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Relationship between plasma norepinephrine at peak exercise and 123I-MIBG imaging of the heart and lower limbs in heart failure.

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 (123)I- metaiodobenzylguanidine (MIBG) scintigraphy.


METHODS AND RESULTS
Twenty patients with organic heart disease underwent exercise testing and (123)I-MIBG scintigraphy. Systemic (123)I-MIBG uptake was measured 4 hours after (123)I-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> or =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.