Ventricular arrhythmias and sudden cardiac death: an insight from recent multicenter randomized clinical trials.

While post-myocardial infarct patients with frequent ventricular premature contractions or nonsustained ventricular tachycardia (NSVT) are at an increased risk of sudden arrhythmic death, the empirical use of antiarrhythmic agents for such patients is no longer justified after the results of the Cardiac Arrhythmia Suppression Trial. A series of major breakthroughs in the design and clinical application of the implantable cardioverter defibrillator (ICD) have taken place over the past two decades since its invention by M Mirowski. Although there is a general consensus for the effectiveness of the ICD therapy in aborting sudden arrhythmic death, it is unknown whether the use of the ICD therapy results in prolonged survival. Three randomized clinical trials directed to the survivors of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation (VF) are currently in progress, comparing the ICD therapy with drug therapy (amiodarone, beta blockers, and sotalol). Already over seventeen hundred patients have been randomized and followed in these three clinical trials. All three trials continue currently indicating no emergence of statistically significant differences in total mortality between the two therapy groups. Prophylactic application of the ICD has been studied in the MADIT (Multicenter Automatic Defibrillator Implantation Trial)--the first randomized clinical trial dealing with implantable defibrillators. This study enrolled post-transmural infarct patients having documented NSVT, left ventricular dysfunction (ejection fraction 35% or lower) and inducible and nonsuppressible NSVT. The study was recently terminated because of an emergence of a highly significant lower mortality with the ICD therapy than with conventional drug therapy. The future for patients at an increased risk of sudden cardiac death is much brighter with future refinement of the ICD system and antiarrhythmic drug therapy, and with further improvement in the therapy directed at the underlying structural heart disease.