An extrapolation of electrophysiological findings to a specific clinical situation is not always feasible since successful arrhythmia analysis frequently is not achieved and even in the presence of a known arrhythmic mechanism, the predominant effect of a given antiarrhythmic agent cannot be predicted with respect to therapeutic relevance. These assertions are additionally supported by the fact that the effects of antiarrhythmic agents, which have been primarily studied in healthy myocardium, may be entirely different in the presence of myocardial ischemia. Furthermore, in spite of a certain degree of agreement among data of experimentally-induced and clinical myocardial ischemia, the findings do not imply complete applicability. Theoretical considerations indicate that a reentry mechanism may not only be favourable influenced by an agent rendering improved conduction velocity and shortened refractory periods but also influenced by an agent effecting oppositely directed changes. Although an effective therapeutic regimen can generally be achieved with no exact knowledge of the arrhythmic mechanism or of the specific action of a given drug, future investigations hould augment existing information to yield a more rational means of treatment and prevention of arrhythmias as well as to aid in the development of new antiarrhythmic agents.