title: Pattern of initiation of monomorphic ventricular tachycardia and implications on tachycardia mechanism.
abstract: The incidence of sudden cardiac death, predominantly caused by ventricular tachycardia and ventricular fibrillation, is high in patients with congestive heart failure. Implantable cardiac defibrillators have improved survival in this population but defibrillator shocks can lead to low quality of life and heart failure progression. The current management of recurrent ventricular tachycardia includes ablation and anti-arrhythmic drugs and both are associated with high recurrence rates. Better understanding the mechanism of ventricular tachycardia allowing individualization of treatment may improve outcomes. Re-entry is currently accepted as the mechanism of the majority of monomorphic ventricular tachycardias in patients with congestive heart failure, being responsible for more than 90% of the ventricular tachycardia in patients with ischemic cardiomyopathy. On the other hand, some studies show a greater participation of focal arrhythmias in the genesis of ventricular tachycardia in this population. The pattern of initiation of ventricular tachycardia is divided into sudden, when the first beat of the tachycardia is morphologically similar to the rest of the tachycardia, and non-sudden, when its morphology is dissimilar. An association between the pattern of the initiation and the mechanism of ventricular tachycardia has been proposed. The pattern of initiation of ventricular tachycardia is a readily available from data stored in current generation implantable cardiac defibrillators. The association with tachycardia mechanism may allow individualization of the therapy, however evidence is lacking and further research is required.
authors.affiliation: McGill University, Montreal, QC, Canada.|Hospital Albert Sabin, Juiz de Fora, MG, Brazil.
authors.forename: Rodrigo S
authors.initials: RS
authors.lastname: Barbosa
authors.affiliation: Department of Physiology, McGill University Health Centre Research Institute, Montreal, QC, Canada.
authors.forename: Leon
authors.initials: L
authors.lastname: Glass
authors.affiliation: Morriston Hospital, Swansea, UK.
authors.forename: Riccardo
authors.initials: R
authors.lastname: Proietti
authors.affiliation: McGill University, Montreal, QC, Canada.
authors.forename: Barry
authors.initials: B
authors.lastname: Burstein
authors.affiliation: Department of Physiology, McGill University Health Centre Research Institute, Montreal, QC, Canada.
authors.forename: Lyndon
authors.initials: L
authors.lastname: Sobolik
authors.affiliation: Department of Physiology, McGill University Health Centre Research Institute, Montreal, QC, Canada.
authors.forename: Zhubo D
authors.initials: ZD
authors.lastname: Zhang
authors.affiliation: McGill University, Montreal, QC, Canada.
authors.forename: Guillaume
authors.initials: G
authors.lastname: Viart
authors.affiliation: Department of Physiology, McGill University Health Centre Research Institute, Montreal, QC, Canada.
authors.forename: Alvin
authors.initials: A
authors.lastname: Shrier
authors.affiliation: McGill University, Montreal, QC, Canada - vidal.essebag@mcgill.ca.|Sacré-Coeur Hospital, Montreal, QC, Canada.
authors.forename: Vidal
authors.initials: V
authors.lastname: Essebag
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D016757:Death, Sudden, Cardiac / Q000453:epidemiology; D017147:Defibrillators, Implantable; D006333:Heart Failure / Q000150:complications / Q000453:epidemiology / Q000628:therapy; D006801:Humans; D011788:Quality of Life; D017180:Tachycardia, Ventricular / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy*; D014693:Ventricular Fibrillation / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy*
chemical_list: D000889:Anti-Arrhythmia Agents