Cardiac sympathetic denervationmodulates the sympathoexcitatoryresponse to acute myocardial ischemia
Shuji Joho, MD*,
Hidetsugu Asanoi, MD*,*,
Junya Takagawa, MD*,
Tomoki Kameyama, MD*,
Tadakazu Hirai, MD*,
Takashi Nozawa, MD*,
Katsumi Umeno, BS
,
Masashi Shimizu, MD
,
Hikaru Seto, MD
and
Hiroshi Inoue, MD, FACC*
* Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan
First Department of Physiology, Toyama Medical and Pharmaceutical University, Toyama, Japan
Department of Radiology, Toyama Medical and Pharmaceutical University, Toyama, Japan

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Figure 2 Polar map of 123I-MIBG images and three-dimensional diagram of wavelet analysis of RR interval variability in two representative patients with mild myocardial ischemia provoked during BCO. These patients had a fall in LVEF (<10%) by BCO. The LF components were augmented in the patient without cardiac denervation (left), whereas no change in the spectral components was found in the patient with cardiac denervation (right). Abbreviations as in Figure 1.
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Figure 3 Changes in LVEF by BCO (ordinate) were plotted against the minimal 123I-MIBG counts of the artery of interest in all lesions (abscissa). Six of seven patients with a substantial fall in LVEF ( 10%) had augmentation of the LF components, regardless of the conditions of cardiac sympathetic innervation. In contrast, in 16 patients with mild ischemia provoked by a fall in LVEF of <10%, the prevalence of augmentation of LF components was significantly less in lesions with cardiac denervation (minimal count of MIBG <52.2%) than in those without cardiac denervation. Solid squares = patients with augmentation of LF components; open circles = patients without augmentation of LF components. Abbreviations as in Figure 1.
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Copyright © 2002 by the American College of Cardiology Foundation.