Relationship of frequent postinfarction premature ventricular complexes to the reentry circuit of scar-related ventricular tachycardia.

Background Postinfarction reentrant ventricular tachycardia (VT) is usually scar-related. However, the sites of origin of premature ventricular complexes (PVCs) in the setting of healed myocardial infarction have not been well characterized. Objective The purpose of this study was to determine the site of origin of frequent PVCs in postinfarction patients with VT and to determine the relationship to VT exit sites. Methods Mapping and catheter ablation were performed in 13 consecutive patients (12 men, mean age 62 ± 8 years, mean ejection fraction 0.32 ± 0.12) with prior myocardial infarction, sustained monomorphic VT, and >10 PVCs/h. The mean PVC burden was 12% ± 11% on a 24-hour Holter monitor. Electroanatomical left ventricular voltage maps were constructed during sinus rhythm to identify scars. Endocardial activation maps of the PVCs were correlated with the voltage maps, and the most prevalent PVCs were ablated. The effect of PVC ablation on the inducibility of VT was determined. Results Seventeen sustained monomorphic VTs were reproducibly inducible. There were a total of 34 different PVC morphologies. The site of origin was identified for 18 of the 34 PVC morphologies in 12 of 13 patients. The 18 PVCs for which the site of origin could be identified accounted for 89% of the PVC burden in these patients. The site of PVC origin was in the infarct scar in 11 patients, the border zone in 1 patient, and unidentifiable in 1 patient. The site of PVC origin corresponded to the VT exit site for 14 of 17 reproducibly inducible VTs. The PVCs that were successfully mapped were ablated, and this rendered VT no longer inducible. Conclusion Postinfarction PVCs usually arise from the infarct scar, and their site of origin often corresponds to the exit site of a reentrant VT. Therefore, catheter ablation of the PVCs often is associated with the loss of inducible VT.