Wenckebach Atrioventricular Block Research Articles

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

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. 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. 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). 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.

533 MOBITZ TYPE I AND HIGH-DEGREE ATRIO-VENTRICULAR BLOCK AS LATE SEQUELAE OF ASYMPTOMATIC COVID-19 INFECTION: A CASE REPORT

Abstract Background It is now well-acknowledged that patients with overt COVID-19 are at increased risk of a broad range of acute cardiovascular disorders including myocardial infarction, myocarditis, pericarditis, pulmonary embolism, vasculitis and thromboembolic disease. However, long-term cardiac sequelae of COVID-19 are still poorly understood, especially in young asymptomatic patients. Case summary A 40 years-old man, with a history of COVID-19 infection 8 weeks earlier, was admitted to the Emergency Department for detection of type 2 atrio-ventricular block (AVB) Mobitz I at 12-lead ECG during regular medical checkup. The patient was asymptomatic and hemodynamically stable (resting blood pressure 125/75 mmHg). An ECG performed 10 weeks earlier showed no conduction abnormalities. At echocardiographic examination, a preserved left ventricular ejection fraction, no abnormal regional wall motion and no valvular abnormalities were found. Routine laboratory tests showed normal values of blood count, electrolytes, thyroid hormones, C-reactive protein and no elevation in high-sensitivity troponin-I levels. Renal function was preserved. A maximal ECG treadmill test was performed using the Bruce protocol that showed no ectopy during exercise, no ST segment changes during exercise or recovery. During the exercise, the patient remained asymptomatic and the AVB disappeared at stage IV and came back at the end of the test. During in-hospital stay, a paroxysmal high-grade AVB was also detected at ECG telemetry monitoring. The electrophysiological study revealed normal HV conduction and intranodal Wenckebach AVB. A cardiac magnetic resonance (CMR) was performed which revealed myocardial edema and septal fibrosis. At the end, the patient underwent a loop recorder implantation and was prescribed 600 mg of ibuprofen twice a day and dexamethasone 1 mg with progressively decreasing doses for a total of 4 weeks. At 3-month follow-up the patient remained asymptomatic and a persistence of type 2 AVB Mobitz I yet no events of high-grade AVB, were recorded at loop recorder monitoring. In addition, the 3-month follow-up CMR showed no signs of edema or fibrosis. Discussion Myocardial injury and conduction disorders have been well-described to complicate the acute COVID-19 infection. However, this is the first report of an atrioventricular conduction block as isolated long-term consequence of COVID-19 in asymptomatic patient. The persistence of AVB during follow-up could be probably explained by microscopic affection of conduction system non detectable at CMR imaging. To date, there is no long-term data to suggest whether such isolated conduction abnormalities are temporary or permanent. The decision of implanting a definitive pacemaker should be based on accurate analysis aimed at evaluating the reversible nature of arrhythmia, especially in young patients. In our case, at 3-month follow-up, CMR showed no macroscopic edema/fibrosis of the myocardium and the high grade AVB disappeared. Serious conduction disorders following asymptomatic or mild COVID-19 may occur and a tailored management is advisable.

What is the attributing electrocardiographic phenomenon underlying a concomitant 2:1 and Wenckebach atrio-ventricular block?

We herein describe the case of a spontaneously observed bidirectional block (both entrance and exit block) at the sino-atrial junction. This bidirectional block at the sino-atrial junction associated with the failure of conduction to the ventricle revealed the Wenckebach periodicity of the atrio-ventricular conduction.

Cardiac abnormalities determined by tissue Doppler imaging and arrhythmias in adolescents with anorexia nervosa.

Anorexia nervosa has a prevalence of 0.5-3% in adolescents, placing this population at increased risk of cardiac anomalies including arrhythmias, pericardial effusion, and myocardial dysfunction. Our objective is to describe cardiovascular anomalies observed by tissue Doppler imaging in patients with anorexia nervosa. We retrospectively reviewed electrocardiogram, Holter, and echocardiography findings in 28 patients diagnosed with anorexia nervosa. Electrocardiogram was abnormal in 71% of patients with sinus bradycardia observed in 57%. Holter confirmed sinus bradycardia without significant pauses. Prolonged QTc, low voltage, and ectopic beats were each seen in 14% of patients. Wenckebach atrioventricular block was observed in one patient. Supraventricular or ventricular tachycardia was not observed. Echocardiography showed structurally normal heart in all patients. Pericardial effusion was seen in 7.1% of patients and left ventricular mass was decreased in 10.7%. Mean ejection fraction was 0.73 and mean fractional shortening was 38.4%. Tissue Doppler imaging revealed systolic or diastolic dysfunction in four patients with e', a', and s' velocities in the lateral and septal basal segments more than two standard deviations below the mean. Two patients had decreased left ventricular mass but no significant difference in disease duration from the group. Basal segment velocities below one standard deviation were also observed in an additional seven patients. A trend for decreased tissue Doppler imaging velocities was seen in 25.0% of patients, while significant systolic and diastolic dysfunction was seen in 14.3% of patients, associated with a significant reduction in left ventricular mass and independent of disease duration.

Benign arrhythmias in pediatric patients

An irregular heart rhythm is a common concern among children. Recognizing the cause of the irregular rhythm is crucial for the proper diagnosis and management by primary physicians as well as pediatric specialists. The cause of pediatric arrhythmias can be identified based on the clinical history, physical examination, presenting symptoms, and electrocardiogram. Pediatric arrhythmias are classified as benign and non-benign. Both benign and non-benign arrhythmias can originate from the sinoatrial node, atrial myocardium, atrioventricular node, and ventricle myocardium. The common form of benign arrhythmias, including sinus arrhythmia, premature atrial contraction, premature ventricular contraction, and Wenckebach atrioventricular block, have no clinical significance or need for therapy. On the other hand, non-benign arrhythmias, such as supraventricular tachycardia, ventricular tachycardia, high-degree atrioventricular conduction abnormalities, and genetic arrhythmia, can affect the hemodynamic state and may cause a serious condition in pediatric patients. Most cases of benign arrhythmia are asymptomatic, and the prognosis is favorable for the normal heart. In this article, we review our current understanding of the electrocardiographic characteristics, clinical presentation, etiology, and natural history of benign arrhythmias in pediatric patients.

The Utility of Rapid Atrial Pacing Immediately Post-TAVR to Predict the Need for Pacemaker Implantation

ObjectivesThe aim of this study was to determine the utility of rapid atrial pacing immediately after transcatheter aortic valve replacement (TAVR) to predict the need for permanent pacemaker implantation (PPI). BackgroundRisk stratification for patients without high-grade atrioventricular block (AVB) after TAVR is imprecise and based on anatomic considerations, electrocardiographic characteristics, and clinical suspicion. A more reliable assessment is necessary to minimize inpatient rhythm monitoring and/or reduce unnecessary PPI. MethodsConsecutive patients undergoing TAVR at 2 centers were included. After valve implantation in patients without pacemakers who did not have complete heart block or atrial fibrillation, the temporary pacemaker was withdrawn from the right ventricle and placed in the right atrium. Rapid atrial pacing was performed from 70 to 120 beats/min, and patients were assessed for the development of Wenckebach AVB. Patients were then followed for clinical outcomes, including PPI. ResultsA total of 284 patients were included. Of these, 130 (45.8%) developed Wenckebach AVB. There was a higher rate of PPI within 30 days of TAVR among the patients who developed Wenckebach AVB (13.1% vs. 1.3%; p < 0.001), with a negative predictive value for PPI in the group without Wenckebach AVB of 98.7%. A greater percentage of patients receiving self-expanding valves required PPI than those receiving a balloon-expandable valves (15.9% vs. 3.7%; p = 0.001), though these rates were still relatively low among patients who did not develop Wenckebach AVB (2.9% and 0.8%). ConclusionsAtrial pacing post-TAVR is easily performed and can help identify patients who may benefit from extended rhythm monitoring. Patients who did not develop pacing-induced Wenckebach AVB demonstrated an extremely low likelihood of PPI.

Wenckebach Periodicity at Rest That Normalizes With Tachycardia in a Family With a NKX2.5 Mutation

A family with asymptomatic Wenckebach atrioventricular block (Wenckebach periodicity [WP]) has been followed at the investigators' institution for >4 decades. In contrast to all reported cases of WP (except in top-ranking athletes) family members have WP at rest that promptly converts to regular sinus tachycardia with exercise. They also have mild apical noncompaction that has been quite stable. Because of apparent autosomal dominant inheritance of the structural and arrhythmia disorders, deoxyribonucleic acid was obtained from 4 affected family members in 2 generations for sequence analysis of the cardiac transcription factor gene NKX2.5. A novel frame-shift mutation (c.959delC) was identified that would result in premature truncation of the protein at residue 293, with loss of the C-terminal 31 amino acids. The responsiveness of WP to exercise, the long-term stability of the WP rhythm, and the mild asymptomatic structural features expand the phenotypic presentation of diseases related to mutations in NKX2.5. In addition, the physiology of WP is reviewed in these subjects and in highly conditioned athletes. In conclusion, the investigators report familial stable WP and ventricular noncompaction caused by a mutation in NKX2.5.

Acute effects of ganglionated plexi ablation on sinoatrial nodal and atrioventricular nodal functions

Ganglionated plexus (GP) ablation has been shown effective for eliminating atrial fibrillation (AF), the most common clinical tachyarrhythmia. However, the safety of destroying the main cardiac autonomic structures remains unclear. This study investigated the acute effects of GP ablation on the sinoatrial nodal (SAN) and atrioventricular nodal (AVN) functions in a canine model. In 10 open-chest dogs, multiple electrode catheters were sutured at both atria for recording and pacing. SAN and AVN function were evaluated. GP ablation caused no significant change of sinus rate immediately after GP ablation compared with the baseline state. After GP ablation, the sinus node recovery time (SNRT) and corrected SNRT did not show significant changes at long pacing cycle lengths (CLs), and only showed significant decrease at shorter pacing CLs. The AH interval at different pacing CLs, the Wenckebach atrioventricular block (AVB) CL, 2:1 AVB CL or the ventricular rate during AF were not significantly altered by GP ablations. Vagal suppression of SAN and AVN functions was eliminated by GP ablation. GP staining showed abundant choline acetyl transferase or tyrosine hydroxylase positive neurons. These findings suggest the functions of the SAN and AVN are mainly retained after GP ablation. These results may be partially related to destroying both parasympathetic and sympathetic elements in the GP by ablation.

Atrial Tachycardia with Atypical Wenckebach Atrioventricular Block after Slow Pathway Ablation

A case of a patient with dual supraventricular tachycardias, atrioventricular nodal tachycardia, and atrial tachycardia is presented. The former was successfully ablated, whereas the latter was inducible after the ablation of the former, but without clinical importance during follow-up. However, this tachycardia showed interesting characteristics, including dual atrioventricular Wenckebach periodicity, presumably due to multiple slow pathways.

Impact of sleep on arrhythmogenesis.

Sleep is generally considered to be a protected period, when the cardiovascular system benefits from the restorative influences of the sleeping brain. However, the dynamics of cardiovascular control during sleep can tax the capacity of the diseased coronary circulation and myocardium with surges in sleep-state–related autonomic activity and disruptions in airway function and central nervous system regulation. In this regard, sleep may constitute an autonomic stress test for the heart. The scope of sleep-related risk for atrial and ventricular arrhythmias is substantial. The major subgroups susceptible to adverse influences of surges in autonomic activity during sleep are those with ischemic heart disease, heart failure, and channelopathies (Table).1 It is significant that 20% of myocardial infarctions and 15% of sudden deaths occur at night in the United States.2 Most atrial arrhythmias in patients younger than 61 years of age have nocturnal onset.3 The young are not immune to risk, as sudden infant death syndrome (SIDS) claims 2500 lives in the United States annually.4 Cardiovascular risk is compounded by comorbid factors, most notably apnea, which affects an estimated 4% to 9% of the general population5 and is considerably more prevalent among obese individuals.6 The more common form is obstructive sleep apnea (OSA), with partial or complete collapse of the pharynx. Half of heart failure patients experience either OSA or central sleep apnea (CSA) with central nervous system–mediated periodic breathing, commonly referred to as Cheyne-Stokes respiration. Such cardiorespiratory disturbances profoundly alter autonomic nervous system activity and increase risk of arrhythmia, hypertension, and myocardial infarction. View this table: Table. Patient Groups at Potentially Increased Risk for Nocturnal Cardiac Events It is surprising, as recently underscored by Malhotra and Loscalzo,7 that the significance of cardiovascular risk during sleep may not be duly recognized within the cardiology community. The reasons are …

Apparent AV junctional escape in Wenckebach AV block: markedly slow conduction through the slow AV pathway

We report here two cases of Wenckebach atrioventricular (AV) block in which apparent AV junctional escape was observed, but most likely resulted from markedly slow conduction through the slow pathway of dual AV junctional pathways. In these cases, it seems that a blocked P-wave was followed by an AV junctional escape beat. However, a blocked P-wave occasionally failed to be followed by an escape beat, and the RR interval containing the blocked P-wave was markedly longer than the above escape interval. In one case, apparent AV junctional escape beats with aberrant ventricular conduction were found, and QRS complexes of the same configuration were also found without the preceding ventricular pause. This strengthens the possibility that apparent AV junctional escape occurred because of markedly slow conduction through the slow AV pathway.

Syndrome de Sharp et bloc de conduction auriculo-ventriculaire aigu du second degré. À propos d'une observation

Mixed connective tissue disease (MCTD) is characterized by overlapping features of progressive systemic sclerosis, dermatomyositis and systemic lupus erythematosus, and by high rate of antibodies to an extractable nuclear antigen ribonucleoprotein. Cardiac manifestations in MTCD are rare. A 58 years old man was admitted for mild fever, a impairment of the general status, muscular pain and a Raynaud's phenomenon. Biologic abnormalities were an inflammatory syndrome, elevated serum CPK and high rate anti-RNP antibodies. Diagnosis of mixed connective tissue disease was made. Shortly after, a Wenckebach atrioventricular block occurred. Systemic corticosteroids were efficient. Heart blocks are rarely described in MCTD. Three cases have been reported. It's a systemic complication resulting of an inflammatory process often responsive to steroids.

Resultados a largo plazo de la estimulación auricular permanente (AAI) en la enfermedad del nodo sinusal

AAI is the pacing mode recommended in patients with sinus node dysfunction (SND) but is the less used in our country. Progression to high grade atrioventricular block (AVB) is argued as the reason to implant VVI or DDD pacemakers. We used AAI pacemakers in patients with SND only if Wenckebach AVB appeared at atrial pacing rates > or = 120 beats/min before implantation. A series of 45 patients with permanent atrial pacemaker (AAI-PM) systems, were prospectively followed and retrospectively analyzed to investigate the incidence of atrioventricular (AV) conduction disturbances and chronic atrial tachyarrhythmias. AAI-PM were implanted in patients with sinus node dysfunction (SND) in the absence of bundle branch block, only if Wenckebach AV block appeared at atrial pacing rates > or = 120 beats/min. Four patients were lost during follow-up. In 41 patients (23 males, mean age 68 +/- 12 years) the mean follow-up time was 56 months (10 to 110). There was one case of lead failure but no case of dislodgement. 28 of the 41 patients are still successfully paced in AAI mode after a mean of 68.5 months (44-110). Five patients presented chronic atrial fibrillation at a mean of 23 months (10-39) after PM implantation and remained chronically in this situation. Of these, 4 patients had paroxysmal atrial fibrillation documented before PM implantation. Eight patients died during follow-up (range 10-78 months post PM implantation) at mean age 84 years. Causes of death were noncardiovascular in 5 patients, and a cerebrovascular accident in 3 patients. One patient on digoxin and amiodarone had asymptomatic Wenckebach AV block during night sleep. The AV conduction normalized after cessation of drug therapy. Progression to high degree AV block was not documented in any patient. AAI is a reliable and safe mode of pacing in patients with SND. If appropriate indications for AAI pacing are followed, progression to high degree AV block is rare and the need to implant additional ventricular lead seems unlikely.

Effects of propofol on the human heart electrical system: a transesophageal pacing electrophysiologic study.

Previous studies have shown that infusion of propofol has sometimes been associated with bradyarrhythmias. To evaluate the effects of propofol on the electrical system of the heart, we carried out an electrophysiologic study with transesophageal pacing on ten healthy subjects scheduled for minor elective maxillo-facial surgery. By means of atrial pacing conducted by a progressive increase in stimulation cycles, we determined, in awake patients and during propofol anesthesia (2.5 mg kg-1 for induction, followed by 100 micrograms kg-1 min-1 for maintenance), the correct sinus recovery time and the eventual appearance of Wenckebach atrio-ventricular block. We did not notice sinoatrial node depression or pathologic increase in the atrio-ventricular conduction.

Cardiac fulguration, a new alternative therapy for atrioventricular nodal reentrant tachycardia.

Ten patients underwent endocardial catheter ablation of the atrioventricular junction for atrioventricular nodal reentrant tachycardias. Unipolar cathodic discharges at the distal electrode were administered against an external plate. Bipolar His and atrial deflections showed a mean of 0.15 mv and 0.5 mv respectively. Mean total energy used per patient was 195 J (range: 50-750), with a mean number of ablating discharges of 2.0 per patient, (range: 1-5). Complete atrioventricular block was achieved, but conduction reappeared in all except one patient, after a mean interval of 19.9 min. Electrophysiological evaluation was assessed 3-8 days after ablation. Sustained atrioventricular nodal reentrant tachycardias were no longer inducible in any patient. Retrograde conduction was abolished in six, and was slow and decremental in four. First-degree atrioventricular block, with intranodal delay was diagnosed in six, with an AH interval that ranged from 240 to 130 ms. Mean cycle length for appearance of Wenckebach atrioventricular block was 390 ms after ablation. One patient developed complete atrioventricular block after two discharges of 50 J, another required a repeat ablation for recurrence of intranodal tachycardia and also developed complete anterograde block in a new session of ablation with a 150 J discharge. In these two patients permanent pacing was needed. Eight patients were cured after a mean follow-up of 20 months. Less energy and fewer discharges should be administered to abolish functional dissociation of the atrioventricular node, without complete interruption of anterograde conduction.

A Case of Being Scared to Death

A 21-year-old student had generalized tonic-clonic seizures induced by the mental image of human pain. One ictal event occurred while he was listening to a description of suffering, as read from Fox's Book of Martyrs. While again listening to the offending passage during EEG and ECG monitoring, he had 25 s of asystole terminating in electrocerebral silence and a generalized tonic, tonic-clonic seizure. A 24-hour ambulatory monitor recorded episodes of progressive sinus bradycardia concomitant with PR-interval prolongation and Wenckebach atrioventricular block. Sinoatrial conduction times and sinus node recovery times were normal on atrial pacing. Since implantation of a permanent pacemaker, he has been asymptomatic. This patient demonstrates the advantages of reproducing the circumstances associated with an unexplained loss of consciousness while monitoring the EEG and ECG.

Wenckebach atrioventricular block (Mobitz type I) in children and adolescents

Mobitz type I atrioventricular block in children, adolescents and young adults without overt heart disease or drug intoxication has been considered less significant than Mobitz type II block. In highly trained athletes and some nonathletes it has been presumed to be a benign manifestation of heightened vagal tone. Experience with 16 young patients, 6 female and 10 male, tends to alter the concept of benignity. Known onset of Wenckebach and varying first degree block was between 6 months and 17 years of age. Of eight patients followed up for 5 to 18 years, five have fixed complete heart block and three first degree block. Of eight followed up for 1 to 4 years, two have fixed complete heart block and the others varying first, second and third degree block. Two have required a pacemaker implant. On intracardiac electrography performed in seven patients, four manifested during sinus rhythm a Wenckebach response to atrial pacing at abnormally slow rates; in addition, the His bundle electrograms showed A-H delay in one patient, H-V delay in two patients and delay in both intervals in one patient. Of three patients studied during complete heart block all manifested A-H block and one also H-V prolongation. The occurrence of Wenckebach block in 7 of 16 children and adolescents before the development of fixed complete heart block suggests that such block is probably more common than heretofore recognized and may be a phase in the natural history of the development of idiopathic heart block. It often represents significant disease of the cardiac conduction system, which may be progressive, and it has a guarded prognosis.

A rare form of Wenckebach atrioventricular block

Summary A patient with an acute inferior transmural myocardial infarction demonstrated a rare form of Wenckebach atrioventricular block, characterized by increasing P-R intervals, constant P-R increments, and constant R-R intervals, leading to a non-conducted beat. Constant P-R increments (the change between successive P-R intervals) have not been previously described in Wenckebach atrioventricular block.