Nonsustained ventricular tachycardia in patients without structural heart disease

2017 ◽  
Vol 2 (43) ◽  
pp. 18-22
Author(s):  
Agnieszka Wojdyła-Hordyńska ◽  
Grzegorz Hordyński ◽  
Patrycja Pruszkowska-Skrzep ◽  
Oskar Kowalski
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Beta Blockers ◽  
Structural Heart Disease ◽  
Differential Diagnostics ◽  
Percutaneous Ablation ◽  
Nonsustained Ventricular Tachycardia ◽  
Clinical Consequences ◽  
Exercise Induced ◽  
Genetic Heart Disease

Nonsustained ventricular tachycardia (NSVT) is usually a mild entity without serious clinical consequences. Nevertheless, exercise-induced NSVT, and short cycle length of tachycardia, significant arrhythmia burden may predict increased cardiac mortality. NSVT is defined as 3 or more consecutive ventricular beats with a rate over 100 beats/min or more, lasting less than 30 s, that can be diagnosed on the basis of electrocardiography, Holter, telemetry, cardiac monitors or exercise test, after careful wide QRS tachycardia differential diagnostics, artefacts, supraventricular tachycardia with aberration, Hiss-Purkinje block or additional atrio-ventricular pathway descending conduction exclusion. It is necessary to assess homogeneity of the tachycardia (monomorphic or polymorphic), exclude ischemic, structural and genetic heart disease. The treatment is based on observation, farmacotherapy (mainly with beta-blockers, calcium channels blockers and antiarrhythmics) and percutaneous ablation. Implantable cardioverter-defibrillator is not recommended. The prognosis is usually good.

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.

scholarly journals Exercise-Induced Sustained Ventricular Tachycardia without Structural Heart Disease: A Case Report

2020 ◽  
Vol 21 ◽  
Author(s):  
Michelle Audrey Darmadi ◽  
Axel Duval ◽  
Hanaa Khadraoui ◽  
Alberto N. Romero ◽  
Blanca Simon ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Case Report ◽  
Structural Heart Disease ◽  
Sustained Ventricular Tachycardia ◽  
Exercise Induced

Sustained monomorphic ventricular tachycardia associated with structural heart disease: classification, assessment, and initial treatment

ESC CardioMed ◽  
2018 ◽  
pp. 2265-2270
Author(s):  
Fernando M. Contreras-Valdes ◽  
Peter J. Zimetbaum
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Sudden Death ◽  
Beta Blockers ◽  
Substantial Reduction ◽  
Structural Heart Disease ◽  
Disease Classification ◽  
Implantable Cardioverter Defibrillators ◽  
Monomorphic Ventricular Tachycardia ◽  
Cardioverter Defibrillators

Sustained monomorphic ventricular tachycardia occurs in patients with structural heart disease and may lead to syncope, haemodynamic collapse, or sudden death. The diagnosis is established by the electrocardiogram, with cardiac imaging used to determine the underlying substrate. Initial management requires a combination of electrical cardioversion and antiarrhythmic drugs, mainly amiodarone and beta blockers. Nonetheless, implantable cardioverter defibrillators provide the most substantial reduction in sudden death, with catheter ablation becoming an increasingly favoured strategy to minimize shocks and possibly lower mortality from ventricular arrhythmias in this population.

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.

scholarly journals Additive beneficial effects of beta blockers in the prevention of symptomatic heart failure

2016 ◽  
Vol 72 (1) ◽  
Author(s):  
Alberto Genovesi Ebert ◽  
Furio Colivicchi ◽  
Marco Malvezzi Caracciolo ◽  
Carmine Riccio
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Heart Disease ◽  
Beta Blockers ◽  
Structural Heart Disease ◽  
Symptomatic Heart Failure ◽  
Post Hoc Analysis ◽  
Lv Dysfunction ◽  
History Of ◽  
Post Hoc

The prevention of symptomatic heart failure represents the treatment of patients in the A and B stages of AHA/ACC heart failure classification. Stage A refers to patients without structural heart disease but at risk to develop chronic heart failure. The major risk factors in stage A are hypertension, diabetes, atherosclerosis, family history of coronary artery disease and history of cardiotoxic drug use. In this stage, blockers hypertension is the primary area in which beta blockers may be useful. Beta blockers seem not to be superior to other medication in reducing the development of heart failure due to hypertension. Stage B heart failure refers to structural heart disease but without symptoms of heart failure. This includes patients with asymptomatic valvular disease, asymptomatic left ventricular (LV) dysfunction, previous myocardial infarction with or without LV dysfunction. In asymptomatic valvular disease no data are available on the efficacy of beta blockers to prevent heart failure. In asymptomatic LV dysfunction only few asymptomatic patients have been enrolled in the trials which tested beta blockers. NYHA I patients were barely 228 in the MDC, MERIT and ANZ trials altogether. The REVERT trial was the only trial focusing on NYHA I patients with LV ejection fraction less than 40%. Metoprolol extended release on top of ACE inhibitors ameliorated LV systolic volume and ejection fraction. A post hoc analysis of the SOLVD Prevention trial demonstrated that beta blockers reduced death and development of heart failure. Similar results were reported in post MI patients in a post hoc analysis of the SAVE trial (Asymptomatic LV failure post myocardial infarction). In the CAPRICORN trial about 65% of the patients were not taking diuretics and then could be considered asymptomatic. The study revealed a reduction in mortality and a non-significant trend toward reduction of death and hospital admission for heart failure. Conclusions: beta blockers are not specifically indicated in stage A heart failure. On the contrary, in most of the stage B patients, and particularly after MI, beta blockers are indicated to reduce mortality and, probably, also the progression toward symptomatic heart failure.

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