Nodal Conduction Research Articles

B-PO03-009 DUAL AV NODE PATHWAYS MASQUERADING AS SYMPTOMATIC ATRIOVENTRICULAR CONDUCTION DISEASE: THE IMPORTANCE OF TREADMILL STRESS TESTING IN ESTABLISHING SYMPTOM-ARRHYTHMIA CORRELATION

Markedly prolonged AV conduction intervals (PR intervals >300ms) may represent slow pathway conduction in patients with previously undiagnosed dual AV node physiology. Treadmill stress testing is a simple and effective way to distinguish between dual AV node physiology and true AV nodal disease in patients with exertional dyspnea. 61 yo female with no significant past medical history referred to EP clinic for dual chamber pacemaker implantation. The patient presented with exercise intolerance secondary to exertional dyspnea and AV nodal conduction block thought to be contributing to her symptoms. Baseline EKG showed normal sinus rhythm and markedly prolonged PR interval at 420 ms. All other studies, including echocardiogram and pertinent bloodwork, were within normal limits. The patient agreed to proceed with exercise treadmill stress testing in an attempt to correlate her symptoms with suspected arrhythmias (AV conduction block). N/A Treadmill stress testing was performed. The patient exercised for 7 min 29 sec in a standard Bruce protocol (9.2 METS). Test was terminated secondary to fatigue and dyspnea. She exhibited a normal chronotropic response (86% MPHR). No ST segment changes consistent with ischemia were observed. Importantly, review of EKGs performed during testing revealed abrupt shortening of the PR interval during exercise. This response to exercise was consistent mechanistically with the existence of dual AV node physiology, as well as preferential fast-pathway conduction and retrograde slow-pathway block during exertion. Identification of dual-AVN physiology excluded the need for pacemaker implantation. While a markedly elevated PR interval can cause exertional dyspnea secondary to dyssynchronous atrial systole or progression to AV conduction block (Mobitz Type I/II). Establishing a symptom-arrhythmia correlation is a crucial diagnostic step. As outlined above, treadmill testing identified dual AVN physiology, and revealed benign preferential slow pathway conduction at rest as the source of the prolonged PR interval. This test excluded AV nodal disease as the source of symptoms, and ensured that the patient did not undergo unnecessary pacemaker implantation.

Science, Medicine, and the Anesthesiologist

Science, Medicine, and the Anesthesiologist

Delayed radiofrequency ablation efficacy in slow pathway ablation: a case report.

BackgroundThe delayed effect of radiofrequency (RF) ablation was described in cases of accessory pathway and premature ventricular contraction ablation, as well as delayed atrioventricular (AV) block after slow pathway ablation.Case summaryWe report a case of a female patient with AV nodal re-entry tachycardia (AVNRT), in whom the first electrophysiology study ended with acute failure of slow pathway ablation, despite using long steerable sheath, both right and left-sided ablation with >15 min of RF energy application and repeatedly achieving junctional rhythm. Six weeks afterwards, during scheduled three-dimensional electroanatomical mapping procedure, there was no proof of dual AV nodal conduction nor could the tachycardia be induced. Also, the patient did not have palpitations between the two procedures nor during the 12-month follow-up period.DiscussionThis case illustrates that watchful waiting for delayed RF ablation efficacy in some cases of AVNRT ablation could be reasonable, in order to reduce the risk of complications associated with slow pathway ablation.

Minor allele of GJA1 gene polymorphism is associated with higher heart rate during atrial fibrillation

Atrial fibrillation (AF) tachycardia causes heart failure and requires more attention. The genetic background of individual heart rate (HR) variations during AF are unclear. We hypothesized that HR-associated single nucleotide polymorphisms (SNPs) reported in Genome-Wide Association Studies (GWAS) are also associated with HR during AF. We enrolled patients with persistent AF (311 for screening and 146 for replication) who underwent AF ablation and were genotyped for the 21 h-associated SNPs reported in GWAS. The patients underwent 24-h Holter monitoring before AF ablation and electrophysiological study after AF ablation during sinus rhythm. Only the GJA1 SNP rs1015451 (T>C) was significantly associated with total HR (TT 110,643 ± 17,542 beats/day, TC 116,350 ± 19,060 beats/day, CC 122,163 ± 25,684 beats/day, P = 8.5 × 10−4). We also confirmed this significant association in the replication set. The intra-atrial conduction was faster in AF patients with the GJA1 minor allele than in those without it. Multivariate analysis revealed the presence of a GJA1 SNP rs1015451 additive model, female gender, lower left ventricular ejection fraction, and higher 1:1 atrioventricular nodal conduction were independently associated with higher HR during AF. The GJA1 SNP might be a new genetic marker for AF tachycardia.

The bradycardic agent ivabradine decreases conduction velocity in the AV node and in the ventricles in-vivo

Ivabradine blocks hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels, thereby lowering the heart rate, an action that is used clinically for the treatment of heart failure and angina pectoris. We and others have shown previously that ivabradine, in addition to its HCN channel blocking activity, also inhibits voltage-gated Na channels in vitro at concentrations that may be clinically relevant. Such action may reduce conduction velocity in cardiac atria and ventricles.Here, we explore the effect of administration of ivabradine on parameters of ventricular conduction and repolarization in the surface ECG of anesthetized mice. We found that 5 min after i.p. administration of 10 mg/kg ivabradine spontaneous heart rate had declined by ~13%, which is within the range observed in human clinical studies. At the same time a significant increase in QRS duration by ~18% was observed, suggesting a reduction in ventricular conduction velocity. During transesophageal pacing at heart rates between 100 and 220 beats/min there was no obvious rate-dependence of ivabradine–induced QRS prolongation. On the other hand, ivabradine produced substantial rate-dependent slowing of AV nodal conduction. We conclude that ivabradine prolongs conduction in the AV-node and in the ventricles in vivo.

Transcatheter cryo-ablation of septal accessory pathways, multicenter observational study in Japan

BackgroundAblation using radiofrequency energy has to be carefully performed when the arrhythmia substrate is located in close proximity to the atrioventricular (AV) node due to the risk of inadvertent permanent AV block. The aim of this study was to evaluate the efficacy and safety of catheter-based cryo-therapy for septal accessory pathways (APs). MethodsA total of eleven patients (median = 56.3 years, range 13–74 years) with septal APs underwent cryoablation. Ice-mapping was performed during sinus rhythm and an AV reciprocating tachycardia utilizing the APs as a requisite limb with cooling of the catheter tip temperature to a maximum of -30℃ for less than 45 s. Cryo-ablation was performed for 4 min at a temperature of -80℃ only if ice-mapping abolished the pre-excitation or retrograde conduction over the AP without injury to the AV nodal conduction. ResultsCryo-ablation was acutely successful in all eleven patients. No permanent cryo-related complications or adverse outcomes were reported. During the follow-up (range 14–26 months), no patients experienced any arrhythmia recurrences. ConclusionIce-mapping was a feasible and reliable method to determine the exact location of the APs owing to the possibility of validating the ablation site. Cryo-ablation of APs located near the AV junction is a safe and efficacious technique with a high success rate over the long term. IRB informationEthical Committee of Japan Red Cross Yokohama City Bay Hospital #2018−19.

Nodal conduction block: A unifying concept.

A newly introduced term, "axonal conduction block," brought a confusion in the electrodiagnostic diagnosis of Guillain-Barrè syndrome (GBS). I am proposing the term "nodal conduction block" for "axonal conduction block." This unifying concept of nodal conduction block will accommodate both the traditional concept of demyelination as well as the new concept of nodopathy in the "axonal form of GBS,", making the practice of electrodiagnosis much easier.

Inter/Intra-Atrial Dissociation in Patients With Maze Procedure and Its Clinical Implications: Pseudo-Block and Pseudo-Ventricular Tachycardia.

BackgroundSevere conduction delay and inter/intra‐atrial dissociation may occur in patients who undergo an extensive catheter ablation or a maze procedure for atrial tachyarrhythmia. We report a series of patients with inter/intra‐atrial dissociation that mimicked complete atrioventricular block or ventricular tachycardia.Methods and ResultsWe retrospectively reviewed the medical records of 7 patients who were referred for the evaluation of atrioventricular block (patients 1–6) or ventricular tachycardia (patient 7) that occurred after biatrial maze procedure and valvular surgery. During the electrophysiologic study, slow atrial or junctional escape rhythm dissociated from isolated atrial activity mimicked complete atrioventricular blocks. Intra‐atrial dissociation of the right atrium or left atrium was observed. Atrioventricular nodal conduction from the nondissociated atrium to the ventricle was preserved in all patients, while the conduction from the dissociated atrium was blocked. In patient 7, the pacing of the ventricle by tracking of atrial tachycardia from the nondissociated left atrium/coronary sinus mimicked ventricular tachycardia during pacemaker interrogation. A total of 5 patients received new permanent pacemaker implantations during the index hospitalization for the surgery (n=2) or as a deferred procedure (n=3) according to the treatment for sick sinus syndrome.ConclusionsPseudo‐atrioventricular block or pseudo‐ventricular tachycardia may occur because of inter/intra‐atrial dissociation after a maze procedure. The selection of patients for permanent pacemaker implantation should be determined based on the patient’s symptoms and the status of the escape pacemaker and not on the apparent atrioventricular block. Proper diagnosis is important to avoid unnecessary implantation of a pacemaker or a defibrillator.

Micra Transcatheter Pacing System Implant under Direct Visualization During Minimally Invasive Tricuspid Valve Surgery

Atrioventricular nodal conduction abnormalities are common after open heart surgery and more so during or after valve surgery. The incidence of atrioventricular (AV) block after tricuspid valve (TV) surgery is higher than what is observed following coronary artery bypass surgery or left sided valve interventions due to the proximity of the TV annulus to the AV node and hence requirements for cardiac pacing are high. However, the mechanical interference between pacing leads and TV leaflet mobility and coaptation can result in regurgitation rendering such an approach counterintuitive. We report a case of Micra Transcatheter pacing system (TPS) implant under direct visualization at the time of tricuspid valve surgery performed via a right mini-thoracotomy approach.

Abstract 14912: Sotalol-induced Wide Complex Rhythm: What is the Mechanism?

Introduction: Delta waves associated with atrioventricular accessory pathways (APs) may manifest with autonomic tone, heart rate, and rhythm changes. Rarely, drugs like sotalol can block AV nodal conduction, revealing latent WPW, one treatable cause of sudden death. Case report: A 38-year-old man was admitted for sotalol loading due to frequent typical atrial flutter and SVT and a desire to avoid catheter ablation. He had a history of cardiac arrest with adenosine and tachycardia-induced cardiomyopathy. After recovery, cardiac MRI showed a normal heart without scar. Admission 12-lead ECG ( Figure A ) revealed normal sinus rhythm without other abnormality. With administration of sotalol, the patient developed a wide complex rhythm ( Figure B ). Interpretation of the rhythm indicated presence of a latent AP and a repeat ECG ( Figure C ) confirmed manifest preexcitation. After consenting to electrophysiology study, the patient developed a short RP tachycardia ( Figure D ) which terminated with Valsalva. The patient underwent successful catheter ablation of the pathway located at the anterior floor of the coronary sinus body and the cavotricuspid isthmus. Discussion: The differential diagnosis for a wide complex rhythm in this setting includes rate-related aberrancy, idioventricular rhythm, phase 4 aberrancy, and preexcitation from an AP. Shortened and consistent PR intervals in the tracing lead to preexcitation as the only possible mechanism. APs that are capable of anterograde conduction but are not manifest in sinus rhythm are termed latent APs. Conditions that may cause this phenomenon include opposite autonomic effects on the AP and the AV node, increased atrial conduction time, or concealed retrograde conduction into the AP. Sotalol typically increases the retrograde effective refractory period of the AP but has variable anterograde effect. Sotalol has not previously been reported to reveal a latent AP but may have acted through one of the stated mechanisms.

Smoking Accelerates Atrioventricular Conduction in Humans Concordant with Increased Dopamine Release.

Smoking is associated with cardiac arrhythmia, stroke, heart failure, and sudden cardiac arrest, all of which may derive from increased sympathetic influence on cardiac conduction system and altered ventricular repolarization. However, knowledge of the effects of smoking on supraventricular conduction, and the role of the sympathetic nervous system in them, remains incomplete. Participants with intermediate-high cardiovascular disease risk were measured for urinary catecholamines and cotinine, and 12-lead electrocardiograms (ECGs) were measured for atrial and atrioventricular conduction times, including P duration, PR interval, and PR segment (lead II), which were analyzed for associations with cotinine by generalized linear models. Statistical mediation analyses were then used to test whether any significant associations between cotinine and atrioventricular conduction were mediated by catecholamines. ECG endpoints and urinary metabolites were included from a total of 136 participants in sinus rhythm. Atrial and atrioventricular conduction did not significantly differ between smokers (n = 53) and non-smokers (n = 83). Unadjusted and model-adjusted linear regressions revealed cotinine significantly and inversely associated with PR interval and PR segment, but not P duration. Dopamine, norepinephrine, and epinephrine all inversely associated with PR interval, whereas only dopamine was also inversely associated with PR segment (p < 0.05). Dopamine and norepinephrine (but not epinephrine) also associated positively with cotinine. Dopamine mediated the relationship between cotinine and PR interval, as well as the relationship between cotinine and PR segment. Smoking is associated with accelerated atrioventricular conduction and elevated urinary dopamine and norepinephrine. Smoking may accelerate atrioventricular nodal conduction via increased dopamine production.

Visual representations of canine cardiac arrhythmias with Lorenz (Poincaré) plots.

To characterize the patterns associated with Lorenz plots (LPs) or Poincaré plots derived from the Holter recordings of dogs with various cardiac rhythms. 77 dogs with 24-hour Holter recordings. A 1-hour period from the Holter recordings from each of 20 dogs without arrhythmias and from each of 57 dogs with arrhythmias (10 each with supraventricular premature complexes, complex supraventricular ectopy, ventricular premature complexes, complex ventricular ectopy, and atrial fibrillation, and 7 with high-grade second-degree atrioventricular block) were used to generate the LPs. Patterns depicted in the LPs were described. Arrhythmia-free Holter recordings yielded LPs with a Y-shaped pattern and variable silent zones. Recordings with single premature complexes yielded LPs with double side and triple side lobes. Complex ectopy was denoted by dots clustered in the lower left corner of the LPs. The LPs of recordings with atrial fibrillation had fan patterns consistent with a nonlinear relationship between atrial electrical impulses and atrioventricular nodal conduction. The recordings with atrioventricular block yielded LPs with island patterns consistent with variable atrioventricular nodal conduction. Distinct LP patterns were identified for common cardiac rhythms of dogs, supportive of nonrandom mechanisms as the cause of most rhythms. Visual interpretation of an LP generated from a Holter recording may aid in determining the arrhythmia type and understanding the arrhythmia's mechanism in dogs and other species.

Resynchronizing Right and Left Ventricles With Right Bundle Branch Block intheCongenitalHeart Disease Population.

This study describes a single center experience with the use of cardiac resynchronization therapy (CRT) in a difficult patient population, including single systemic right ventricles (RVs), subpulmonary RVs, and left ventricles (LVs) with right bundle branch block (RBBB). CRT remains challenging in the congenital heart disease population. Consecutive patients undergoing resynchronization of single RVs, subpulmonary RVs, or LVs in the setting of RBBB were identified between 2016 and 2019. Patients who had CRT performed for complete heart block or had <3months of follow-up were excluded. Patients underwent pre-procedural advanced imaging by echocardiogram, computed tomography, or cardiac magnetic resonance to assess ventricular function and synchrony; intraoperative mapping was performed to identify optimal lead placement. All patients undergoing resynchronization presented with at least moderate systolic ventricular dysfunction in the setting of intrinsic atrioventricular nodal conduction and RBBB. Seven patients were identified. Two patients underwent CRT of a single RV, 3 with subpulmonary RVs and 2 with systemic LVs. The median age at CRT was 5 years (range 0.6 to 48 years). The median follow-up was 9months (range 3 to 18months). The median baseline QRS duration was 180ms (range 115 to 260ms). Post-CRT, the QRS duration decreased by a median of 34% (range 19% to 38%). All patients had improvement in their systolic ventricular function. Targeted resynchronization in systemic and subpulmonary RVs can be used to improve ventricular function and heart failure in the congenital heart disease population. Similar techniques can be applied to successfully treat patients with LV dysfunction and RBBB and improve their long-term outcomes.

Para-Hisian Pacing During Sinus Rhythm: Establishing Threshold Values to Distinguish Nodal From Septal Pathway Conduction.

This study sought to identify minimum threshold values below which conduction over the atrioventricular (AV) node would be unexpected. Para-Hisian pacing is used to evaluate for the presence of a septal accessory pathway (AP); however, threshold values to differentiate nodal from AP conduction are unknown. The authors performed high- and low-output para-Hisian pacing during sinus rhythm to capture the His and para-Hisian ventricular myocardium (H+V) and para-Hisian ventricular myocardium (V) alone, respectively. The change in stimulation (stim)-to-atrial electrogram interval after loss of His bundle capture in patients with (AP+) and without (AP-) aseptal AP was evaluated. Stim-to-proximal coronary sinus (PCS) and stim-to-high right atrium (HRA) intervals were measured and within-patient differences (△) for V and H+V capture were calculated. A total of 23 AP+ and 45 AP- patients were evaluated. The difference in stimulus to earliest atrial signal in the high right atrial catheter seen with the loss of His bundle capture (△-stim-HRA) (21ms; interquartile range [IQR]: 3to 43ms vs. 64ms; IQR: 56 to 73ms; p<0.001) and difference in stimulus to earliest atrial signal in the proximal coronary sinus catheter seen with the loss of His Bundle capture (△-stim-PCS) (11ms; IQR: 0 to 30ms vs. 61ms; IQR: 52to 72ms; p<0.001) were shorter in AP+ patients. The shortest △-stim-PCS and △-stim-HRA in AP- patients were 37 ms and 32ms, respectively, whereas the longest corresponding intervals in AP+ patients were 51 ms and 75ms, respectively. A △-stim-PCS<37ms or △-stim-HRA<32ms confirmed the presence of a septal AP, whereas a value >51ms for △-stim-PCS or >75ms for △-stim-HRA excluded it. Alternatively, the minimum △-stim-PCS with loss of His capture compatible with AV nodal conduction in isolation was 37ms, and a △-stim-PCS >51ms effectively ruled out the presence of a septal AP.

First-degree atrioventricular block in patients with atrial fibrillation and atrial flutter: the prevalence of intra-atrial conduction delay

PurposePR interval prolongation > 200 ms resulting in the diagnosis of first-degree atrioventricular block (AVB1) is caused by a delay in the AV nodal/His conduction and/or the right intra-atrial conduction (RIAC). The aim of the study was to assess the prevalence of AVB1 due to RIAC delay (AVB1 with normal AH and HV) in patients with atrial fibrillation (AF) and atrial flutter (AFlu).MethodsWe included 1067 consecutive patients (33% female, age 63 ± 13 years) referred for catheter ablation of AF (AF-group) (453 patients), AF and AFlu (136 patients), AFlu (292 patients), and AVNRT/AVRT (186 patients). AH-, HV-, PR-interval, and P-wave duration were measured on the 12-lead ECG and the intracardiac electrograms in sinus rhythm. RIAC delay was defined as a prolonged PR interval > 200 ms with normal AH and HV intervals.ResultsThe prevalence of AVB1 is higher in patients with AFlu (41%) and AF (21%) and patients with both arrhythmias (30%) as compared with a reference group (8%) of patients with AVNRT/AVRT. AVB1 was due to RIAC delay in 42 of 67 patients (63%) in the AF-group, in 37 of 96 patients (39%) in the AFlu-group, and in 17 of 36 patients (47%) in the AF/AFlu group, respectively. AV nodal conduction delay was more common in AFlu patients compared with AF patients.ConclusionRIAC delay is a common underlying cause of AVB1 in patients with AF and AFlu. These findings may impact the prescription of antiarrhythmic and AV-nodal blocking drugs.

P927Electrophysiological features in children with premature ventricular contractions

Abstract Background Premature ventricular contractions (PVCs) is the one of the most frequent arrhythmias in children. There is no clear understanding regarding the causes of PVCs in children without structural heart diseases. There is also little information about the state of the conduction system (CS) of the heart in children with PVCs. Purpose:The aims of the study were to estimate the electrophysiological properties of the sinus node (SN) and atrioventricular node (AVN) in children with PVCs, and to evaluate the effect of atropine test on the frequency and nature of the PVCs. Methods: 167 children(54(32,3%) girls and 113(67,7%) boys with PVCs without structural heart disease were examined. Mean age at the time of the first examination was 14,5 ± 5,3years (6-18 years). Examination included: ECG, 24-hour Holter monitor (HM), echocardiogram, treadmill test, transesophageal pacing study (TEPS), atropine test.Results:The duration of the PVCs was 3,3 ± 1,5years (6-14 years). The burden of the PVCs was 7-29% according to HM data. 5(3%) children had syncope. Frequent PVCs were recorded in 43(25,7%) patients, single PVC in 59 (35,3%), and the rest of children did not have PVCs during TEPS. SN recovery time (SNRT) was 1118,1 ± 292,4ms (541-2300ms) which exceeded the age-dependent limit in 23(13,7%) children. Corrected SNRT was 350,1 ± 171,1ms (41-1317ms), which exceeded the age-dependent limit in 15(8,9%) children. Max.rate of 1:1 conduction through AVN was 166,7 ± 39,1 imp/min (90-220 imp/min); in 16(9,6%) children it was less than 120 imp/min, while 8 (4,8%) children had enhanced AV nodal conduction (more than 200imp/min). The effective refractory period (ERP) of AVN was 325,1 ± 91,7ms (190-650ms), exceeding the age norm in 18(10,7%) children. 16(9,6%) children had a discontinuous AV nodal conduction. The frequency of stimulation which suppressed PVCs was 100-160imp/min. Atropine test was performed in 100(59,9%) children (0,1% sol. Atropini sulfatis 0,02 mg/kg IV). After administration of atropine the increase in heart rate constituted 7-131%, with an average of 57%. The SNRT was 665,5 ± 154,4 ms (406-1512ms), maximal rate of 1:1 conduction through AVN was 213,2 ± 31,9 imp/min (150-270 imp/min). Among patients who initially had PVCs during TEPS, after atropine test PVCs disappeared in 61(59,8%) children, in 16(15,7%) children there was a significant decrease, and 4(3,9%) patients had an increase in the number of PVCs and episodes of stable ventricular bigeminy, and in 1(0.9%) child there were short runs of ventricular tachycardia (up to 8 QRS complexes).Conclusions: In children with PVCs normal electrophysiological parameters of cardiac CS were noted in most cases. In 35% of children there was a hypervagotonic influence on SN or AVN, and in 75,5% cases there was a disappearance or decrease in PVCs after atropine test. This suggests that the preferential nature of PVCs in children without structural heart diseases is autonomic system dependent

Transcriptional Patterning of the Ventricular Cardiac Conduction System.

The heartbeat is organized by the cardiac conduction system (CCS), a specialized network of cardiomyocytes. Patterning of the CCS into atrial node versus ventricular conduction system (VCS) components with distinct physiology is essential for the normal heartbeat. Distinct node versus VCS physiology has been recognized for more than a century, but the molecular basis of this regional patterning is not well understood. To study the genetic and genomic mechanisms underlying node versus VCS distinction and investigate rhythm consequences of failed VCS patterning. Using mouse genetics, we found that the balance between T-box transcriptional activator, Tbx5, and T-box transcriptional repressor, Tbx3, determined the molecular and functional output of VCS myocytes. Adult VCS-specific removal of Tbx5 or overexpression of Tbx3 re-patterned the fast VCS into slow, nodal-like cells based on molecular and functional criteria. In these cases, gene expression profiling showed diminished expression of genes required for VCS-specific fast conduction but maintenance of expression of genes required for nodal slow conduction physiology. Action potentials of Tbx5-deficient VCS myocytes adopted nodal-specific characteristics, including increased action potential duration and cellular automaticity. Removal of Tbx5 in vivo precipitated inappropriate depolarizations in the atrioventricular (His)-bundle associated with lethal ventricular arrhythmias. TBX5 bound and directly activated cis-regulatory elements at fast conduction channel genes required for fast physiological characteristics of the VCS action potential, defining the identity of the adult VCS. The CCS is patterned entirely as a slow, nodal ground state, with a T-box dependent, physiologically dominant, fast conduction network driven specifically in the VCS. Disruption of the fast VCS gene regulatory network allowed nodal physiology to emerge, providing a plausible molecular mechanism for some lethal ventricular arrhythmias.

Electropharmacological Characterization of Aciclovir in the Halothane-Anesthetized Dogs: A Proposal of Evaluation Method for Cardiovascular Safety Pharmacology of Anti-virus Drugs.

Given limited information regarding the pathophysiology underlying aciclovir-associated, clinically observed cardiovascular adverse events including chest pain, tachycardia, bradycardia, palpitation, arrhythmia, hypertension and hypotension, we investigated its electropharmacological effects using the halothane-anesthetized beagle dogs. Aciclovir in doses of 2 and 20mg/kg was sequentially infused over 10min with an interval of 20min (n = 4), which would achieve sub-therapeutic to supra-therapeutic levels of plasma concentrations. Aciclovir decreased the total peripheral vascular resistance along with the blood pressure in a dose-related manner, which increased the heart rate, ventricular contraction and atrioventricular nodal conduction speed probably via a reflex-mediated increase of sympathetic tone. No significant change was detected in the intra-atrial or intra-ventricular conduction, indicating that aciclovir may not inhibit atrial or ventricular INa. Aciclovir prolonged the repolarization period in a dose-related as well as in a reverse frequency-dependent manners, indicating that aciclovir may inhibit IKr, which was supported by the Tpeak - Tend prolongation. Aciclovir transiently prolonged the J - Tpeakc possibly through a reflex-mediated increase of sympathetic tone, indicating an increase of net inward current in the early repolarization phase. Thus, aciclovir may directly inhibit IKr, and also have the potential to indirectly induce Ca2+ overload leading to early afterdepolarization. These in vivo electropharmacological profile of aciclovir would partly explain the onset mechanism of clinical adverse events.

Atrioventricular Nodal Reentrant Tachycardia in Very Elderly Patients: A Single-center Experience.

We present a series of elderly patients older than 80 years who had recurrent palpitations for decades and who were subsequently diagnosed with atrioventricular (AV) nodal reentrant tachycardia (AVNRT). Through a retrospective chart analysis, we identified 12 patients (nine females and three males) aged 88 years ± 3.7 years (range: 80–92 years) seen at our center from 2015 to 2016 for recurrent palpitations and supraventricular tachycardia (SVT) who were ultimately diagnosed with AVNRT. These patients had palpitations and had been treated for anxiety and panic attacks for decades. They underwent electrophysiology (EP) study and successful ablation of the slow pathway. The demographic data, symptoms, and EP characteristics during the EP studies of the patients were evaluated. All 12 patients experienced palpitations and all but three had documented SVT on a loop recorder or an event monitor. During EP study, all patients displayed slow-pathway conduction. Nine patients demonstrated discontinuous AV nodal conduction curves, while three showed continuous AV nodal conduction curves. The observed tachycardia rates were 496.7 ms ± 25.7 ms. Three patients had atrial fibrillation (AF), which was noted during monitoring with the implanted loop recorders. Tachycardia was induced with both burst atrial pacing and atrial extrastimuli in five patients and with extrastimuli only in two patients. In five patients, no tachycardia induction was noted, but these individuals showed evidence of dual AV node physiology. Successful elimination of residual slow-pathway conduction postablation and/or noninducibility of tachycardia in the postablation period were achieved in all patients. All patients remained symptom-free over a period of one year. The patients who had AF in addition to AVNRT also did not present any recurrent AF following AVNRT ablation but are being monitored for recurrence. AVNRT in elderly people is often confused with panic attacks; hence, reports of panic attacks in elderly people should be properly evaluated for an arrhythmic etiology.

What is the Diagnosis?

One image and tracings were obtained during the para-Hisian stimulation maneuver in an electrophysiological study. The question is: is there any retrograde nodal or extranodal conduction behavior?