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Reversal of Vascular ¹⁸F-FDG Uptake with Plasma High-Density Lipoprotein Elevation by Atherogenic Risk Reduction

¹ Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea; and ² Division of Cardiology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

Correspondence: For correspondence or reprints contact: Kyung-Han Lee, Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwondong, Kangnamgu, Seoul, Korea. E-mail: khnm.lee{at}samsung.com

Vascular ¹⁸F-FDG uptake marker represents inflammation in atherosclerotic lesions, but whether inflammation can be reversed by risk-modifying interventions has not, to our knowledge, been demonstrated. In this study, we evaluated the change of vascular ¹⁸F-FDG uptake in response to lifestyle intervention on serial PET/CT scans and further assessed how the findings relate to atherogenic risk reduction. Methods: A total of 60 healthy adults underwent ¹⁸F-FDG PET/CT scans and atherogenic risk-factor assessment at baseline and again after 17.1 ± 8.3 mo of practicing lifestyle modification. The PET/CT images were evaluated for the presence of vascular ¹⁸F-FDG lesions, and vessel–to–blood-pool ¹⁸F-FDG ratios were measured. Indices from summed ratios of positive lesions were compared and correlated to atherogenic risk factors. Results: At follow-up, significant reductions in diastolic blood pressure (P < 0.05), total cholesterol (P < 0.05), and low-density lipoprotein level (P < 0.05) and an increase in high-density lipoprotein (HDL) level (P < 0.0001) were demonstrated. On the initial PET/CT scan, 50 of 60 subjects showed 1 or more ¹⁸F-FDG–positive lesions (5.9 ± 5.0/subject), leading to a total of 352 vascular sites. On follow-up, ¹⁸F-FDG–positive lesions were significantly reduced to 2.1 ± 2.2 sites per subject (P < 0.0001) and a total of 124 sites (64.8% reduction). Follow-up ¹⁸F-FDG–positive rates were significantly reduced for the aorta and iliac arteries. In addition, significant reductions in the whole-body ¹⁸F-FDG index from 1.39 ± 1.23 to 0.53 ± 0.59 (P < 0.0001) and carotid ¹⁸F-FDG index from 0.08 ± 0.16 to 0.03 ± 0.06 (P = 0.01) were shown. The whole-body ¹⁸F-FDG index correlated with total cholesterol (P < 0.05) and HDL level (P < 0.05), and the magnitude of reduction in the ¹⁸F-FDG index closely correlated to the amount of increase in plasma HDL level (P = 0.005). Conclusion: Our study demonstrated that vascular ¹⁸F-FDG uptake is reversed in response to atherogenic risk reduction by lifestyle intervention and that the magnitude of improvement correlates to increases in plasma HDL levels. Thus, serial ¹⁸F-FDG PET/CT may be useful for monitoring improvements in the inflammatory component of atherosclerotic lesions in response to risk modification.

Key Words: atherosclerosis • ¹⁸F-FDG PET • atherogenic risk factor • risk modification

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

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