Bundle Branch Reentry Tachycardia Research Articles

Recurring episodes of bundle branch reentry ventricular tachycardia due to aortitis preceded by SARS-CoV-2 infection: a case report

BackgroundSARS-CoV-2 may trigger both vasculitis and arrhythmias as part of a multisystem inflammatory syndrome described in children as well as in adults following COVID-19 infection with only minor respiratory symptoms. The syndrome denotes a severe dysfunction of one or more extra-pulmonary organ systems, with symptom onset approximately 2–5 weeks after the COVID-19 infection. In the present case, a seemingly intractable ventricular tachycardia preceded by SARS-CoV2 infection was only managed following the diagnosis and management of aortitis.Case presentationA 69-year-old woman was hospitalized due to syncope, following a mild COVID-19 infection. She presented with paroxysmal atrial fibrillation and intermittent ventricular tachycardia interpreted as a septum-triggered bundle branch reentry ventricular tachycardia, unaffected by amiodaron, lidocaine and adenosine. A CT-scan revealed inflammation of the aortic arch, extending into the aortic root. In the following days, the tachycardia progressed to ventricular storm with intermittent third-degree AV block. A temporary pacemaker was implanted, and radiofrequency ablation was performed to both sides of the ventricular septum after which the ventricular tachycardia was non-inducible. Following supplemental prednisolone treatment, cardiac symptoms and arrythmia subsided, but recurred after tapering. Long-term prednisolone treatment was therefore initiated with no relapse in the following 14 months.ConclusionWe present a rare case of aortitis complicated with life-threatening ventricular tachycardia presided by Covid-19 infection without major respiratory symptoms. Given a known normal AV conduction prior to the COVID-19 infection, it seems likely that the ensuing aortitis in turn affected the septal myocardium, enabling the reentry tachycardia. Generally, bundle branch reentry tachycardia is best treated with radiofrequency ablation, but if it is due to aortitis with myocardial affection, long-term anti-inflammatory treatment is mandatory to prevent relapse and assure arrhythmia control. Our case highlights importance to recognize the existence of the multisystem inflammatory syndrome in adults (MIS-A) following COVID-19 infection in patients with alarming cardiovascular symptoms. The case shows that the early use of an CT-scan was crucial for both proper diagnosis and treatment option.

Importance of the Activation Sequence of the His or Right Bundle for Diagnosis of Complex Tachycardia Circuits.

In this review, we emphasize the unique value of recording the activation sequence of the His bundle or right bundle branch (RB) for diagnoses of various supraventricular and fascicular tachycardias. A close analysis of the His to RB (H-RB) activation sequence can help differentiate various forms of supraventricular tachycardias, namely atrioventricular nodal reentry tachycardia from concealed nodofascicular tachycardia, a common clinical dilemma. Furthermore, bundle branch reentry tachycardia and fascicular tachycardias often are included in the differential diagnosis of supraventricular tachycardia with aberrancy, and the use of this technique can help the operator make the distinction between supraventricular tachycardias and these other forms of ventricular tachycardias using the His-Purkinje system. We show that this technique is enhanced by the use of multipolar catheters placed to span the proximal His to RB position to record the activation sequence between proximal His potential to the distal RB potential. This allows the operator to fully analyze the activation sequence in sinus rhythm as compared to that during tachycardia and may help target ablation of these arrhythmias. We argue that 3 patterns of H-RB activation are commonly identified-the anterograde H-RB pattern, the retrograde H-RB (right bundle to His bundle) pattern, and the chevron H-RB pattern (simultaneous proximal His and proximal RB activation)-and specific arrhythmias tend to be associated with specific H-RB activation sequences. We show that being able to record and categorize this H-RB relationship can be instrumental to the operator, along with standard pacing maneuvers, to make an arrhythmia diagnosis in complex tachycardia circuits. We highlight the importance of H-RB activation patterns in these complex tachycardias by means of case illustrations from our groups as well as from prior reports.

Atypical Surface ECG Complicating the Diagnosis of Bundle Branch Reentry Tachycardia

Typical left bundle branch block (LBBB) during ventricular tachycardia (VT) is a diagnostic criterion of bundle branch reentry tachycardia (BBRT) with activation of the right bundle in the anterograde direction. Eleven patients (seven male, 60 ± 12 years) with nonischemic cardiomyopathy (left ventricular ejection fraction 37 ± 16%) presenting with BBRT were successfully treated by ablation of the right bundle. Among them, five patients had atypical surface electrocardiograms (ECGs) differing from a typical LBBB during the VT. Three patients with severe enlargement and dysfunction of the left ventricle had broadened irregular QRS complexes with rR or RS configuration in lead V6 during the BBRT. Two patients with enlargement and/or hypokinesia of the right ventricle had entirely or almost entirely negative complexes (QS) in the chest leads (V1-V6) during the VT. Activation mapping in these two patients revealed that the exit site of the BBRT was in the anterior right ventricle generating a negative concordance in the precordial leads. Atypical surface ECGs with broadened irregular QRS complexes or negative concordance in the precordial leads can complicate the correct diagnosis of BBRT in patients with severe left ventricular dysfunction and involvement of the right ventricle.

The risk of delayed atrioventricular and intraventricular conduction block following ablation of bundle branch reentry

The aim of the study was to determine the long-term reliability of atrioventricular and intraventricular conduction and the implications for cardiac resynchronization therapy (CRT-D) following catheter ablation of bundle branch reentry tachycardia (BBRT) and interfascicular tachycardia. Fourteen patients with recurrent monomorphic ventricular tachycardia (VT) (n = 11) and incessant VT (n = 3) underwent catheter ablation of BBRT (n = 7), interfascicular tachycardia (n = 5) or both arrhythmias (n = 2). Successful ablation was achieved in all patients without intraprocedural atrioventricular (AV) block. Within 2 months after ablation, three patients with BBRT and pre-existing prolonged QRS developed a delayed third-degree AV block. During the follow-up of 2 years, two patients with interfascicular tachycardia developed a new left bundle branch block (LBBB) associated with worsening of heart failure. Three patients underwent upgrading of implantable cardioverter defibrillator therapy to CRT-D early after ablation which improved heart failure during the 6 months follow-up. During the long-term follow-up of 39 ± 13 months, VT storm recurred in one patient. Four of the 14 patients died of deterioration of heart failure and one had to undergo heart transplantation. Catheter ablation for BBRT in patients with prolonged QRS is associated with a high risk of delayed third-degree AV block. Ablation of interfascicular tachycardia can be associated with delayed LBBB. After ablation of bundle branch reentry, patients with prolonged QRS are candidates for cardiac resynchronization therapy but the mortality remains high.

Transcatheter Cryoablation Part I: Preclinical Experience

The concept of cooling to treat medical disorders dates back to the ancient Egyptian Edwin Smith Papyrus on surgical trauma, written between 3000 and 2500 B.C. Hypothermic therapy was recommended for abscesses that were “oily, like fluid under thy hand, [which] produce some clamminess of the surface.”1 Modern forms of cryothermal tissue ablation have been used surgically for decades in numerous organ systems and for various pathologies. Unlike heat that destroys cells by coagulation and tissue necrosis with potential for thrombus formation and aneurysmal dilatation, cryoablation involves a distinct pathophysiological process. As such, it carries a unique safety and efficacy profile. While not novel as an energy modality, harnessing cryoenergy into a steerable transcatheter format represents a more recent landmark in the history of arrhythmia therapy. In Part I of this two-part series, we will focus on the body of knowledge underlying the development of a transcatheter cryoablation system. Pertinent features related to biophysics and mechanisms of cryothermal tissue injury will be highlighted, key historical developments considered, and experience gained from cryosurgery with hand-held probes summarized. Preclinical studies with transcatheter cryoablation will be detailed, setting the framework for human applications. Part II of this series will review the current state of knowledge regarding clinical experience with transcatheter cryoablation.

Reinitiation of Ventricular Macroreentry within the His‐Purkinje System by Back‐Up Ventricular Pacing—A Mechanism of Ventricular Tachycardia Storm

We describe immediate reinitiation of macroreentry ventricular tachycardia (VT) involving the His-Purkinje system by ventricular pacing from the electrode of an implantable cardioverter defibrillator (ICD) as a mechanism of VT storm refractory to ICD therapy. Repetitive reinitiation of bundle branch reentry tachycardia (BBRT), interfascicular tachycardia, or both VTs by ventricular pacing was identified in four ICD patients presenting with VT storm or incessant VT. All patients had a pre-existing prolonged HV interval (75 +/- 9 ms) and left bundle branch block (LBBB) or bifascicular block during sinus rhythm. The VTs included BBRT with LBBB in three patients and interfascicular tachycardia with right bundle branch block (RBBB) and left anterior or left posterior fascicular block in two patients. The paced beats from the ICD electrode exhibited a LBBB pattern of depolarization in two patients and a RBBB contour in V1 and V2 with left axis deviation in two patients. The QRS complex during pacing from the ICD electrode closely resembled that of the recurrent VT in all four patients suggesting that the pacing site of the ICD electrode was in proximity to the myocardial exit site of the bundle fascicle used for antegrade conduction during the reinitiated VT. Ventricular pacing from the ICD electrode after termination of the VT apparently encountered the retrograde refractoriness of this bundle fascicle and allowed immediate re-propagation of the wavefront orthodromically along the VT circuit. BBRT was eliminated by ablation of the right bundle branch. Successful ablation of the interfascicular tachycardias was achieved by targeting (1) an abnormal potential of the distal left posterior Purkinje network or (2) a diastolic potential during VT in the midinferior left ventricular (LV) septum. Repetitive reinitiation of BBRT and interfascicular tachycardia by ventricular pacing from the ICD electrode should be considered as a mechanism of VT storm refractory to ICD therapy in patients with a pre-existing conduction delay within the His-Purkinje system.

Are electrophysiological studies needed prior to defibrillator implantation?

At present, patients with documented sustained VT or resuscitated cardiac arrest (CA) are treated with ICDs. The aim of this study was to retrospectively evaluate if a routine electrophysiological study should be recommended prior to ICD implantation. In 462 patients referred for ICD implantation because of supposedly documented VT (n = 223) or CA (n = 239), electrophysiological study was routinely performed. In 48% of the patients with CA, sustained VT or VF was inducible. Electrophysiological study suggested conduction abnormalities (n = 11) or supraventricular tachyarrhythmias (n = 3) in conjunction with severely impaired left ventricular function to have been the most likely cause of CA in 14 (5.9%) of 239 patients. Likewise, sustained VT was only inducible in 48% of patients with supposedly documented VT. Of these inducible VTs, nine were diagnosed as right ventricular outflow tract tachycardia or as bundle branch reentry tachycardia. Supraventricular tachyarrhythmias judged to represent the clinical event were the only inducible arrhythmia in 35 (16%) patients (AV nodal reentrant tachycardia [n = 7], AV reentry tachycardia [n = 4], atrial flutter [n = 19], and atrial tachycardia [n = 5]). Based on findings from the electrophysiological study, ICD implantation was withheld in 14 (5.9%) of 239 patients with CA and in 44 (19.7%) of 223 patients with supposedly documented VT. During electrophysiological study, VT or VF was only reproducible in about 50% of patients with supposedly documented VT or CA. Electrophysiological study revealed other, potentially curable causes for CA or supposedly documented VT in 12.6% (58/462) of all patients, indicating that ICD implantation can potentially be avoided or at least postponed in some of these patients. Based on these retrospective data, routine electrophysiological study prior to ICD implantation seems to be advisable.

Ventricular tachycardia with QRS configuration similar to that in sinus rhythm and a myocardial origin: differential diagnosis with bundle branch reentry.

Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported. The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia. A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.

Etiology and management of sustained ventricular tachycardia.

Ventricular tachyarrhythmias secondary to a variety of underlying cardiovascular problems pose a therapeutic challenge to the clinician. The initial presentation may be as sudden cardiac death, which underlies its public health problem. The underlying conditions predisposing to this arrhythmia include ischemic heart disease, dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmiogenic right ventricle dysplasia and certain postoperative states including corrective surgery for tetralogy of Fallot and valve replacement. Other causes include prolonged QT syndrome, idiopathic right and left ventricle tachycardia and bundle branch re-entry tachycardia. Ischaemic heart disease is the most common cause of ventricular tachycardia and therapy has evolved considerably over the past two decades. The development of and refinements in the implantable cardioverter-defibrillator (ICD) have introduced a new dimension in therapeutic options and markedly improved survival in these patients. Insights in the dichotomy between arrhythmia suppression and total mortality have reoriented drug therapy with a decrease in the use of sodium channel blockers. beta-blockers have emerged as antiarrhythmic drugs in their own right and their synergistic effects with amiodarone have strengthened the antiarrhythmic drug arm. The role of these drugs in patients with hemodynamically stable ventricular tachycardia, especially in relatively preserved ventricles needs to be explored. Catheter ablation techniques have provided curative therapy in patients with idiopathic and bundle branch reentry tachycardia. Further advances in radiofrequency ablation, including use of newer mapping techniques, promise a greater role for ablation of ischemic ventricular tachycardia in the future. A hybrid approach consisting of drugs, catheter ablation and/ or ICD may provide effective therapeutic approach in some situations. Further innovations and technologic developments promise a further reorientation in therapy towards identification and treatment of the underlying arrhythmogenic substrate.

Bundle branch reentry tachycardia: why is the HV interval often longer than in sinus rhythm? The critical role of anisotropic conduction.

Bundle branch reentry tachycardia: why is the HV interval often longer than in sinus rhythm? The critical role of anisotropic conduction.

Uncommon Forms of Ventricular Tachycardia

Radiofrequency catheter ablation has been increasingly used in the treatment of ventricular tachycardia (VT). The success rates have been high in the management of patients with bundle branch reentry tachycardia and idiopathic ventricular tachycardia. Ablation of the right bundle branch provides a permanent cure for patients with bundle branch reentrant tachycardia. Similarly, using pace mapping and endocardial activation mapping, the tachycardia focus can be eliminated in more than 90% of patients with idiopathic VT. In this article, we review the clinical characteristics, electrophysiologic features and management of these arrhythmias, with an emphasis on the role of radiofrequency catheter ablation.

Effects of Sotalol on His-Purkinje Conduction and Refractoriness in Humans.

BACKGROUND: The effects of sotalol on refractoriness in human ventricular and atrial muscles have been well established, but the drug's effect on the electrical properties of the His-Purkinje system in humans is not known, especially whether sotalol's effect is due solely to its action on prolonging repolarization or in combination with its beta-blocking properties. We studied the electrophysiologic effects of intravenous sotalol and propranolol in patients undergoing electrophysiologic studies of cardiac arrhythmias. METHODS AND RESULTS: We studied 22 patients (19 men, 3 women; mean age, 60 +/- 6 years) who had coronary artery disease and assessable anterograde, retrograde, or both, His-Purkinje system function. Fifteen patients underwent electrophysiologic studies before and after intravenous sotalol (1.5 mg/kg), and 7 patients underwent electrophysiologic studies before and after intravenous propranolol (0.15 mg/kg). Both sotalol and propranolol had no significant effect on the H-V interval, but sotalol significantly increased ventricular refractoriness and His-Purkinje refractoriness, both in anterograde and retrograde conduction, whereas propranolol did not, Sotalol's effect on His-Purkinge refractoriness also caused atrioventricular block distal to the His bundle during atrial pacing at a moderately fast rate. Sotalol was not effective in preventing bundle branch re-entry tachycardia, nevertheless, it increased cycle length of bundle branch re-entry tachycardia by increasing refractoriness. CONCLUSIONS: Sotalol increased His-Purkinje refractoriness in humans but had no effect on His-Purkinje conduction. The drug must be used judiciously in patients with a diseased His-Purkinje system because it may cause atrioventricular block distal to His at fast heart rates. Sotalol had no effect on macrore-entry utilizing bundle branches.

Progression to complete atrioventricular block in a patient with bundle branch re-entry tachycardia

A 38-year-old man with no significant structural heart disease suffered from one episode of wide QRS tachycardia. The electrocardiogram showed a PR interval of 0.20 second and a QRS duration of 0.10 second. His bundle recording revealed an HV interval of 90–100 ms. The tachycardia was inducible with programmed stimulation and displayed a QRS morphology of complete left bundle branch block. It was characterized by an atrioventricular dissociation, a cycle length of 280 ms, and an H deflection preceding each QRS complex. Pacing from the right ventricular apex at a cycle length of 270 ms entrained the tachycardia, while at a cycle length of 260 ms, the tachycardia was terminated. Four years later, the patient presented with complete atrioventricular block with a wide QRS escape rhythm. An electrophysiologic study conducted while he was in 1:1 atrioventricular conduction showed an HV interval of 100 ms. Second-degree infrahisian block developed at an atrial paced cycle length of 700 ms. There was no induction of tachycardia with programmed stimulation before or after isoproterenol. The patient was treated with an implantation of a permanent pacemaker.

Bidirectional Bundle Branch Reentry Tachycardia Associated with Ebstein's Anomaly: Cured by Extensive Cryoablation of the Right Bundle Branch

A 30-year-old woman with Ebstein's anomaly presented with a sustained, wide QRS complex tachycardia exhibiting a left bundle branch block morphology. Serial electrophysiological studies revealed right and left bundle branch reentry tachycardias refractory to many conventional antiarrhythmic drugs. Radiofrequency and direct current catheter ablation of the right bundle branch failed to control the tachycardias. The patient subsequently underwent extensive endocardial cryoablation to the right bundle branch resulting in cure of her arrhythmia.

Mechanism‐Specific Therapy of Ventricular Tachycardia

Arrhythmia Mechanisms and Therapy. An understanding of the mechanisms responsible for experimental and clinical arrhythmias has led to the development of mechanism‐specific therapies for ventricular tachycardia. These include: (1) beta blockade for catecholamine‐sensitive ventricular tachycardia; (2) verapamil for ventricular tachycardia possibly due to triggered activity; (3) pacing, isoproterenol and magnesium therapy for torsade de pointes possibly due to early afterdepolarizations; (4) catheter ablation of the right bundle for bundle branch reentry tachycardia; and (5) catheter ablation of the zone of slow conduction for ventricular tachycardia due to reentry. Hopefully, further progress will be made in removing some of the empiricism from antiarrhythmic therapy.

Mechanisms of clinical tachycardias

Animal data suggest that cardiac arrhythmias can result from a variety of mechanisms. In clinical settings, arrhythmias that are easily initiated and terminated with programmed electrical stimulation are often designated as reentry tachycardias. However, proof of reentry is contingent upon demonstration of the entire circuit; this relation has been proposed for arrhythmias associated with large circuits, such as those seen in the Wolff-Parkinson-White syndrome. Reentry has also been proposed as the mechanism responsible for a variety of other tachycardias, including bundle branch and atrioventricular nodal reentry tachycardia, permanent junctional reentrant tachycardia, reentry tachycardia associated with nodoventricular Mahaim fibers and inducible atrial and ventricular tachycardia. Documentation of triggered rhythms as the mechanism responsible for clinical arrhythmias has been even more difficult. Examples of arrhythmias resulting from triggered activity may include those associated with digitalis toxicity arising from the atria, the atrioventricular junction or the ventricles. Clinical arrhythmias due to triggered activity in the absence of digitalis have also been described. Cardiac arrhythmias that cannot be induced by electrical stimulation are presumably due to normal or abnormal automaticity. Examples of normal automaticity in the human heart are sinus rhythm and junctional and idioventricular escape rhythms. Tachycardias by abnormal automaticity have seldom been investigated for the purpose of documenting the mechanism and therefore the limited data available make it difficult to draw any final conclusions.