Post-TAVR conduction abnormalities leading to permanent pacemaker implantation: Risk factors, prevention, and management.

Transcatheter aortic valve replacement (TAVR) often leads to conduction abnormalities, necessitating pacemaker implantation. This review of 38 meta-analyses identified preexisting right bundle branch block (RBBB), LAHB, and new-onset left bundle branch block as key risk factors, with a higher PPM risk in male and older patients. Procedural factors like transfemoral access and self-expandable valves also increase this risk. Prevention focuses on tailoring TAVR to individual electrophysiological and anatomical profiles. However, there's a lack of consensus in managing these conduction disturbances post-TAVR, highlighting the need for further research and standardized treatment strategies.

Conduction Disturbances and Permanent Pacemaker Implantation After Transcatheter Aortic Valve Replacement: Predictors and Prevention.

Conduction disturbances and permanent pacemaker implantation (PPMI) remain a frequent and important consequence of transcatheter aortic valve replacement (TAVR). Understanding risk factors for TAVR-related conduction disturbances could improve patient selection, procedural techniques, and periprocedural efforts for monitoring and treatment of heart block. Several studies have identified patient-related and procedural factors associated with new-onset left bundle branch block, high-degree atrioventricular block, and the need for PPMI after TAVR. Notable patient-related predictors include preexisting right bundle branch block, membranous septal length, and calcification of the left ventricular outflow tract. Modifiable procedural predictors include device implantation depth, prosthesis oversizing, and valve type. This review aims to summarize the current literature examining predictors of conduction disturbances and PPMI after TAVR, particularly with regard to the newer-generation valve types. We also propose a management algorithm for the management of conduction disturbances postprocedure.

Effect of antihypertensive therapy on development of incident conduction system disease in hypertensive patients.

BACKGROUND: Previous work has demonstrated that treatment of hypertensive patients with the angiotensin-converting enzyme inhibitor lisinopril was associated with a reduced incidence of a composite conduction system disease endpoint and also left bundle branch block (LBBB) compared with chlorthalidone therapy. The relationship of incident conduction system disease to angiotensin receptor blocker therapy has not been examined. METHODS: Risk of new right (RBBB) or LBBB in relation to losartan-based vs. atenolol-based treatment was assessed in 8342 hypertensive patients without baseline RBBB or LBBB. Risk of incident intraventricular conduction delay (IVCD), defined as new QRS duration at least 110 ms was assessed in the 7110 patient subset who also had baseline QRS duration less than 110 ms. QRS duration and BBB were determined on in-study ECGs done at 6 months, 1 year and then yearly. RESULTS: During 4.8 ±â€Š1.0 years follow-up, 459 patients developed new LBBB (5.5%), 184 (2.2) new RBBB and 1173 (16.5%) a new IVCD. In univariate Cox analyses, losartan-based treatment was not associated with a significantly reduced risk of either new LBBB (hazard ratio 0.95, 95% CI 0.79-1.14, P = 0.583) or RBBB (hazard ratio 1.02, 95% CI 0.76-1.36, P = 0.903), but resulted in a 15% lower risk of new IVCD (hazard ratio 0.85, 95% CI 0.76-0.95, P = 0.005). In a multivariable Cox model that adjusted for other statistically significant predictors of incident IVCD in this population (age, sex, race, history of ischemic heart disease, MI, heart failure, diabetes or atrial fibrillation, prior antihypertensive treatment, baseline total and HDL cholesterol, serum glucose and creatinine and baseline QRS duration as standard covariates and incident MI and on-treatment systolic and diastolic pressure, BMI and Cornell voltage as time-dependent covariates), losartan treatment remained associated with a 13% lower risk of new IVCD (hazard ratio 0.87, 95% CI 0.77-0.98, P = 0.021). CONCLUSION: Incident IVCD, but not BBB, is significantly reduced by losartan-based treatment. Further study is warranted to assess the potential differential impact of this therapy on QRS prolongation vs. development of more discrete conduction system block. CLINICAL TRIALS REGISTRATION: .

Patients with left bundle branch block and left axis deviation show a specific left ventricular asynchrony pattern: Implications for left ventricular lead placement during CRT implantation.

BACKGROUND: Left bundle branch block (LBBB) and left axis deviation (LAD) patients may have poor response to resynchronization therapy (CRT). We sought to assess if LBBB and LAD patients show a specific pattern of mechanical asynchrony. METHODS: CRT candidates with non-ischemic cardiomyopathy and LBBB were categorized as having normal QRS axis (within -30° and +90°) or LAD (within -30° and -90°). Patients underwent tissue Doppler imaging (TDI) to measure time interval between onset of QRS complex and peak systolic velocity in ejection period (Q-peak) at basal segments of septal, inferior, lateral and anterior walls, as expression of local timing of mechanical activation. RESULTS: Thirty patients (mean age 70.6years; 19 males) were included. Mean left ventricular ejection fraction was 0.28±0.06. Mean QRS duration was 172.5±13.9ms. Fifteen patients showed LBBB with LAD (QRS duration 173±14; EF 0.27±0.06). The other 15 patients had LBBB with a normal QRS axis (QRS duration 172±14; EF 0.29±0.05). Among patients with LAD, Q-peak interval was significantly longer at the anterior wall in comparison to each other walls (septal 201±46ms, inferior 242±58ms, lateral 267±45ms, anterior 302±50ms; p<0.0001). Conversely, in patients without LAD Q-peak interval was longer at lateral wall, when compared to each other (septal 228±65ms, inferior 250±64ms, lateral 328±98ms, anterior 291±86ms; p<0.0001). CONCLUSIONS: Patients with heart failure, presenting LBBB and LAD, show a specific pattern of ventricular asynchrony, with latest activation at anterior wall. This finding could affect target vessel selection during CRT procedures in these patients.

[Right Bundle Branch Block, Left Bundle Branch Block, Pace Maker in Case of Acute Coronary Syndrome - is the ECG of any Value?] / Rechtsschenkelblock, Linksschenkelblock, Schrittmacher bei akutem Koronarsyndrom ­ kann man das EKG hier vergessen?

The 12 lead ECG is difficult to evaluate if there is a persistent right or even left bundle block or a pace maker continually stimulating the right ventricle. Despite these pre-existing or new ECG changes it might still be possible to detect variations which can hint to an ST-elevation myocardial infarction (STEMI). Diagnosing significant ST elevations in a case of right bundle block is not very challenging. If the ECG shows a left bundle block the modified Sgarbossa criteria should be used for evaluation. These criteria can also be used in a pace maker ECG. If a patient is not pacemaker-dependent the stimulation can be paused transiently to reveal changes of the ST segment. At first medical contact it can be very important to assess these changes correctly in order to classify the ECG as a STEMI.

The value of electrophysiologic study in decision-making regarding the need for pacemaker implantation after TAVI.

PURPOSE: The purpose of this study was to evaluate electrophysiologic study (EPS) in risk stratification of relative indications for pacemaker implantation (PMI) after transcatheter aortic valve implantation (TAVI). METHODS: We reviewed files of all patients who had a left bundle branch block (LBBB) and underwent EPS after TAVI between 3/2009 and 5/2015. The indications for EPS were new-onset LBBB and the presence of an old or a new-onset LBBB associated with either PR prolongation after TAVI (∆PR >20 ms) or with "slow" atrial fibrillation (<100/min). Pacemakers were implanted when significant infranodal disease was demonstrated. The control group comprised of 55 consecutive patients who underwent TAVI and had an indication for an EPS per our definitions. These patients were discharged without further intervention. All patients were followed during 1 year for the composite endpoint of mortality or PMI after hospital discharge. RESULTS: Indications for EPS were new LBBB (n = 8, 30.8%), new LBBB + ∆PR >20 ms (n = 9, 34.6%), baseline LBBB + ∆PR >20 ms (n = 7, 26.9%) and new LBBB + slow AF <100 bpm (n = 2, 7.7%). Multilevel conduction disturbances involving the AV node (n = 19, 73.1%), the His (n = 3, 11.5%), and the infra-His system (n = 4, 15.4%) were found. Post discharge, there were 5 (9%) deaths and 3 (5.5%) PMI in the control group compared to none in the EPS group corresponding to event-free survival of 85 and 100%, respectively (p = 0.04). CONCLUSIONS: Patients with LBBB with or without ∆PR >20 ms are at a higher risk of mortality and late PMI at 1-year follow-up. EPS can be used to safely identify patients in whom a PMI is needed.

Functional aspects of His bundle physiology and pathophysiology: Clinical implications.

In this review we present evidence from many experimental studies which challenge the concept of predestination of His bundle fibers. Using both intra- and extracellular His bundle pacing in the context of atrio-ventricular block and the development of bundle branch blocks these experimental studies provide the underlying mechanisms for the recent clinical findings showing the benefits of permanent His bundle pacing.

History of His bundle pacing.

Chronic right ventricular (RV) pacing has been shown over the years to exert detrimental physiological changes including increased risk for heart failure and atrial fibrillation. His bundle pacing offers the promise of physiological activation of the ventricular tissue, with the potential for reducing the detrimental effects of RV pacing. We describe His bundle pacing in a historical context and briefly highlight several clinical trials that have helped shape the landscape of permanent His bundle pacing.

[Optimisation of subcutaneous defibrillator programming after inappropriate shocks due to new onset of right bundle branch block]. / Optimierung der Geräteeinstellung eines subkutanen Defibrillators nach inadäquaten Schocks durch neu aufgetretenen Rechtsschenkelblock.

The subcutaneous implantable defibrillator (S-ICD) has become an established tool for the prevention of sudden cardiac death. Based on its detection properties, the S­ICD is essentially dependent on correct morphology discrimination of the QRS complex and avoidance of potential T­wave sensing. We report on a patient who experienced multiple inappropriate S­ICD shocks due to T­wave oversensing in the setting of new onset of right bundle branch block. Strategies for the optimisation of the device programming are discussed.

His bundle pacing: Initial experience and lessons learned.

Direct His bundle pacing provides the most physiologic means of artificial pacing of the ventricles with a preserved His-Purkinje system and may play a role in patients with a diseased intrinsic conduction system. We describe our initial motivations and experience with permanent direct His bundle pacing and important lessons learned since that time.

Physiological mechanisms of QRS narrowing in bundle branch block patients undergoing permanent His bundle pacing.

His bundle pacing is increasingly used to avoid chronic right ventricular pacing, and electrically resynchronize ventricular activation by narrowing or normalizing the QRS interval in left and right bundle branch block. The mechanisms by which this occurs remain poorly understood. In this review, the proposed mechanisms and evidence supporting them are discussed. Also discussed are aspects of mechanisms that are not completely supported by the evidence. We also review the differences and physiological bases for direct vs. indirect His bundle capture, and the physiological mechanisms for QRS narrowing vs. normalization following His bundle pacing.

Spontaneous resolution of left bundle branch block and biventricular stimulation lead to reverse remodeling in dyssynchronopathy.

Left bundle branch block (LBBB) is considered a marker of underlying structural cardiac disease. To determine whether LBBB is cause or consequence of deterioration of left ventricular (LV) function is difficult as both are often diagnosed concomitantly. We discuss a patient where reversal of LBBB and subsequent normalization of LV function was observed after 2 different therapies, first after start of heart failure medication, and years later after implantation of a cardiac resynchronization device. This indicates that LBBB per se may result in the development of non-ischemic cardiomyopathy and that LBBB resolution can lead to reverse remodeling in dyssynchronopathy.

Diagnosis of myocardial infarction and ischemia in the setting of bundle branch block and cardiac pacing.

The diagnosis of myocardial infarction (MI) in the presence of left bundle branch block (LBBB) or during ventricular pacing (VP) is challenging because of inherent changes in the sequence of ventricular depolarization and repolarization associated with both conditions. Although LBBB and right ventricular (RV) pacing may both produce abnormalities in the ECG, it is often possible to diagnose an acute MI (AMI) or an old MI based on selected morphologic changes. Primary ST-segment changes scoring 3 points or greater according to the Sgarbossa criteria are highly predictive of an AMI in patients with LBBB or RV pacing. The modified Sgarbossa criteria are useful for the diagnosis of AMI in patients with LBBB; however, these criteria have not yet been studied in the setting of RV pacing. Although changes of the QRS complex are not particularly sensitive for the diagnosis of an old MI in the setting of LBBB or RV pacing, the qR complex and Cabrera sign are highly specific for the presence of an old infarct. Diagnosing AMI in the setting of biventricular (BiV) pacing is challenging. To date there is minimal evidence suggesting that the traditional electrocardiographic criteria for diagnosis of AMI in bundle branch block may be applicable to patients with BiV pacing and positive QRS complexes on their ECG in lead V1. This report is a careful review of the electrocardiographic criteria facilitating the diagnosis of acute and remote MI in patients with LBBB and/or VP.

Anatomical approach to permanent His bundle pacing: Optimizing His bundle capture.

Permanent His bundle pacing is a physiological alternative to right ventricular pacing. In this article we describe our approach to His bundle pacing in patients with AV nodal and intra-Hisian conduction disease. It is essential for the implanters to understand the anatomic variations of the His bundle course and its effect on the type of His bundle pacing achieved. We describe several case examples to illustrate our anatomical approach to permanent His bundle pacing in this article.

Electrophysiological observations of acute His bundle injury during permanent His bundle pacing.

BACKGROUND: Permanent His bundle pacing (HBP) is a physiological alternative to right ventricular pacing (RVP). Catheter manipulation during HBP can cause trauma to the His bundle during implantation. We sought to determine acute and long-term incidence of His bundle (HB) injury with HBP. METHODS: Patients undergoing permanent HBP at Geisinger Wyoming Valley Medical Center from 2006 to 2014 formed the study group. Patients with pre-existing His-Purkinje disease (HPD) were excluded from the study. Any development of new bundle branch block (BBB) or AV block (B) during acute HBP lead-induced block was recorded. Resolution of AVB and/or BBB was documented. RESULTS: HBP was attempted in 450 patients. In 358 patients without HPD, 28 (7.8%) developed acute HB injury in the form of complete AVB (4, 1.1%), RBBB (21, 5.9%) or LBBB (3, 0.8%) during HBP lead placement. In all 7 patients with AVB or LBBB, conduction completely recovered. The HB electrogram from the lead displayed injury current in all 7 patients. Lead-induced RBBB resolved in 12 of 21 patients and persisted in 9 (2.5%) patients. Pacing from the HBP lead resulted in correction of acute conduction block in 27 of 28 patients and 8 of 9 patients with chronic RBBB. None of the patients with transient conduction block developed new conduction disease during follow-up of 21±19months. CONCLUSIONS: Despite acute trauma to HB in 7.8% of patients undergoing permanent HBP, complete resolution of conduction block occurred in 19 of 28 patients (68%). RBBB persisted in 9 patients (32%) but mostly normalized with HBP.

The Complexity of the His Bundle: Understanding Its Anatomy and Physiology through the Lens of the Past and the Present.

In this paper, we describe the anatomy and physiology of the His bundle and describe the mechanisms by which permanent His-bundle pacing can be accomplished.

How to Perform Permanent His Bundle Pacing: Tips and Tricks.

Right ventricular pacing can cause ventricular dyssynchrony and result in reduced left ventricular systolic function and heart failure. Permanent His bundle pacing is a more physiologic form of pacing, but can be technically challenging. In this article, we describe our technique for permanent His bundle pacing including special considerations and limitations associated with His bundle pacing.