DEFIBRILLATION SHOCKS OVER EPICARDIAL PATCHES PRODUCE SYMPATHETIC NEURAL DYSFUNCTION IN MAN

Introduction: The purpose of this study was to determine the effect of direct current (DC) shocks on cardiac sympathetic innervation in huma ns using I-123-metaiodobenzylguanidine (MIBG) scintigraphy. Decreased efferent sympathetic neural function has been demonstrated following > 10-J DC shocks delivered through epicardial patch electrodes in dogs. To evaluate the effect of DC shocks on cardiac sympathetic innervatio n in humans, we performed MIBG scintigraphy in 11 patients (ages 46 to 75 years) prior to and after receiving shocks from an implantable car dioverter defibrillator (ICD). Methods and Results: This study was per formed during an ICD generator change in 7 patients with epicardial pa tch electrodes and at the time of initial ICD implantation in 4 patien ts: 2 with epicardial patch electrodes, and 2 with a transvenous ICD s ystem. All patients had spontaneous and inducible ventricular tachycar dia. Prior to ICD implantation and remote from any cardioversions or s hocks, baseline MIBG and thallium-201 scintigraphy were performed. Rep eat MIBG scintigraphy was performed after delivery of ICD shocks and c ompared with the baseline scans to determine the effect of the shock o n sympathetic neural function. The baseline scans revealed focal areas of reduced MIBG uptake in areas of thallium perfusion defects in all patients except the patient without structural heart disease whose sca ns were normal. Postshock, patients with epicardial patch electrodes w ho received at least one 24-J shock and had the postshock MIBG scan pe rformed within 4 hours demonstrated no cardiac uptake of MIBG. Two pat ients with epicardial patch electrodes had no change in the postshock MIBG scans: 1 had a maximal shock of 20 J, and the other had the posts hock scan delayed for 11 hours. The 2 patients with a transvenous lead system demonstrated no change in the postshock MIBG scan when compare d with baseline. Conclusions: This study demonstrates that following D C shocks delivered over epicardial patch electrodes, there is diffuse reduction in MIBG uptake that probably represents cardiac sympathetic neural dysfunction that appears to be transient. Sympathetic function does not appear to be affected by shocks delivered over a transvenous lead system.