Incessant ventricular tachycardia: a lost case or new hope?

Editorials Incessant ventricular tachycardia: a lost case or new hope? Ventricular tachycardia remains a difficult problem in spite of all the recent advances. Anti-arrhythmic drugs continue to fail in more and more trials, and it is unlikely that we will have effective (and safe) drugs based on new principles in the near future'' 1. In contrast, the results of implantable cardioverter/ defibrillator therapy remain very encouraging, in particular in patients with ventricular tachycardia. Furthermore, implantable anti-arrhythmic devices are being continually improved, and implantable cardioverters/defibrillators now resemble the shape of the early pacemakers. Therefore, it is very tempting to skip anti-arrhythmic drug treatment, and to proceed immediately to implantable cardioverter/defibrillator therapy. However, the paper of Cao and Gonska in this issue is an illustration of the fact that such an approach is not always the right one' 21. If implantable cardioverters/defibrillators give a shock, and terminate a sustained tachycardia, they do what we expect them to do. However, ventricular tachycardia does not always behave as we would like, and when such an arrhythmia becomes 'incessant' this poses a major problem with respect to survival. On such occasions implantable cardioverters/ defibrillators usually give multiple shocks or intervene with antitachycardia pacing, but fail to prevent immediate recurrences. We expect anti-arrhythmic drugs to prevent recurrences but the clinical status of those patients with incessant tachycardia will often deteriorate because of the myocardial depressant or vasodilating effect of the therapy. Drugs are even incriminated in the pathogenesis of the incessant mechanism because they slow conduction, and enhance re-entry, sustaining arrhythmias which would otherwise have been short and sometimes even asymptomatic. This pro-arrhythmic mechanism is well known for drugs such as procainamide, disopyramide, flecainide, propaf-enone, cibenzoline, and probably all other sodium-channel-blockers' 3 ' 4 '. We have also observed several patients who were referred for treatment only after episodic tachycardia became incessant in the course of amiodarone loading, causing severe left ventricular dysfunction. This rather specific pro-arrhythmic property of amiodarone might be the most important one from the clinical point of view. Furthermore, it is now well established that amiodarone increases the defibrillation threshold, and this corresponds with earlier clinical observations' 51. This may be another reason to avoid the use of amiodarone in the setting of incessant tachycardia. Therefore, even amio-darone, a drug that we have used for about 20 years in Europe, has no definite place in the treatment of incessant ventricular tachycardia. It …