The multifactorial pathogenesis of sudden death explains, on the one hand, the inadequacy of an unilateral approach to its mechanism and, on the other hand, the failure of its prevention. Antiarrhythmics have been widely used clinically after myocardial infarction in the hope of reducing mortality due to arrhythmias and/or global mortality. Since the publication of the CAST study, the arrhythmia hypothesis, according to which the suppression of asymptomatic arrhythmias would decrease mortality, has been disproved. Class Ic antiarrhythmic agents were associated with a higher mortality rate than placebo. Class IV antiarrhythmics have not been shown to improve survival in the post-infarction period though the results are not definitive because of the great difference between drugs of this class. For the moment, only Class II antiarrhythmics have been shown to be beneficial including patients with low ejection fractions. The Class III antiarrhythmics and, in particular, amiodarone, have been shown to have a beneficial effect in the prevention of sudden death and a recent meta-analysis has demonstrated a 33% increase in survival with amiodarone. Three large scale prospective trials are currently under way and their results should confirm the positive impression already gained: EMIAT (European Myocardial Infarction Amiodarone Trial) will include 1,500 patients after myocardial infarction with poor left ventricular function (EF < 40%); CAMIAT (Canadian Myocardial Infarction Amiodarone Trial) will include 1,200 patients with myocardial infarction and asymptomatic arrhythmias (> 10 VES per hour); VA320 is an American trial under way in Veteran Administration Centres; 720 patients with dilated cardiomyopathy (EF < or = 40%) and arrhythmias (> 10 VES per hour) have been included.(ABSTRACT TRUNCATED AT 250 WORDS)