[Ventricular arrhythmias].
Tachycardias arise from an arrhythmogenic substrate triggered by a random factor (generally an extrasystole) and modulated by the autonomic nervous system. The three components are interactive, but their intensity and conjunction vary continuously. During the last decade, major achievements have been made to clarify definition and classification of data reported in the literature, helping our understanding of the mechanisms of ventricular arrhythmias. Nowadays, the pathophysiology of cardiac arrhythmias is well-known at the cellular and molecular ion channel activity. The progress of epidemiology and molecular genetics have allowed a better knowledge of the genotype-phenotype correlation in young patients presenting syncopes due to torsades de pointes or polymorphic ventricular tachychardia episodes which may degenerate into ventricular fibrillation and cause sudden death. The data of numerous large prospective randomised studies have led to more rational treatments with the progressive withdrawal of class I antiarrhythmics and their replacement by betablocking agents. The surgical approach of ventricular tachycardia has been overcome by the automatic implantable defibrillator and in some well-defined clinical situations, catheter ablation is used.
Waleffe
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Service de Cardiologie, CHU Liège.
Piérard
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D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000367:Age Factors; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D016757:Death, Sudden, Cardiac; D017147:Defibrillators, Implantable; D005838:Genotype; D006801:Humans; D010641:Phenotype; D016032:Randomized Controlled Trials as Topic; D017180:Tachycardia, Ventricular / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D014693:Ventricular Fibrillation / Q000188:drug therapy* / Q000517:prevention & control
D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents