[Cardiac insufficiency: prevention of ventricular arrhythmias]

Ventricular arrhythmias are particularly common in cardiac failure and their mechanisms are very complex. The prevention of these ventricular arrhythmias is only worthwhile if it results in benefits in terms of reduction of the risk of sudden death and in improvement in life expectancy. However, the relationship between complex ventricular arrhythmias and sudden death is far from established. The first problem is, therefore, to select the patients at high risk of sudden death. Unfortunately, there are no reliable markers of arrhythmic risk; only patients at low risk can be reasonably well identified on clinical and haemodynamic assessment and the results of ambulatory and signal averaged ECG. When an antiarrhythmic treatment seems to be required, the choice is very limited 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 arrhythmias, 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 discordance 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 special profile such as carvedilol, has been clearly established. In association with conventional diuretics and angiotensin converting enzyme inhibitors, they reduce global mortality by about 35% and sudden death by 40%. However, the future possibly lies with non-pharmacological approaches such as the implantable defibrillator, at least in patients clearly identified as being at high risk of arrhythmic death, resuscitated from cardiorespiratory arrest due to documented ventricular fibrillation or presenting with haemodynamically poorly tolerated ventricular tachycardia. The automatic defibrillator could improve the prognosis of these patients, irrespective of their functional status (NYHA, Classes I, II or III). In practice, "rhythmological" management of cardiac failure cannot be dissociated from the haemodynamic and neuro-hormonal aspects of the affection, and only a multi-factorial approach is being realistic.