Ventricular Tachycardia on Previous Myocardial Infarction: Effective by Nifekalant, Bepridil and Two Sessions of Catheter Ablation

A 74-year-old man with previous myocardial infarction and CABG was admitted our hospital because of sustained VT. VT’s cycle length (CL) was 460 ms and QRS morphology was RBBB+LAD (VT1). As he had intestinal pneumonia, amiodarone was contraindicated. Thus we started nifekalant and d-sotalol. VT was controlled by nifekalant, but relapsed and became uncontrollable after discontinuation of nifekalant, even with increased dosage of d-sotalol. Temporary pacing from RVA wasn’t effective, and QT interval became be more prolonged after increased dosage of nifekalant and d-sotalol. Thus catheter ablation was performed. Clinical VT couldn’t induced by programmed stimulations at RVA and RVOT. Perfect pacemap site was existed at inferoseptal wall. At this site, purkinje potential preceded ventricular potential. Radiofrequency (RF) energy was delivered around this site. Next evening, altenated VT was appeared. QRS morphologies were LBBB+LAD (VT2, CL: 440 ms) and RBBB+superior axis (VT3, CL: 520 ms). After we administration of nifekalant, VT was supressed. After ICD implantation, we stopped d-sotalol and started bepridil. VT duration became shorter, but its frequency showed no change. We performed catheter ablation again because of repetitive VT. VT couldn’t induced on this session, either. RF energy was delivered at perfect (VT2, midseptal) and good (VT3, inferoseptal, slightly anterior of VT1) pacemap site. Linear lesion was made in low voltage zone between two pacemap sites and between septal and anterior wall. After ablation, VT dissappeared with low dose bepridil. Conclusion: Alterated VT modified by focal ablation was effective linear ablation at low voltage zone and pottasium channel blocker.