Background: Termination of ventricular tachycardia (VT) by mechanical pressure has been described for fascicular and postinfarction VT. Mechanical interruption of idiopathic ventricular arrhythmias (VT/premature ventricular complexes [PVCs]) arising in the right ventricular outflow tract (RVOT) has not been described in systematic fashion.
Methods: Eighteen consecutive patients (13 females, age 49 +/- 13 years, ejection fraction 0.55 +/- 0.12) underwent mapping and ablation of RVOT VT or PVCs. In 7 patients, 9 distinct VTs (mean cycle length 440 +/- 127 ms), and in 11 patients, 11 distinct PVCs originating in the RVOT were targeted. Mechanical termination was considered present if a reproducibly inducible VT was no longer inducible or if frequent PVCs suddenly ceased with the mapping catheter at a particular location. Endocardial activation time, electrogram characteristics, and pace-mapping morphology were assessed at this location. Radiofrequency energy was delivered if mechanical termination was observed.
Results: All targeted arrhythmias were successfully ablated. In 7 of 18 patients (39%), catheter manipulation terminated the arrhythmia with the mapping catheter located at a particular site. Local endocardial activation time was earlier at sites of mechanical termination (-31 +/- 7 ms) compared with effective sites without termination (-25 +/- 3 ms, P = 0.04). The 10-ms isochronal area was smaller in patients with mechanical interruption (0.35 +/- 0.2 cm(2)) than in patients without mechanical termination (1.33 +/- 0.9 cm(2), P = 0.01). At all sites susceptible to mechanical trauma, the pace map displayed a match with the targeted VT/PVC. All sites where mechanical termination of VT or PVCs occurred were effective ablation sites.
Conclusions: Mechanical suppression at the site of origin of idiopathic RVOT arrhythmias frequently occurs during the mapping procedure and is a reliable indicator of effective ablation sites. Mechanical termination of RVOT arrhythmias may be indicative of a more localized arrhythmogenic substrate.