Effects of pharmacological and non-pharmacological interventions on ventricular late potentials.

The purpose of this paper is to review the presently available information on the effect of antiarrhythmic drugs and of map-guided antitachycardia surgery on ventricular late potentials. Studies in experimental myocardial infarction have shown that antiarrhythmic drugs are able to prolong regional low-amplitude fractionated electrical activity. However, no correlation between changes in duration of low-amplitude electrical activity and antiarrhythmic drug efficacy could be demonstrated. A similar lack of correlation between changes in duration of late potentials as recorded by the signal averaging technique from the body surface and inducibility or suppression of ventricular tachycardia were observed. Neither changes in duration or amplitude nor in the frequency content of ventricular late potentials showed an unequivocal correlation with drug efficacy. By contrast, there is convincing evidence that exclusion of arrhythmogenic tissue by map-guided antitachycardia surgery correlates with the loss of late potentials postoperatively in a high percentage of cases. If, however, late potentials persist after surgery, there is a high chance of ventricular tachycardia being still inducible postoperatively. A loss of ventricular late potentials by surgery may be the result of isolation of the arrhythmogenic tissue, devitalization and/or removal. In conclusion, there is presently no convincing evidence that any of the parameters for characterization of ventricular late potentials is clinically useful to predict the efficacy of antiarrhythmic drug therapy. On the other hand, ventricular late potentials have proved useful for prediction of the success of map-guided antitachycardia surgery.