Mechanisms of tachyarrhythmias, past and present.

Several hypotheses, developed in the early years of arrhythmology, and frequently used for the explanation of many types of clinical tachyarrhythmias, are often based on experiments on unusual models, unphysiologic interventions, or, in some instances, on erroneously interpreted histologic findings. However, it can be demonstrated that several of these hypotheses are valid. Focal activity, unidirectional block, extremely slow conduction velocity, differences in conduction velocity in closely adjacent regions, reentry of the excitation wave, circulating excitation waves in small or large regions of the heart and other postulated mechanisms as, for example, entrance and exit block, local ventricular fibrillation, appear to be involved in the causative mechanisms of clinical tachyarrhythmias. A multicausal genesis of at least some of these must be considered seriously, particularly those which occur in acute or chronic coronary heart disease. A recent suggestion that the injury current might be involved in the genesis of ventricular tachyarrhythmias in acute myocardial ischemia and infarction is supported by observations on several properties of this current. Progress has been made in recent years but large gaps in our knowledge of mechanisms causing arrhythmias are still present.