as ventricular tachycardia is the leading cause for inappropriate shocks in patients with implantable cardiac defibrillators (ICD). These inappropriate shocks are associated with significant morbidity and mortality and cause great discomfort and stress.Case presentationWe report the case of a patient with ischemic cardiomyopathy, permanent atrial fibrillation, and a single-chamber DF-1 ICD implanted for the primary prevention of sudden cardiac death, who presented for multiple inappropriate internal shocks due to very fast-conducting atrial fibrillation, which was mislabeled as ventricular fibrillation by the ICD. Since the patient was under maximal atrioventricular nodal blocking medical therapy (beta-blockers and digitalis) and we didn`t find any reversible causes for the heart rate acceleration, we opted for rate control with atrioventricular node ablation. To counteract the risk of pacing-induced cardiomyopathy in this patient who would become totally pacemaker-dependent, we successfully performed left bundle branch area pacing. Because the patient`s ICD had a DF-1 connection and the battery had a long life remaining, we connected the physiological pacing lead to the IS-1 sense-pace port of the ICD. The 6-month follow-up showed an improvement in left ventricular function with no more inappropriate shocks.ConclusionsLeft bundle branch area pacing and atrioventricular node ablation in patients with an implantable single-chamber DF-1 defibrillator and fast-conducting permanent atrial fibrillation is a cost-efficient and very effective method to prevent and treat inappropriate shocks, avoiding the use of an additional dual-chamber or CRT-D device.

Voltage and propagation mapping: New tools to improve successful ablation of atrioventricular nodal reentry tachycardia.

Mapping system is useful in ablation of atrioventricular nodal reentry tachycardia (AVNRT) and localization of anatomic variances. Voltage mapping identifies a low voltage area in the Koch trianglecalled low-voltage-bridge (LVB); propagation mapping identifies the collision point (CP) of atrial wavefront convergence. We conducted a prospective study to evaluate the relationship between LVB and CP with successful site of ablation and identify standard value for LVB. Three-dimensional (3D) maps of the right atria were constructed from intracardiac recordings using the ablation catheter. Cut-off values on voltage map were adjusted until LVB was observed. On propagation map, atrial wavefronts during sinus rhythm collide in the site representing CP, indicating the area of slow pathway conduction. Ablation site was selected targeting LVB and CP site, confirmed by anatomic position on fluoroscopy and atrioventricular ratio. Twenty-seven consecutive patients were included. LVB and CP were present in all patients. Postprocedural evaluation identified standard cut-off of 0.3-1 mV useful for LVB identification. An overlap between LVB and CP was observed in 23 (85%) patients. Procedure success was achieved in all patient with effective site at first application in 22 (81%) patients. There was a significant correlation between LVB, CP, and the site of effective ablation (p = .001). We found correlation between LVB and CP with the site of effective ablation, identifying a voltage range useful for standardized LVB identification. These techniques could be useful to identify ablation site and minimize radiation exposure.

HE EFFECT OF PROBENECID ON α-1-ADRENOCEPTOR STIMULATION INDUCED PROARRHYTHMIC CONDUCTION IN THE ATRIOVENTRICULAR NODE OF RAT HEART

Cardiac tissue contains adrenergic receptors (AR) not only of the beta type, but also of the alpha type (α-AR). Both types of ARs play signifi cant role in regulation of cardiomyocytes electrophysiology in diff erent parts of the heart, including the atrioventricular node (AVN). An augmentation of α1-AR mediated component of adrenergic signaling results in impaired conduction of excitation in the heart and onset of various rhythm disturbances including AVNassociated arrhythmias. The activation of α1-AR facilitates anionic transmembrane transport causing electrophysiological changes in myocytes. Current study is aimed to the investigation of the eff ects of anion/chloride blockade on α1-AR-mediated proarrhythmic alteration of AVN functioning. Functional characteristics of AVN including AVN conduction time, AVN refractoriness and the AVN conduction alterations were examined via recording of surface electrograms in Langendorff -perfused isolated rat heart (Wistar, 250 ± 30 g). Phenylephrine was used as α1-AR agonist. Probenecid demonstrating anion/chloride transmembrane conductance blocking activity was used to modify Phe-induced α1-AR-mediated eff ects in AVN. The activation of α1-AR by Phe results in a signifi cant increase in the duration of AV intervals (N = 10, p &lt; 0.001) and eff ective refractory period (ERP) in the AVN (by 9.8% ± 1.2%, n = 10, p &lt; 0.001). Also, Phe induces AV-blocks of conduction and oscillations in atrioventricular delay (N = 10) at the stimulation rates close to ERP. Probenecid signifi cantly reduces the magnitude of AVD oscillations during non-stationary conduction in the AV node. In addition, probenecid attenuates ERP prolongation caused by Phe (107 ± 4 ms, N = 6) and 114.2 ± 5.35 ms (N = 10) in presence of only Phe and Phe with probenecid, respectively, returning its values toward typical for normal conditions. In conclusion, probenecid maintains physiological mode of AVN conduction when α1-AR are stimulated. This also suggests that chloride ion channels and anion carriers may contribute to the α1-AR-mediated AVN arrhythmias.

3D models of the cardiac conduction system in healthy neonatal human hearts

Iatrogenic damage to the cardiac conduction system (CCS) remains a significant risk during congenital heart surgery. Current surgical best practice involves using superficial anatomical landmarks to locate and avoid damaging the CCS. Prior work indicates inherent variability in the anatomy of the CCS and supporting tissues. This study introduces high-resolution, 3D models of the CCS in normal pediatric human hearts to evaluate variability in the nodes and surrounding structures. Human pediatric hearts were obtained with an average donor age of 2.7 days. A pipeline was developed to excise, section, stain, and image atrioventricular (AVN) and sinus nodal (SN) tissue regions. A convolutional neural network was trained to enable precise multi-class segmentation of whole-slide images, which were subsequently used to generate high- resolution 3D tissue models. Nodal tissue region models were created. All models (10 AVN, 8 SN) contain tissue composition of neural tissue, vasculature, and nodal tissues at micrometer resolution. We describe novel nodal anatomical variations. We found that the depth of the His bundle in females was on average 304 μm shallower than those of male patients. These models provide surgeons with insight into the heterogeneity of the nodal regions and the intricate relationships between the CCS and surrounding structures.

The optimal slow pathway ablation site in atrioventricular nodal reentrant tachycardia cases with an inferiorly located His bundle.

The optimal slow pathway (SP) ablation site in cases with an inferiorly located His bundle (HIS) remains unclear. In 45 patients with atrioventricular nodal reentrant tachycardia, the relationship between the HIS location and successful SP ablation site was assessed in electroanatomical maps. We assessed the location of the SP ablation site relative to the bottom of the coronary sinus ostium in the superior-to-inferior (SPSI), anterior-to-posterior (SPAP), and right-to-left (SPRL) directions. The HIS location was assessed in the same manner. The HIS location in the superior-to-inferior direction (HISSI), SPSI, SPAP, and SPRL were 17.7±6.4, 1.7±6.4, 13.6±12.3, and -1.0±13.0mm, respectively. The HISSI was positively correlated with SPSI (R2=0.62; P<.01) and SPAP (R2=0.22; P<.01), whereas it was not correlated with SPRL (R2=0.01; P=.65). The distance between the HIS and SP ablation site was 17.7±6.4mm and was not affected by the location of HIS. The ratio of the amplitudes of atrial and ventricular potential recorded at the SP ablation site did not differ between the high HIS group (HISSI≥13mm) and low HIS group (HISSI<13mm) (0.10±0.06vs. 0.10±0.06; P=.38). In cases with an inferiorly located HIS, SP ablation should be performed at a lower and more posterior site than in typical cases.

Novel near-field detection algorithm–guided slow pathway ablation in atrioventricular nodal reentrant tachycardia

Novel near-field detection algorithm–guided slow pathway ablation in atrioventricular nodal reentrant tachycardia

Reduced kinase function in two ultra-rare TNNI3K variants in families with congenital junctional ectopic tachycardia.

Genetic missense variants in TNNI3K, encoding troponin-I interacting kinase, have been associated with dilated cardiomyopathy (DCM) and observed in families with supraventricular tachycardias (SVT). Previously, a family harboring the TNNI3K-c.1615A > G (p.Thr539Ala) variant presented with congenital junctional ectopic tachycardia (CJET), an arrhythmia that arises from the atrioventricular (AV) node and His bundle. However, this was a relatively small four-generational family with limited genetic testing (N = 3). We here describe a multigenerational family with CJET harboring a novel ultra-rare TNNI3K variant: TNNI3K-c.1729C > T (p.Leu577Phe). Of all 18 variant carriers, 13 individuals presented with CJET, resulting in a genetic penetrance of 72%. In addition, CJET is reported in another small family harboring TNNI3K-c.2225C > T (p.Pro742Leu). Similar to the previously published CJET family, both TNNI3K variants demonstrate a substantial reduction of kinase activity. Our study contributes novel evidence supporting the involvement of TNNI3K genetic variants as significant contributors to CJET, shedding light on potential mechanisms underlying this cardiac arrhythmia.