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First published online August 14, 2008, 10.2967/jnumed.108.052340
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Journal of Nuclear Medicine Vol. 49 No. 9 1458-1464
© 2008 by Society of Nuclear Medicine

doi: 10.2967/jnumed.108.052340

Clinical Investigation

Myocardial Sympathetic Innervation in Patients with Symptomatic Coronary Artery Disease: Follow-up After 1 Year with Neurostimulation

Eva Fricke1, Siegfried Eckert2, Aristidis Dongas3, Harald Fricke1, Rainer Preuss1, Oliver Lindner1, Dieter Horstkotte2 and Wolfgang Burchert1

1 Institute of Radiology, Nuclear Medicine and Molecular Imaging, Heart and Diabetes Centre North Rhine–Westphalia, Bad Oeynhausen, Germany; 2 Department of Cardiology, Heart and Diabetes Centre North Rhine–Westphalia, Bad Oeynhausen, Germany; and 3 Institut of Anesthesiology, Heart and Diabetes Centre North Rhine–Westphalia, Bad Oeynhausen, Germany

Correspondence: For correspondence or reprints contact: Eva Fricke, Institut für Radiologie, Nuklearmedizin und Molekulare Bildgebung, Herz- und Diabeteszentrum Nordrhein-Westfalen, Georgstrasse 11, 32545 Bad Oeynhausen, Germany. E-mail: efricke{at}hdz-nrw.de

In both diabetic and nondiabetic patients, there is a loose correlation between coronary flow reserve (CFR) and sympathetic innervation in viable myocardial segments. The loose correlation implies that sympathetic innervation may be preserved even with major impairment of myocardial blood supply. In some patients, denervation is due to repetitive episodes of ischemia in areas with severely reduced CFR. We investigated the long-term effect of reduced CFR on myocardial sympathetic innervation in diabetic and nondiabetic patients with spinal cord stimulation. Methods: We analyzed 23 patients (10 diabetic and 13 nondiabetic) with coronary artery disease and without known cardiac autonomic neuropathy. At baseline, we determined quantitative myocardial blood flow using 13N-ammonia PET, myocardial viability using 18F-FDG PET, and cardiac innervation using 11C-hydroxyephedrine (HED) PET. At the 1-y follow-up we measured CFR and 11C-HED retention. During follow-up, no cardiac intervention was performed and no myocardial infarction occurred. In all patients, spinal cord stimulation was performed for relief of angina. Results: There was no significant difference in segmental 11C-HED retention between baseline and follow-up in the whole patient group. In diabetic patients, as well as in segments with severely reduced CFR (<1.5), 11C-HED retention showed a small but significant decrease (P < 0.05). Linear regression of segmental 11C-HED retention between baseline and follow-up was high (r2 = 0.81), confirming good reproducibility of the investigation on the one hand and little change in regional sympathetic innervation on the other hand. Conclusion: In patients with stable chronic coronary artery disease, sympathetic innervation of the myocardium is almost unchanged in both diabetic and nondiabetic patients in a 1-y follow-up. In myocardial segments with severely altered blood supply, a small but significant decrease in 11C-HED retention most probably reflects ischemic neuronal damage. The prognostic relevance of sympathetic denervation in viable myocardium still has to be determined.

Key Words: coronary artery disease • sympathetic nervous system • ischemia • positron emission tomography

COPYRIGHT © 2008 by the Society of Nuclear Medicine, Inc.


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