TORSADES-DE-POINTES

Torsades de pointes are defined and characterised by specific, polymor phic but organised ventricular activation on the surface electrocardio gramme. They constitute episodes of rapid tachycardia which are usuall y short lasting and terminate spontaneously. However, they may recur a nd persist, leading to syncope or sudden death. They occur typically i n cases with abnormalities of ventricular repolarisation with prolonga tion of the QTU interval and variable deformations of the TU waves. Th e basal abnormalities may be modest or intermittent. A bigeminy with a long coupling interval and alternating long and short cycles often pr ecede the burst of arrhythmia. Abnormalities of ventricular repolarisa tion and torsades de pointes may be the result of congenital syndromes (catecholamine-dependant torsades) or acquired factors (pause-dependa nt torsades) such as paroxysmal bradycardia, drugs which prolong the r epolarisation and potassium and magnesium deficiencies. The electrophy siological mechanisms comprise reentry and after depolarisation induce d activity genetic factors causing abnormalities of the G-proteins, po tassium currents or adrenergic receptors may also play a role. Emergen cy treatment consists of intravenous magnesium salts, sometimes of bet ablockers or verapamil for maintenance therapy. The association of a p otassium-sparing drug may be useful. Cardiac pacing may be necessary. Left sympathetic denervation or implantation of an automatic defibrill ator are exceptional therapeutic options in refractory congenital tors ades de pointes.