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Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752
Online ISSN 1827-1618
Sanders P., Hsu L. F., Hocini M., Jaïs P., Takahashi Y., Rotter M., Sacher F., Pasquié J. L., Arentz T., Scavée C., Garrigue S., Clémenty J., Haïssaguerre M.
Sudden cardiac death frequently results from ventricular fibrillation (VF). While VF is frequently the eventual mode of death in patients with abnormal ventricular substrates, it has also been described in patients with structurally normally hearts. Until recently, the management of patients who have survived sudden cardiac death has focused on treating the consequences by implantation of a defibrillator. However, such therapy remains restricted in many countries, is associated with a prohibitive cost to the community, and may be a cause of significant morbidity in patients with frequent episodes or storms of arrhythmia. Evidence emerging from the study of fibrillation both in the atria and the ventricle suggests an important role for triggers arising from the Purkinje network or the right ventricular outflow tract in the initiation of VF. Initial experience in patients with idiopathic VF and even those with VF associated with abnormal repolarization syndromes (LQT or Brugada syndrome) or myocardial infarction suggests that long term suppression of recurrent VF may be feasible by the elimination of these triggers. With the development of new mapping and ablation technologies, and greater physician experience, catheter ablation of VF, with the ultimate aim of curing such patients at risks of sudden cardiac death, may not be an unrealistic goal in the future.