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Defibrillation Shocks Over Epicardial Patches Produce Sympathetic Neural Dysfunction in Man
Author(s) -
RIGDEN LAWRENCE B.,
MITRANI RAUL D.,
WELLMAN HENRY N.,
KLEIN LAWRENCE S.,
MILES WILLIAM M.,
ZIPES DOUGLAS P.
Publication year - 1996
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1996.tb00545.x
Subject(s) - medicine , cardiology , scintigraphy , shock (circulatory) , defibrillation , thallium , perfusion , implantable cardioverter defibrillator , tachycardia , nuclear medicine , inorganic chemistry , chemistry
ICD Shocks Produce Sympathetic Neural Dysfunction. Introduction: The purpose of this study was to determine the effect of direct current (DC) shocks on cardiac sympathetic innervation in humans using I‐123‐metaiodobenzylguanidine (MIBG) sciutigraphy. 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 innervation in humans, we performed MIBG scintigraphy in 11 patients (ages 46 to 75 years) prior to and after receiving shocks from an implantable cardioverter defibrillator (ICD). Methods and Results: This study was performed during an ICD generator change in 7 patients with epicardial patch electrodes and at the time of initial ICD implantation in 4 patients: 2 with epicardial patch electrodes, and 2 with a transvenous ICD system. All patients had spontaneous and inducible ventricular tachycardia. Prior to ICD implantation and remote from any cardioversions or shocks, baseline MIBG and thallium‐201 scintigraphy were performed. Repeat MIBG scintigraphy was performed after delivery of ICD shocks and compared with the baseline scans to determine the effect of the shock on 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 scans were normal. Postshock, patients with epicardial patch electrodes who received at least one 24‐J shock and had the postshock MIBG scan performed within 4 hours demonstrated no cardiac uptake of MIBG. Two patients with epicardial patch electrodes had no change in the postshock MIBG scans: I had a maximal shock of 20 J, and the other had the postshock scan delayed for 11 hours. The 2 patients with a transvenous lead system demonstrated no change in the postshock MIBG scan when compared with baseline. Conclusions : This study demonstrates that following DC shocks delivered over epicardial patch electrodes, there is diffuse reduction in MIBG uptake that probably represents cardiac sympathetic neural dysfunction that appears to he transient. Sympathetic function does not appear to be affected by shocks delivered over a transvenous lead system.