-Original-

Relationship between Plasma Norepinephrine at Peak Exercise and ¹²³I-MIBG Imaging of the Heart and Lower Limbs in Heart Failure

Takaya Tsuchida¹, Nagaharu Fukuma¹, Keiko Oikawa¹, Kazuyo Kato¹, Yuko Kato¹, Teruo Takano¹ and Shinichiro Kumita²

¹Department of Functional Pathophysiology for Human Organs, Graduate School of Medicine, Nippon Medical School
²Department of Clinical Radiology, Graduate School of Medicine, Nippon Medical School

Background: Past studies suggested that plasma norepinephrine during exercise originates in sympathetic nerve endings and that the main origin differs among pathophysiological conditions.
Aims: This study investigated the most important site of sympathetic terminals as an origin of plasma norepinephrine during exercise in patients with heart failure using ¹²³I-metaiodobenzylguanidine (MIBG) scintigraphy.
Methods and Results: Twenty patients with organic heart disease underwent exercise testing and ¹²³I-MIBG scintigraphy. Systemic ¹²³I-MIBG uptake was measured 4 hours after ¹²³I-MIBG injection, and the heart-to-brain (H/B) and lower limb-to-brain ratios (L/B) were calculated. Plasma norepinephrine concentration was measured at rest and at peak exercise. Subjects were divided into two groups: those with preserved left ventricular ejection fraction (LVEF≥45%, n=8) and those with reduced LVEF (<45%, n=12). Plasma norepinephrine at rest did not correlate with H/B or L/B. In the preserved LVEF group, plasma norepinephrine at peak exercise was correlated with H/B (r=0.722), but not with L/B. In the reduced LVEF group, the norepinephrine response to peak exercise correlated with L/B (r=0.642), but not with H/B.
Conclusion: The present findings suggest that norepinephrine concentration is regulated by sympathetic terminal function of working muscles in patients with impaired LVEF and by that of the heart in patients with preserved LVEF.

J Nippon Med Sch 2007; 74: 114-122

Keywords
exercise, norepinephrine, heart failure, sympathetic nerve, ¹²³I-metaiodobenzylguanidine

Correspondence to
Takaya Tsuchida, MD, Department of Functional Pathophysiology for Human Organs, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan
tsutchy@dc4.so-net.ne.jp

Received, December 19, 2006
Accepted, December 29, 2006