Mental activity, adrenergic modulation, and cardiac arrhythmias in patients with heart disease. All of the electrophysiological mechanisms of arrhythmias are sensitive to the influences of the autonomic nervous system, particularly to its adrenergic limb. Arrhythmogenic areas may also be dependent on the inhomogeneity of these influences because of their pathophysiological structure and/or the neurogenic or humoral nature of the vector of modulation. The complexity of the various possible scenarios, combined with the role of the rate dependence, explains why standardized protocols exploring the autonomic nervous system in clinical arrhythmias are difficult to define. Invasive electrophysiology is not adapted to address the problem. Isoprenaline infusion only reproduces the humoral adrenergic stimulation to which only a few types of arrhythmias are sensitive. The exercise test is a very complex investigation if the multiple parameters involved are considered. Only a part of its limitations are obviated by the mental stress. Under natural conditions, the neurogenic origin, the intensity of the sympathetic stimulation, and its suddenness are all critical factors responsible for severe tachyarrhythmias. Arrhythmias of the long QT syndrome are particularly demonstrative of the importance of the autonomic nervous system, but this evidence can also be documented in more trivial circumstances of diseased or apparently undiseased hearts. Exploring the autonomic nervous system behavior through heart rate variability in ambulatory recordings is the most recent and fruitful method of investigation. This nonprovocative approach has technical obstacles and practical and theoretical limitations related to the fundamental nature of the autonomic nervous system, which is both a marker of the cardiac status and a determinant of arrhythmias. 