Abstract

A 66-year-old man, with a long history of rheumatic heart disease, valvular cardiomyopathy, and congestive heart failure, underwent a mechanical mitral and aortic valve replacement in 1995. In 2005, an implantable cardioverter defibrillator (ICD) was implanted because of nonsustained ventricular tachycardia (VT) and a reduced left ventricular function (left ventricular ejection fraction, 30%). In 2010, the patient developed a VT storm refractory to amiodarone, sotalol, lidocaine and beta-blockers, and received multiple ICD shocks. There were at least 3 clinical VTs. VT1 exhibited a right bundle-branch block (RBBB) morphology, northwest axis, and a cycle length (CL) of 560 ms; VT2 exhibited an RBBB morphology, right-axis deviation, and CL of 490 ms; and VT3 had a left bundle-branch block (LBBB) morphology, right-axis deviation, and CL of 430 ms. During the electrophysiological study, the VTs were induced by programmed ventricular stimulation, hence bundle branch reentry was ruled out. Mapping in the coronary veins during VT suggested an epicardial circuit of the tachycardia. Electroanatomical mapping in the epicardium using a NaviStar catheter (Biosense-Webster, Diamond Bar, California) revealed the presence of a wide low-voltage area in the apical region. During the induced VT1 a presystolic potential (PP) was recorded from this area, which preceded the onset of the QRS by 60 ms (Fig. 1A). Entrainment pacing with a 9.9 V output (1.0 ms width) was performed from this site at a CL of 500 ms. The surface ECG during entrainment pacing showed some degree of fusion. The interval between the pacing stimulus and onset of the QRS complex (S-QRS) was 160 ms, whilst the interval from the electrogram recorded at the pacing site to the QRS onset during the VT (Eg-QRS) was just 60 ms. The post-pacing interval (PPI) was 680 ms (120 ms longer than the VT–CL). A radiofrequency (RF) energy application using open irrigation (30 ml/min, 35 W)

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