Pathophysiological mechanisms of ventricular tachyarrhythmias

The pathophysiological background for ventricular tachyarrhythmias based on experimental and clinical evidence is presented. Sudden cardiac death may occur as the first manifestation of coronary artery disease without antecedent complaints or it may occur in patients with a previous myocardial infarction. In the latter situation, a circumscribed area of cardiac tissue may be responsible for the genesis and maintenance of a ventricular tachyarrhythmia which may be called the 'arrhythmogenic substrate'. This zone of electrically abnormal ventricular myocardium is usually located at the border of a previous myocardial infarction, and is characterized by islands of relatively viable muscle alternating with areas of necrosis and, later, fibrosis. The consequent fragmentation of the propagating electromotive forces leads to the development of high-frequency components that can be recorded directly or non-invasively using signal-averaging techniques. These signals have been called ventricular late potentials. The 'arrhythmogenic substrate' may be present permanently or may rise acutely and be present only transiently in the case of extensive ischaemia or acute myocardial infarction. In the setting of a chronic 'arrhythmogenic substrate', this electrically abnormal tissue may be triggered by spontaneously occurring ventricular ectopic beats or salvoes or by programmed ventricular stimulation, as well as by transient episodes of ischaemic causing spontaneous arrhythmias. These trigger factors modify the 'arrhythmogenic substrate' in such a way that ventricular tachyarrhythmias are sustained. It is apparent that sudden cardiac death is due to a wide spectrum of pathophysiological mechanisms which may be interrelated. There is obviously no single parameter that helps the clinician to predict the propensity for sudden cardiac death in the individual patient.