Radiofrequency Ablation of Infarct Scar-Related Ventricular Tachycardia: Correlation of Electroanatomical Data with Post-Mortem Histology


  • Dr. Koa-Wing and Professor Peters are funded by the British Heart Foundation.

  • Manuscript received 29 January 2007; Revised manuscript received 7 March 2007; Accepted for publication 19 March 2007.

Address for correspondence: Dr. Michael Koa-Wing, B.Sc., M.R.C.P., Imperial College and St. Mary's Hospital, Waller Cardiology Department, St. Mary's Hospital, Praed Streeet, London W2 1NY, UK; Fax: +44-0207-8862210; E-mail:


Introduction: Histological data after VT ablation in humans is rare. We present a case of a patient who had ablation for VT storm and who died remotely from non-arrhythmic causes.

Methods and Results: A 69-year-old male with ischemic cardiomyopathy and a dual-chamber implantable cardioverter defibrillator (ICD) presented with VT storm and multiple ICD therapies. A voltage map of the left-ventricular (LV) scar was created using CARTO™. VT was induced. An isochronal map identified the VT exit site at the scar border. No diastolic potentials were seen in this territory, so VT exit site ablation was performed, as well as at a putative entry site. VT cycle length and morphology changed during ablation, but termination only occurred with burst pacing. Post-ablation, the patient had no further shocks. He died seven months later from acute pancreatitis. The two ablation sites were identified on the post-mortem heart and used to correlate with the electroanatomical map. Scar area correlated well, measuring approximately 58.4 cm2 macroscopically and 63.3 cm2 on the electroanatomical map. Histology at VT exit site demonstrated areas of viable epicardial myocardium, suggesting that the circuit was at the epicardial scar border, which would explain the lack of diastolic potentials. Ablation scar did not reach the epicardium and therefore, ablation may have modified the exit site without complete interruption of the VT circuit.

Conclusions: In this case, ablation was unable to terminate the VT due to failure to reach the epicardium, but was sufficient to modify the tachycardia, thereby reducing ICD therapy.