Abstract

Decreased efferent sympathetic neural function has been demonstrated following > 10J DC shocks delivered through epicardial patch electrodes in dogs. To evaluate the effect of DC shocks on cardiac sympathetic innervation in humans, we performed 1–123-metaiodobenzylguanidine (MIBG) scintigraphy in 5 patients (age 46–73 years, mean 64) prior to and after receiving shocks from implanted cardiac defibrillators (ICD). Four patients had coronary artery disease (CAD) with prior myocardial infarction and one had an idiopathic dilated cardiomyopathy (IDCM). All patients had spontaneous and inducible ventricular tachycardia. One patient was receiving amiodarone at the time of this study. One patient had had prior coronary artery bypass surgery (CABG), and two had concurrent CABG at the time of ICD implantation. This study was performed during an ICD generator change in 2 patients and at the time of initiallCD implantation in 3 patients. Four patients (3 CAD, 1 IDCM) received epicardial patch electrodes, and one patient had a transvenous lead system. Baseline MIBG and thallium-201 scintigraphy performed > 1 week preoperatively and remote from any cardioversions or shocks revealed focal areas of reduced MIBG uptake in areas of thallium perfusion defects in all patients. Repeat MIBG scans were performed > four hours after shocks delivered during either the surgical implantation orfollow-up EPS. All patients had received at least one 24J shock (mean 2.4 shocks, range 1–4), In all patients with epicardial patch electrodes, there was minimal or no cardiac uptake of MIBG post-Shock, consistent with diffuse sympathetic dysfunction. In the patient with a transvenous lead system the post-shock MIBG scan was unchanged from baseline. This study demonstrates that following DC shocks delivered through epicardial patches there is diffuse cardiac sympathetic neural dysfunction, which may contribute to the arrhythmic “storm” that has been reported following some ICD implantations.

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