Atrial Septal Defect (ASD) Repair Unveiling an Unusual Conduction Conundrum: A Wenckebach Case Report.

Atrial septal defects are a common congenital malformation that can lead to an elevated risk for stroke due to the bypass of the lungs by deep vein thrombosis, as well as the expected repercussions of pulmonary hypertension if left untreated. Surgical intervention is definitive; however, recent advancements in treatment options, such as percutaneous intervention, represent a safer and equally effective way to treat this congenital complication. While safer, percutaneous interventions can also lead to adverse events that may force patients to present to the emergency department. Here, we present a unique case of a patient with congenital atrial septal defect status post-percutaneous intervention who developed a new-onset second-degree AV block, Mobitz type 1 Wenckebach rhythm.

Clinical/electrophysiologic characteristics of infranodal Wenckebach in patients with indication for permanent ventricular pacing: A prospective study.

BACKGROUND: Infranodal Wenckebach is rare and not well characterized. OBJECTIVE: We prospectively studied clinical and electrophysiologic characteristics of patients with atrioventricular (AV) Wenckebach with an indication for permanent ventricular pacing. METHODS: During a 2-year period, all patients with an indication for permanent ventricular pacing underwent targeted preimplantation electrophysiologic study. Clinical and electrophysiologic characteristics at presentation and ventricular pacing percentage at 6-month follow-up were evaluated. RESULTS: A total of 163 patients (median age, 68 [interquartile range, 60-74] years; male, 59%; median QRS duration, 110 [90-130] ms; complete AV block in 123 [75.5%]) were included. AV Wenckebach was noted in 22 (13.4%) patients (median age, 70 [63-76.5] years; male, 54%; median QRS duration, 120 [110-140] ms) and classified as infranodal (12/163 [7.3%]) vs AV nodal (10/163 [6.1%]). Patients with infranodal Wenckebach (infrahisian in all), compared with AV nodal Wenckebach, demonstrated higher frequency with left ventricular ejection fraction ≤40% (41.7% vs 0%; P = .04), longer median HV interval (90 vs 49 ms; P = .005), lower frequency of isolated first-degree AV block (8.3% vs 60%; P = .02), higher frequency of right bundle branch block with left anterior fascicular block (75% vs 10%; P = .003), lesser PR increment at onset of AV Wenckebach (20.5 vs 80 ms; P = .002), and onset of 2:1 AV block at longer cycle lengths (91.7% vs 20%; P = .002). CONCLUSION: Of patients referred for pacemaker implantation, infranodal Wenckebach was present in 27.5% (11/40) without complete AV block. It was as frequent as AV nodal Wenckebach and associated with characteristic electrophysiologic findings.

A case of exaggerated exuberance: Iatrogenic atrioventricular block/intra-Hisian Wenckebach during conduction system pacing.

Isolated sinus node dysfunction with its pursuant long-term risk for atrioventricular (AV) conduction disease poses a unique dilemma for proponents of CSP due to paucity of imprimatur guidelines. In such scenarios, the risk and prognosis of iatrogenic AV block is not well elucidated but is a valid concern. We report a case where CSP was complicated by iatrogenic AV block and peculiarly the rare phenomenon of intra-Hisian Wenckebach.

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.

Intra-Hisian Wenckebach after surgical closure of conoventricular ventricular septal defect.

We report a 5-year-old girl with transient complete atrioventricular (AV) block following surgical closure of a symptomatic conoventricular ventricular septal defect (VSD) which recovered on post-operative day 9. She later presented with exertional dizziness and fatigue. While congenital cardiac defect repairs are occasionally complicated by complete heart block, this patient was found to have intra-Hisian Wenckebach which is rare in the pediatric population and can be very difficult to discern from surface electrocardiograms and by Holter monitoring. Mechanisms of post-surgical AV block, including intra-Hisian Wenckebach, are not well characterized in the pediatric population.

Definitions and Pitfalls in the Diagnosis of Atrioventricular Block.

The widespread use of disparate definitions of atrioventricular block has created important diagnostic problems. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation. This review focuses on the clinical importance of the definitions in the diagnosis of the various types of atrioventricular (AV) block and the associated diagnostic pitfalls.

Profound First-Degree Atrioventricular Block in a High-Level Basketball Athlete.

First-degree atrioventricular (AV) block (PR interval >200 ms) is commonly observed among screening electrocardiogram (ECG) in athletes. Profound first-degree AV block (PR interval >400 ms) and Mobitz type I (Wenckebach) second-degree AV block are generally uncommon and often require further workup on a case-by-case basis, particularly when there is concern for a structural cardiac abnormality. In this case, we present an example of an asymptomatic profound first-degree AV block with Mobitz type I (Wenckebach) second-degree AV block. Transthoracic echocardiogram and stress echocardiogram were unremarkable and the patient was cleared to participate in sports without any restriction. Physicians managing athletes should be aware of ECG features that require additional evaluation and cardiology consultation.

Utility of rapid atrial pacing before and after TAVR with balloon-expandable valve in predicting permanent pacemaker implantation.

BACKGROUND: High-grade or complete atrioventricular block (AVB) requiring permanent pacemaker (PPM) implantation is a known complication of transcatheter aortic valve replacement (TAVR). Wenckebach AVB induced by rapid atrial pacing (RAP) after TAVR was previously demonstrated in an observational analysis to be an independent predictor for PPM. We sought to investigate the utility of both pre- and post-TAVR RAP in predicting PPM implantation. METHODS: In a single-center, prospective study, 421 patients underwent TAVR with balloon-expandable valves (BEV) between April 2020 and August 2021. Intraprocedural RAP was performed in patients without a pre-existing pacemaker, atrial fibrillation/flutter, or intraprocedural complete AVB to assess for RAP-induced Wenckebach AVB. The primary outcome was PPM within 30 days after TAVR. RESULTS: RAP was performed in 253 patients, of whom 91.3% underwent post-TAVR RAP and 61.2% underwent pre-TAVR RAP. The overall PPM implantation rate at 30 days was 9.9%. Although there was a numerically higher rate of PPM at 30 days in patients with RAP-induced Wenckebach AVB, it did not reach statistical significance (13.3% vs. 8.4%, p = 0.23). In a multivariable analysis, RAP-induced Wenckebach was not an independent predictor for PPM implantation at 30 days after TAVR. PPM rates at 30 days were comparable in patients with or without pre-TAVR pacing-induced Wenckebach AVB (11.8% vs. 8.2%, p = 0.51) and post-TAVR pacing-induced Wenckebach AVB (10.2% vs. 5.8%, p = 0.25). CONCLUSION: In patients who underwent TAVR with BEV, there were no statistically significant differences in PPM implantation rates at 30 days regardless of the presence or absence of RAP-induced Wenckebach AVB. Due to conflicting results between the present study and the prior observational analysis, future studies with larger sample sizes are warranted to determine the role of RAP during TAVR as a risk-stratification tool for significant AVB requiring PPM after TAVR.

Mobitz type II second-degree atrioventricular block during sleep: true or false?

A number of publications have claimed that Mobitz type II second-degree atrioventricular (AV) block can occur during sleep apnea. None has provided a definition of type II block used in the articles, and representative electrocardiograms have been generally missing. Despite these reports, the existence of type II AV block during sleep must remain questionable.

Intermittent Normal Ventricular Conduction in Left Bundle Branch Block After TAVR.

In a patient who previously developed left bundle branch block after transcatheter aortic valve replacement, intermittent narrow QRS complexes were recorded on ambulatory electrocardiography monitoring. The peculiar distribution of wide and narrow QRS complexes suggested the presence of a window of supernormality in the refractory period of a branch block that on other occasions exhibited the Wenckebach phenomenon. (Level of Difficulty: Intermediate.).

Electrocardiography of Atrioventricular Block.

Delayed atrioventricular (AV) conduction most commonly occurs in the AV node, resulting from AH prolongation on an intracardiac electrocardiogram and PR prolongation on a surface electrocardiogram. AV conduction may be blocked in a 2:1 manner, with a normal PR interval and wide QRS suggesting infranodal disease, whereas a prolonged PR interval and narrow QRS are more suggestive of AV nodal disease. Block within the His is suspected when there is 2:1 AV block with normal PR and QRS intervals. Complete heart block occurs when the atrial rhythm is totally independent of a junctional or lower escape rhythm.

Ivabradine for inappropriate sinus tachycardia-induced symptomatic Mobitz type I atrio-ventricular block: a case summary.

Background: Inappropriate sinus tachycardia (IST) is characterized by a continuum of symptoms, and the aetiology of IST is imprecise. IST-induced autonomic dysfunction is well known, but IST-induced atrio-ventricular block is not reported to our knowledge. Case summary: A 67-year-old female presented with a 4-day history of random intermittent difficulty in breathing, chest tightness, palpitations, and dizziness, with a recorded heart rate of 30 beats per minute (BPM) on home monitoring equipment. The initial electrocardiogram (ECG) demonstrated sinus rhythm with intermittent Mobitz type I second degree atrio-ventricular (AV) block, with continuous cardiac monitoring demonstrating frequent episodes of Wenckebach phenomenon throughout the day, with a sinus rate of 100-120 BPM. Echocardiogram showed no significant structural abnormalities. The patient was on bisoprolol, and hence, it was suspected Wenckebach may be due to that and so stopped. However, there was no tangible effect on rhythm 48 hours after stopping bisoprolol, leading to a suspicion of IST-induced Mobitz type I second degree AV block; and so decided to introduce ivabradine 2.5 mg twice daily. After 24 hours of Ivabradine, the patient remained in sinus rhythm with no documented episodes of Wenckebach phenomenon on cardiac monitor, a finding subsequently confirmed by 24-hour Holter monitoring. During a recent follow-up visit in clinic, the patient remained symptom-free, with an ECG demonstrating sinus rhythm at a physiological rate. Discussion: Mobitz type I second degree AV block is usually due to reversible conduction block at the level of the AV node whereby malfunctioning AV nodal cells tend to progressively fatigue until they fail to conduct an impulse. Under conditions of increased vagal tone and autonomic dysfunction, Wenckebach occurrence will be increased. Thus, selective impulse conduction within the sinoatrial (SA) node by ivabradine to reduce beat conduction to the AV node in patients with IST/dysautonomia-induced Mobitz type I AV will reduce the occurrence of Wenckebach.

Conduction delays across the specialized conduction system of the heart: Revisiting atrioventricular node (AVN) and Purkinje-ventricular junction (PVJ) delays.

Background and significance: The specialized conduction system (SCS) of the heart was extensively studied to understand the synchronization of atrial and ventricular contractions, the large atrial to His bundle (A-H) delay through the atrioventricular node (AVN), and delays between Purkinje (P) and ventricular (V) depolarization at distinct junctions (J), PVJs. Here, we use optical mapping of perfused rabbit hearts to revisit the mechanism that explains A-H delay and the role of a passive electrotonic step-delay at the boundary between atria and the AVN. We further visualize how the P anatomy controls papillary activation and valve closure before ventricular activation. Methods: Rabbit hearts were perfused with a bolus (100-200 µl) of a voltage-sensitive dye (di4ANEPPS), blebbistatin (10-20 µM for 20 min) then the right atrial appendage and ventricular free-wall were cut to expose the AVN, P fibers (PFs), the septum, papillary muscles, and the endocardium. Fluorescence images were focused on a CMOS camera (SciMedia) captured at 1K-5 K frames/s from 100 × 100 pixels. Results: AP propagation across the AVN-His (A-H) exhibits distinct patterns of delay and conduction blocks during S1-S2 stimulation. Refractory periods were 81 ± 9, 90 ± 21, 185 ± 15 ms for Atrial, AVN, and His, respectively. A large delay (>40 ms) occurs between atrial and AVN activation that increased during rapid atrial pacing contributing to the development of Wenckebach periodicity followed by delays within the AVN through slow or blocked conduction. The temporal resolution of the camera allowed us to identify PVJs by detecting doublets of AP upstrokes. PVJ delays were heterogeneous, fastest in PVJ that immediately trigger ventricular APs (3.4 ± 0.8 ms) and slow in regions where PF appear insulated from the neighboring ventricular myocytes (7.8 ± 2.4 ms). Insulated PF along papillary muscles conducted APs (>2 m/s), then triggered papillary muscle APs (<1 m/s), followed by APs firing of septum and endocardium. The anatomy of PFs and PVJs produced activation patterns that control the sequence of contractions ensuring that papillary contractions close the tricuspid valve 2-5 ms before right ventricular contractions. Conclusions: The specialized conduction system can be accessed optically to investigate the electrical properties of the AVN, PVJ and activation patterns in physiological and pathological conditions.

Mobitz type I as manifestation of acute lithium cardiotoxicity.

Lithium induced cardiotoxicity is associated with several electrocardiographic (ECG) findings. The most commonly observed cardiac effects include QT prolongation, Twave abnormalities, and to lesser extent SA node dysfunction and ventricular arrythmias. We present a case of a 13-year-old female with acute lithium overdose whodeveloped Mobitz I, a manifestation of lithium associated cardiotoxity not previously reported. The patient had no significant past medical history and presented to the emergency department 1 h after intentional overdose of 10 tablets of unknown drug. Parents reported that the patient had visited her grandmother, who "regularly took many different kinds of medications," earlier that same evening. On physical examination the patient had reassuring vital signs, was in no acute distress,cardiopulmonary examination was normal, had clear sensorium, and no evidence of a toxidrome. On serological examination complete blood count, chemistries panel, and liver function tests did not show significant derangements. 4 h post-ingestion acetaminophen concentration was 28 mcg/ml and below indication for n-acetylcysteine antidote therapy. During her ED course she showed evidence of Mobitz I (Wenckebach) on 12-lead ECG. No prior ECGs were available for comparison. Medical toxicology was consulted at that time given concern for potential cardiotoxicity from an unknown xenobiotic. Serum dioxin and lithium concentrations were subsequently requested. Serum digoxin concentration was undetectable. Serum lithium concentrations was 1.7 mEq/L (0.6-1.2 mEq/L therapeutic range). The patient was treated with intravenous hydration at twice maintenance rate. Repeat lithium concertation 14 h post-ingestion was undetectable. During her admission, the patient remained hemodynamically stable and asymptomatic despite occasional episodes of Mobitz I, lasting seconds to minutes. Repeat 12-lead ECG obtained 20 h post-ingestion showed normal sinus rhythm. Cardiology recommendations included ambulatory Holter monitoring upon discharge and follow-up in clinic within two weeks. The patient was medically cleared after 36 h of monitoring and discharged after psychiatric evaluation. Our case demonstrates that patients who develop a new Mobitz I atrioventricular block of unclear etiology in the setting of acute ingestion should be screened for lithium exposure, even if otherwise free of more typical manifestations of lithium toxicity.

Increased in vivo perpetuation of whole-heart ventricular arrhythmia in heterozygous Na+/Ca2+ exchanger knockout mice.

Aims: Na+/Ca2+ exchanger (NCX) upregulation in cardiac diseases like heart failure promotes as an independent proarrhythmic factor early and delayed afterdepolarizations (EADs/DADs) on the single cell level. Consequently, NCX inhibition protects against EADs and DADs in isolated cardiomyocytes. We here investigate, whether these promising cellular in vitro findings likewise apply to an in vivo setup. Methods/Results: Programmed ventricular stimulation (PVS) and isoproterenol were applied to a murine heterozygous NCX-knockout model (KO) to investigate ventricular arrhythmia initiation and perpetuation compared to wild-type (WT). KO displayed a reduced susceptibility towards isoproterenol-induced premature ventricular complexes. During PVS, initiation of single or double ectopic beats was similar between KO and WT. But strikingly, perpetuation of ventricular tachycardia (VT) was significantly increased in KO (animals with VT - KO: 82 %; WT: 47 %; p = 0.0122 / median number of VTs - KO: 4.5 (1.0, 6.25); WT: 0.0 (0.0, 4.0); p = 0.0039). The median VT duration was prolonged in KO (in s; KO: 0.38 (0.19, 0.96); WT: 0.0 (0.0, 0.60); p = 0.0239). The ventricular refractory period (VRP) was shortened in KO (in ms; KO: 15.1 ± 0.7; WT: 18.7 ± 0.7; p = 0.0013). Conclusions: Not the initiation, but the perpetuation of provoked whole-heart in vivo ventricular arrhythmia was increased in KO. As a potential mechanism, we found a significantly reduced VRP, which may promote perpetuation of reentrant ventricular arrhythmia. On a translational perspective, the antiarrhythmic concept of therapeutic NCX inhibition seems to be ambivalent by protecting from initiating afterdepolarizations but favoring arrhythmia perpetuation in vivo at least in a murine model.

CineECG illustrating the ventricular activation sequence in progressive AV-junctional conduction block.

We present the use of CineECG in visualizing abnormal ventricular activation in a case of a complex conduction disorder. CineECG combines the standard 12­lead surface ECG with a 3D anatomical model of the heart. It projects the location and direction of the average ventricular activation and recovery on the heart model over time. In this case, CineECG was able to visualize the different type of fascicular conduction in this progressive conduction block. This novel imaging technique was able to provide additional insight in this complex case, and might be of use in other complex ECG patterns.

Atrioventricular conduction in PM recipients after transcatheter aortic valve implantation: Implications using Wenckebach point measurement.

Background: Atrioventricular (AV) conduction disturbances requiring permanent pacemaker implantation (PPI) are a common complication after transcatheter aortic valve implantation (TAVI). However, a significant proportion of patients might recover AV conduction at follow-up. Objectives: The aim of our study was to evaluate the recovery of AV conduction by determination through Wenckebach point in patients with PPI and therefore identify patients who could benefit from device reprogramming to avoid unnecessary RV pacing. Methods: We enrolled 43 patients that underwent PM implantation after TAVI at our Department from January 2018 to January 2021. PM interrogation was performed at follow-up and patients with native spontaneous rhythm were further assessed for AV conduction through WP determination. Results: A total of 43 patients requiring a PM represented the final study population, divided in patients with severely impaired AV conduction (no spontaneous valid rhythm or WP < 100; 26) and patients with valid AV conduction (WP ≥ 100; 17). In the first group patients had a significantly higher number of intraprocedural atrioventricular block (AVB) (20 vs. 1, p < 0.005), showed a significant higher implantation depth in LVOT (7.7 ± 2.2 vs. 4.4 ± 1.1, p < 0.05) and lower ΔMSID (-0.28 ± 3 vs. -3.94 ± 2, p < 0.05). Conclusion: AV conduction may recover in a significant proportion of patients. In our study, valve implantation depth in the LVOT and intraprocedural AV block are associated with severely impaired AV conduction. Regular PM interrogation and reprogramming are required to avoid unnecessary permanent right ventricular stimulation in patients with AV conduction recovery.

A Case Report of a Wenckebach Phenomenon Occurring during a His-Bundle Pacing Procedure: Is It Atrioventricular Node Pacing?

A 70-year-old man with severe valvular cardiomyopathy, permanent atrial fibrillation (AF) with a slow ventricular response, and transient atrioventricular (AV) block, was admitted to our center for severe heart failure and recurrent presyncope. While hospitalized, the coronary computed tomography angiography (CTA) showed huge atriums. We tried His bundle pacing (HBP). HB potential was observed at site A, and the His-ventricular (HV) interval was 68 ms. The duration from the stimulus signal to the onset of paced QRS (S-QRSonset) at site A was 232 ms when pacing at 60 beats per minute (BPM) with the pacing threshold of 2.0 V/0.5 ms. The S-QRSonset was longer than the HV interval and had a notable and progressive prolongation from 252 ms to 456 ms during the pacing at 90 BPM. Then, we pushed another lead a little forward, and the S-QRSonset shortened back to 68 ms, and the paced QRS morphology was the same as the intrinsic QRS morphology with the pacing threshold of 1.5 V/0.5 ms. The progressively prolonged S-QRSonset demonstrated a Wenckebach phenomenon (WP), a well-known electrophysiological characteristic of the AV node (AVN). It is the first time to report an intraoperative AVN-pacing related-WP in a patient with persistent AF. The enlarged atrium might be convenient for capturing the AVN. There are some other potential explanations for this phenomenon. The diameters of atriums decreased significantly, and the symptoms improved after the procedure. This is the first reported case in which we might achieve AVN capture in a patient with persistent AF. Although we ultimately chose HBP for better long-term pacing thresholds, the result of this case suggested that AVN pacing may be possible.