[Torsade de pointes syndromes. Variations and limits].
Advances in cardiac rhythm studies have led to more precise definitions of wave burst arrhythmias since they were first described by Dessertenne. This progress has also broadened the scope of these arrhythmias and the initially defined limits no longer apply. Prolonged Q-T syndromes, whether inherited or acquired, remain the standard, characterized by the ECG so typical of tachycardiac rhythms with long coupling of the initial extrasystole. In the congenital forms, neurogenic, sympathetic stimulation plays a triggering role, whereas sympathetic hypertonia of humoral origin protects acquired forms. Catecholaminergic ventricular tachycardia is clearly related to congenital Q-T syndrome and involves the same treatment, but tends to show idiosyncrasy to quinidine compounds, in common with acquired forms of Q-T syndrome. Short-coupling wave burst arrhythmias are congenital and in principle idiopathic. They have triggering factors in common with acquired prolonged Q-T syndromes, but their interactions with the autonomic nervous system are more complex; the vagus and sympathetic nerves are equally implicated and these interactions are curiously sensitive to calcium antagonists. These four related syndromes form an "ill-defined group" the limits of which will become clearer as more knowledge is acquired regarding the substrate and the interactions with the autonomic nervous system.
D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology; D001919:Bradycardia / Q000503:physiopathology; D002648:Child; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008133:Long QT Syndrome / Q000151:congenital / Q000209:etiology / Q000503:physiopathology; D008297:Male; D005082:Physical Exertion; D011802:Quinidine / Q000009:adverse effects; D013610:Tachycardia / Q000503:physiopathology*; D014883:Water-Electrolyte Imbalance / Q000503:physiopathology
D011802:Quinidine
Les syndromes de torsades de pointes. Variétés et limites.