DRUG-INDUCED VENTRICULAR-TACHYCARDIA

Certain drugs can induce ventricular tachycardia (VT) by creating reen try, ventricular after potentials or exaggerating the slope of phase 4 . These may or may not be symptomatic, sustained or non-sustained and have variable ECG appearances : monomorphic or polymorphic, bidirectio nal, torsades de pointes, They risk degenerating into ventricular flut ter or fibrillation and have been held responsible for the increased m ortality observed unexpectedly in some long-term treatments. The drugs responsible are mainly those used in cardiology, probably due to pred isposing circumstances (cardiomegaly, cardiac failure, previous severe ventricular arrhythmias, therapeutic associations, metabolic abnormal ities). These include primarily the antiarrhythmic drugs (IA, IC, sota lol and bepridil), digitalis, sympathomimetics and phosphodiesterase i nhibitors. These complications may be toxic or idiosyncratic, in patie nts with or without cardiac disease, and may also occur with other dru gs : vasodilators and anti-anginal drugs (lidoflazine, vincamine, feno xedil), psychotropic agents (phenothiazine and imipramine), antimitoti cs, antimalarials (chloroquine) or antibiotics (erythromycine, pentami dine). The prognosis is severe and the treatment is often difficult wh ich makes prevention, helped by repeated surface ECG (or Holter monito ring), very important with careful assessment of patients at risk.