Cardiac failure: Prevention of ventricular arrhythmias.

Ventricular arrhythmias are particularly common in cardiac failure and thei r mechanisms are very complex. The prevention of these ventricular arrhythm ias is only worthwhile if it results in benefits in terms of reduction of t he risk of sudden death and in improvement in life expectancy. However, the relationship between complex ventricular arrhythmias and sudden death is f ar from established. The first problem is, therefore, to select the patient s at high risk of sudden death. Unfortunately, there are no reliable marker s of arrhythmic risk: only patients at low risk can be reasonably well iden tified on clinical and haemodynamic assessment and the results of ambulator y and signal averaged EGG. When an antiarrhythmic treatment seems to be required, the choice is very l imited in practice. There is no role for Class I antiarrhythmics to play in this indication. Amiodarone, with its complex electrophysiological profile enabling an interaction with all potential mechanisms of ventricular arrhy thmias, is a first-line drug in cardiac failure because of its efficacy and good myocardial tolerance. However, the benefits of amiodarone therapy in terms of reduction of global mortality have not been demonstrated, especially in view of the discordanc e between the results of the GESICA and CHF STAT trials. On the other hand, the Value of betablockers, whether conventional molecules like bisoprolol (CIBIS II study) or metoprolol (MERIT-HF study), or molecules with a specia l profile such as carvedilol, has been clearly established. In association with conventional diuretics and angiotensin converting enzyme inhibitors, t hey reduce global mortality by about 35% and sudden death by 40%. However, the future possibly lies with non-pharmacological approaches such as the im plantable defibrillator, at least in patients clearly identified as being a t high risk of arrhythmic death, resuscitated from cardiorespiratory arrest due to documented ventricular fibrillation or presenting with haemodynamic ally poorly tolerated ventricular tachycardia. The automatic defibrillator could improve the prognosis of these patients, irrespective of their functi onal status (NYHA, Classes I, II or III). In practice, "rhythmoIogical" management of cardiac failure cannot be disso ciated from the haemodynamic and neuro-hormonal aspects of the affection, a nd only a multi-factorial approach is being realistic.