Sudden cardiac death is a leading cause of death in industrially developed countries and accounts for approximately 90 000 deaths yearly in the FRG. While the majority of victims have severe coronary heart disease, sudden cardiac death is infrequently caused by acute myocardial infarction (20%) but is predominantly related to malignant ventricular arrhythmias (i.e., ventricular fibrillation or sustained ventricular tachycardia). Patients with a history of such malignant ventricular arrhythmias are at high risk for sudden death. Spontaneous occurrence of sustained ventricular tachycardia and of ventricular fibrillation is critically related to two factors: 1. trigger-arrhythmias consisting usually of complex ventricular extrasystoles (Lown classification IV to V); 2. increased vulnerability of the myocardium representing the target organ for trigger-arrhythmias. While trigger-arrhythmias can be easily recorded by noninvasive techniques including Holter monitoring or exercise and stress ECG, ventricular vulnerability is more difficult to determine and often requires ventricular stimulation with intracardiac electrocatheters. In patients with documented spontaneous malignant ventricular arrhythmias, two aspects of programmed stimulation must be considered: 1. diagnostic, and more importantly, 2. therapeutic purposes of this method. Diagnostic purposes include determination of the mode of initiation and unequivocal ventricular localization of the tachycardia excluding other arrhythmias with broad QRS complex. In patients with spontaneous sustained ventricular tachycardia, programmed stimulation can reproducibly initiate the clinical arrhythmia in 85% (sensitivity and specificity of the method approximately 90%). In patients with cardiac arrest due to ventricular fibrillation, programmed stimulation is less reliable (50%). However, the main purpose of programmed stimulation in patients with documented clinical malignant arrhythmias is not diagnostic or prognostic evaluation but is serial electrophysiological studies for individual optimization of antiarrhythmic therapy.