For the acute myocardial infarction and sudden cardiac death a circadian variation can be observed. There are several, mostly epidemiological studies that demonstrate this non-uniform distribution of events in different day-time periods. These studies are in the vast majority based on eye-witness reports, medical documents and retrospective evaluation of the timing of the event. Moreover, they represent only singular observations in a heterogeneous population. With the introduction of implantable cardioverter-defibrillators which provide extensive diagnostic features such as stored RR-intervals, endocardial electrograms of each episode and internal time storage, an exact analysis of the circadian variation of malignant ventricular tachyarrhythmias became feasible. Ventricular tachyarrhythmias follow a different circadian distribution with increased number of events at certain day-time periods. For patients with a coronary artery disease a significantly higher risk to experience a potentially fatal arrhythmia could be shown for the mid-morning hours and a secondary peak occurrence for the late afternoon and the early evening. Patients with idiopathic dilated cardiomyopathy tend to have a higher probability of events in the evening hours. With respect to beta-blockers and other antiarrhythmic drugs most of the studies failed to confirm a blunting influence on the degree of variability for fast arrhythmias. Others showed similar patterns for fast and slow tachycardias. Another clinical parameter, the degree of congestive heart failure was in some studies found to influence the pattern in the sense of causing a distinct difference in occurrence frequency. A higher vairation was determined for lower NYHA classes < III. Other studies were contrary to these findings. The activity level before the onset of arrhythmias has yet been only insufficiently analyzed regarding the day-time-variability. But first results make believe, that patients younger than 50 years and still involved in the working process seem to follow a more varying circadian distribution. More substudies will have to be performed to compare working and nonworking patients and patients with different structural heart diseases. Furthermore ther influence of antiarrhythmic agents on the day-time-variation of ventricular tachyarrhythmias should be assessed. Finally, there, should be systematic prospective studies that evaluate the influence of drug administration on triggers of ventricular tachyarrhythmias such as sympathoadrenergic activity, premature ventricular beats, reduction of heart rate variability and others with respect to their day-time-variability.