scholarly journals Arrhythmias from the Right Ventricular Moderator Band: Diagnosis and Management

2020 ◽  
Vol 8 (4) ◽  
pp. 294-299
Author(s):  
Megan Barber ◽  
Jason Chinitz ◽  
Roy John
Keyword(s):  
Ventricular Tachycardia ◽  
Right Ventricle ◽  
Ventricular Arrhythmias ◽  
Structural Heart Disease ◽  
Conduction System ◽  
Polymorphic Ventricular Tachycardia ◽  
Management Options ◽  
Premature Ventricular Contractions ◽  
Moderator Band ◽  
The Right

The moderator band in the right ventricle is being increasingly recognised as a source for arrhythmias in the absence of identifiable structural heart disease. Because it carries part of the conduction system from the right ventricle septum to the free wall, it is a source of Purkinje-mediated ventricular arrhythmias that manifest as premature ventricular contractions (PVC) or repetitive ventricular tachycardia. More importantly, short coupled PVCs triggering polymorphic ventricular tachycardia and VF have been localised to the moderator band and ablation of these Purkinje mediated PVCs can effectively prevent recurrent VF. The exact mechanism of arrhythmogenesis is still debated but stretch, fibrosis and ion channel alterations might be responsible. Arrhythmias originating in this region of the right ventricle may thus be another cause for idiopathic VF that is potentially treatable with catheter-based ablation techniques. Recognition of the typical PVC morphology can point to the moderator band as the source of idiopathic VF and an opportunity for timely intervention. The available data on the anatomy, electrophysiology and management options are reviewed.

scholarly journals Proarrhythmic Effect of RF ablation on the Right Ventricular Moderator Band

2021 ◽  
Author(s):  
Jonathan Willner ◽  
Parth Makker ◽  
Roy John
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Right Ventricular ◽  
Ventricular Arrhythmias ◽  
Conduction System ◽  
Rf Ablation ◽  
Moderator Band ◽  
Coupling Interval ◽  
The Right ◽  
Durable Suppression

The right ventricular moderator band (MB) is increasingly being recognized as a source for PVCs and PVC-mediated ventricular fibrillation. Monomorphic PVCs, non-sustained monomorphic VT and ventricular fibrillation are all documented arrhythmias originating from the MB. The benign PVCs usually have a coupling interval in excess of 400 msec. When PVCs trigger VF, coupling intervals are typically short, less than 300 msec. We report here a case of long-standing frequent monomorphic PVCs with a coupling interval of > 400 msec from the right ventricular distal conduction system embedded in the moderator band that progressed to non-sustained ventricular tachycardia. Following suppression of the arrhythmia with RF ablation, the arrhythmia recurred with PVCs at a shorter coupling interval (<300 msec), with frequent repetitive non-sustained polymorphic VT and triggering of sustained ventricular fibrillation. The use of a cryoballoon to ablate over the course of the moderator band resulted in complete and durable suppression of ventricular arrhythmias.

scholarly journals Electrocardiographic Criteria for Differentiating Left from Right Idiopathic Outflow Tract Ventricular Arrhythmias

2021 ◽  
Vol 10 (1) ◽  
pp. 10-16
Author(s):  
Marco V Mariani ◽  
Agostino Piro ◽  
Domenico G Della Rocca ◽  
Giovanni B Forleo ◽  
Naga Venkata Pothineni ◽  
...  
Keyword(s):  
Ventricular Arrhythmias ◽  
Right Ventricular Outflow Tract ◽  
Structural Heart Disease ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Premature Ventricular Contractions ◽  
Left Ventricular Outflow ◽  
The Right ◽  
Ecg Criteria

Idiopathic ventricular arrhythmias are ventricular tachycardias or premature ventricular contractions presumably not related to myocardial scar or disorders of ion channels. Of the ventricular arrhythmias (VAs) without underlying structural heart disease, those arising from the ventricular outflow tracts (OTs) are the most common. The right ventricular outflow tract (RVOT) is the most common site of origin for OT-VAs, but these arrhythmias can, less frequently, originate from the left ventricular outflow tract (LVOT). OT-VAs are focal and have characteristic ECG features based on their anatomical origin. Radiofrequency catheter ablation (RFCA) is an effective and safe treatment strategy for OT-VAs. Prediction of the OT-VA origin according to ECG features is an essential part of the preprocedural planning for RFCA procedures. Several ECG criteria have been proposed for differentiating OT site of origin. Unfortunately, the ECG features of RVOT-VAs and LVOT-VAs are similar and could possibly lead to misdiagnosis. The authors review the ECG criteria used in clinical practice to differentiate RVOT-VAs from LVOT-VAs.

Ventricular Arrhythmias

2020 ◽  
Author(s):  
Roy M. John ◽  
William G Stevenson
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Catheter Ablation ◽  
Sudden Death ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Polymorphic Ventricular Tachycardia ◽  
Left Ventricular Ejection ◽  
Premature Ventricular Contractions ◽  
Increased Risk

Ventricular arrhythmias are common in all forms of heart disease and are an important cause of cardiac arrest and sudden death. Many ventricular arrhythmias are benign but may serve as a marker for underlying disease or its severity. Others are life threatening. The significance of an arrhythmia is determined by the specific characteristics of the arrhythmia and the associated heart disease, and these features guide evaluation and therapy. This review discusses various mechanisms and types of ventricular arrhythmias and management based on clinical presentation (including patients with symptomatic arrhythmia and increased risk of sudden death without arrhythmia symptoms). Genetic arrhythmia syndromes, such as abnormalities of repolarization and the QT interval, catecholaminergic polymorphic ventricular tachycardia (VT), and inherited cardiomyopathies, are discussed in depth. Under the rubric of management of ventricular arrhythmias, drug therapy for ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs), and catheter ablation for VT are also covered. Tables chart out guideline recommendations for ICD therapy, drugs for the management of ventricular arrhythmias, and indications and contraindications for catheter ablation of ventricular arrhythmias. Electrocardiograms are provided, as well as management algorithms for ventricular arrhythmias based on patient presentation, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection less than or equal to 35% who are candidates for consideration of an ICD for primary prevention of sudden cardiac death. This review contains 5 figures, 8 tables, and 61 references. Keywords: Ventricular arrhythmias, implanted cardioverter-defibrillator (ICD), Ventricular tachycardia (VT), Premature Ventricular Contractions (PVC), Myocardial Infarction (MI), Brugada syndrome, Arrhythmogenic right ventricular cardiomyopathy (ARVC), electrocardiographic (ECG)

Ventricular Arrhythmias

2020 ◽  
Author(s):  
Roy M. John ◽  
William G Stevenson
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Catheter Ablation ◽  
Sudden Death ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Polymorphic Ventricular Tachycardia ◽  
Left Ventricular Ejection ◽  
Premature Ventricular Contractions ◽  
Increased Risk

Ventricular arrhythmias are common in all forms of heart disease and are an important cause of cardiac arrest and sudden death. Many ventricular arrhythmias are benign but may serve as a marker for underlying disease or its severity. Others are life threatening. The significance of an arrhythmia is determined by the specific characteristics of the arrhythmia and the associated heart disease, and these features guide evaluation and therapy. This review discusses various mechanisms and types of ventricular arrhythmias and management based on clinical presentation (including patients with symptomatic arrhythmia and increased risk of sudden death without arrhythmia symptoms). Genetic arrhythmia syndromes, such as abnormalities of repolarization and the QT interval, catecholaminergic polymorphic ventricular tachycardia (VT), and inherited cardiomyopathies, are discussed in depth. Under the rubric of management of ventricular arrhythmias, drug therapy for ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs), and catheter ablation for VT are also covered. Tables chart out guideline recommendations for ICD therapy, drugs for the management of ventricular arrhythmias, and indications and contraindications for catheter ablation of ventricular arrhythmias. Electrocardiograms are provided, as well as management algorithms for ventricular arrhythmias based on patient presentation, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection less than or equal to 35% who are candidates for consideration of an ICD for primary prevention of sudden cardiac death. This review contains 5 figures, 8 tables, and 61 references. Keywords: Ventricular arrhythmias, implanted cardioverter-defibrillator (ICD), Ventricular tachycardia (VT), Premature Ventricular Contractions (PVC), Myocardial Infarction (MI), Brugada syndrome, Arrhythmogenic right ventricular cardiomyopathy (ARVC), electrocardiographic (ECG)

scholarly journals Catecholaminergic polymorphic ventricular tachycardia complicated by dilated cardiomyopathy: a case report

2020 ◽  
Author(s):  
Granitz Christina ◽  
Jirak Peter ◽  
Strohmer Bernhard ◽  
Pölzl Gerhard
Keyword(s):  
Heart Failure ◽  
Ventricular Tachycardia ◽  
Dilated Cardiomyopathy ◽  
Sinus Bradycardia ◽  
Clinical Care ◽  
Structural Heart Disease ◽  
Catecholaminergic Polymorphic Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia ◽  
Myocardial Inflammation ◽  
As Stress

Abstract Background  Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe genetic arrhythmogenic disorder characterized by adrenergically induced ventricular tachycardia manifesting as stress-induced syncope and sudden cardiac death. While CPVT is not associated with dilated cardiomyopathy (DCM) in most cases, the combination of both disease entities poses a major diagnostic and therapeutic challenge. Case summary  We present the case of a young woman with CPVT. The clinical course since childhood was characterized by repetitive episodes of exercise-induced ventricular arrhythmias and a brady-tachy syndrome due to rapid paroxysmal atrial fibrillation and sinus bradycardia. Medical treatment included propranolol and flecainide until echocardiography showed a dilated left ventricle with severely depressed ejection fraction when the patient was 32 years old. Cardiac magnetic resonance imaging revealed non-specific late gadolinium enhancement. Myocardial inflammation, however, was excluded by subsequent endomyocardial biopsy. Genetic analysis confirmed a mutation in the cardiac ryanodine receptor but no pathogenetic variant associated with DCM. Guideline-directed medical therapy for HFrEF was limited due to symptomatic hypotension. Over the next months, the patient developed progressive heart failure symptoms that were finally managed by heart transplantation. Discussion  Management in patients with CPVT and DCM is challenging, as Class I antiarrhythmic drugs are not recommended in structural heart disease and prophylactic internal cardioverter-defibrillator implantation without adjuvant antiarrhythmic therapy can be detrimental. Regular echocardiographic screening for DCM is recommendable in patients with CPVT. A multidisciplinary team of heart failure specialists, electrophysiologists, geneticists, and imaging specialists is needed to collaborate in the delivery of clinical care.

scholarly journals Mechanisms and Clinical Management of Ventricular Arrhythmias following Blunt Chest Trauma

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Daniel H. Wolbrom ◽  
Aleef Rahman ◽  
Cory M. Tschabrunn
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Ventricular Arrhythmias ◽  
Blunt Chest Trauma ◽  
Chest Trauma ◽  
Motor Vehicle ◽  
Structural Heart Disease ◽  
Chest Injury ◽  
Chronic Stage ◽  
Chest Wall Injury

Nonpenetrating, blunt chest trauma is a serious medical condition with varied clinical presentations and implications. This can be the result of a dense projectile during competitive and recreational sports but may also include other etiologies such as motor vehicle accidents or traumatic falls. In this setting, the manifestation of ventricular arrhythmias has been observed both acutely and chronically. This is based on two entirely separate mechanisms and etiologies requiring different treatments. Ventricular fibrillation can occur immediately after chest wall injury (commotio cordis) and requires rapid defibrillation. Monomorphic ventricular tachycardia can develop in the chronic stage due to underlying structural heart disease long after blunt chest injury. The associated arrhythmogenic tissue may be complex and provides the necessary substrate to form a reentrant VT circuit. Ventricular tachycardia in the absence of overt structural heart disease appears to be focal in nature with rapid termination during ablation. Regardless of the VT mechanism, patients with recurrent episodes, despite antiarrhythmic medication in the chronic stage following blunt chest injury, are likely to require ablation to achieve VT control. This review article will describe the mechanisms, pathophysiology, and treatment of ventricular arrhythmias that occur in both the acute and chronic stages following blunt chest trauma.

Peritricuspid annular prostate pellet

2021 ◽  
Vol 14 (2) ◽  
pp. e238076
Author(s):  
Bryan O'Sullivan ◽  
Richard Tanner ◽  
Peter Kelly ◽  
Gerard Fahy
Keyword(s):  
Right Ventricle ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Prostate Adenocarcinoma ◽  
Left Ventricular ◽  
Premature Ventricular Contractions ◽  
Left Ventricular Outflow ◽  
Metallic Object ◽  
The Right

A 75-year-old was treated for prostate adenocarcinoma with brachytherapy in September 2018. A routine follow-up chest radiograph 3 months later revealed a metallic object of the same dimensions as a brachytherapy pellet located in the right ventricle. Further imaging showed the brachtherapy pellet was located in the anterobasal right ventricular endocardium close to the tricuspid valve. Frequent asymptomatic premature ventricular contractions were observed with likely origin from the left ventricular outflow tract, an area remote from the site of the pellet. The patient remains asymptomatic and subsequent imaging shows that the position of the pellet has not changed.

Sustained and non-sustained ventricular tachycardia and no associated heart disease (idiopathic ventricular tachycardia)

ESC CardioMed ◽  
2018 ◽  
pp. 2288-2293
Author(s):  
Victor Bazan ◽  
Enrique Rodriguez-Font ◽  
Francis E. Marchlinski
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Drug Therapy ◽  
Catheter Ablation ◽  
Beta Blockers ◽  
Young Patients ◽  
Structural Heart Disease ◽  
Holter Monitoring ◽  
Severe Arrhythmia ◽  
The Right

Around 10% of ventricular arrhythmias (VA) occur in the absence of underlying structural heart disease. These so-called ‘idiopathic’ VAs usually have a benign clinical course. Only rarely do these “benign” arrhythmias trigger polymorphic ventricular tachycardia (PVT) and idiopathic ventricular fibrillation (VF). Due to their focal origin and to the absence of underlying myocardial scar, the 12-lead ECG very precisely establishes the right (RV) or left (LV) ventricular site of origin of the arrhythmia and can help regionalizing the origin of VT for ablation. A 12-lead ECG obtained during the baseline rhythm and 24-hour ECG Holter monitoring are indicated in order to identify structural or electrical disorders leading to PVT/VF and to determine the VA burden. The most frequent origin of idiopathic VAs is the RV outflow tract (OT). Other origins include the LVOT, the LV fascicles (fascicular VTs), the LV and RV papillary muscles, the crux cordis, the mitral and tricuspid annuli and the RV moderator band. Recognizing the typical anatomic sites of origin combined with a 12 lead ECG assessment facilitates localization.  Antiarrhythmic drug therapy (including use of beta-blockers) or catheter ablation may be indicated to suppress or eliminate idiopathic VAs, particularly upon severe arrhythmia-related symptoms or if the arrhythmia burden is high and ‘tachycardia’-induced cardiomyopathy is suspected. Catheter ablation is frequently preferred to prevent lifelong drug therapy in young patients.

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