Mapping and ablation of frequent post-infarction premature ventricular complexes.

INTRODUCTION

Premature ventricular complexes (PVCs) occur frequently in patients with heart disease. The sites of origin of PVCs in patients with prior myocardial infarction and the response to catheter ablation have not been systematically assessed.

METHODS AND RESULTS

In 28 consecutive patients (24 men, age 60 ± 10, ejection fraction [EF] 0.37 ± 0.14) with remote myocardial infarction referred for catheter ablation of symptomatic refractory PVCs, the PVCs were mapped by activation mapping or pace mapping using an irrigated-tip catheter in conjunction with an electroanatomic mapping system. The site of origin (SOO) was classified as being within low-voltage (scar) tissue (amplitude ≤1.5 mV) or tissue with preserved voltage (>1.5 mV). The SOO was confined to endocardial scar tissue in 24/28 patients (86%). The SOO was outside of scar in 3 patients and could not be identified in 1 patient. At the SOO, local endocardial activation preceded the PVC by 46 ± 19 ms, and the electrogram amplitude during sinus rhythm was 0.48 ± 0.34 mV. The PVCs were effectively ablated in 25/28 patients (89%), resulting in a decrease in PVC burden on a 24-hour Holter monitor from 15.6 ± 12.3% to 2.4 ± 4.2% (P < 0.001). The SOO most often was confined to scar tissue located in the left ventricular septum and the papillary muscles.

CONCLUSION

Similar to post-infarction ventricular tachycardia, PVCs after remote myocardial infarction most often originate within scar tissue. Catheter ablation of these PVCs has a high-success rate.