Functional role of the epicardium in postinfarction ventricular tachycardia. Observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation.

BACKGROUND

Conventionally, monomorphic sustained ventricular tachycardia in patients with remote myocardial infarction is believed to originate from the subendocardium. In a previous study, we demonstrated that electrical activation patterns during ventricular tachycardia occasionally suggest a subepicardial rather than subendocardial reentry.

METHODS AND RESULTS

This study prospectively evaluated the functional role of the epicardium in postinfarction ventricular tachycardia with complex intraoperative techniques including computerized electrical activation mapping, entrainment, observation of changes in activation pattern during successful epicardial laser photoblation, and histological study. Five of 10 consecutive patients undergoing intraoperative computerized activation mapping had 10 ventricular tachycardia morphologies displaying epicardial diastolic activation These 10 "epicardial" ventricular tachycardias revealed the following global activation patterns: monoregional spread (two), figure-eight activation (five), and circular macroreentry (three). Entrainment of ventricular tachycardia using epicardial stimulation was successfully performed from an area of slow diastolic conduction in four tachycardia morphologies. During entrainment, global activation remained undisturbed with recordings showing a long stimulus to QRS interval, unchanged QRS morphology, and pacing capture of all components of the reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation was delivered during ventricular tachycardia to epicardial sites of presumed reentry. Epicardial photoablation terminated five of five figure-eight tachycardias, two of three circular macroreentry tachycardias but not the monoregional tachycardias. Electrophysiological recordings during epicardial laser photocoagulation demonstrated progressive prolongation of ventricular tachycardia cycle length and apparent interruption of the presumed reentrant circuit. Histological evaluation of the reentrant region (three patients) showed a rim of surviving myocardium under the epicardial surface.

CONCLUSIONS

This study suggests that 1) chronic postinfarction ventricular tachycardia may result from subepicardial macroreentry, 2) slow conduction within the reentry circuit can be localized by computerized mapping and epicardial entrainment, and 3) ventricular tachycardia interruption by laser photocoagulation results from conduction delay and block within critical elements of the reentrant pathway. Viable subepicardial muscle fibers may constitute the underlying pathology.