Journal
STROKE
Volume 45, Issue 6, Pages 1842-1845Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/STROKEAHA.114.005147
Keywords
atherosclerosis; carotid arteries; magnetic resonance imaging; positron emission tomography
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Funding
- Army Medical Research Funds of China [11BJZ19]
- National Natural Science Foundation of China [81371540]
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Background and Purpose-F-18-fluorodeoxyglucose positron emission tomography and dynamic contrast-enhanced MRI have been proposed to quantitatively assess plaque inflammation by probing macrophages and neovessels, respectively. We examined their correlation to study the in vivo relationship between macrophage and neovessel activities in atherogenesis. Methods-Forty-one patients (34 men; aged 65 +/- 12 years) with a total of 68 carotid plaques (thickness >= 2 mm on ultrasound; 20 symptomatic) were assessed by both F-18-fluorodeoxyglucose positron emission tomography/computed tomography and dynamic contrast-enhanced MRI within 2 weeks, measured as target-to-background ratio and transfer constant (K-trans), respectively. Results-Overall, the correlation between target-to-background ratio and K-trans was weak and marginal (r=0.22; P=0.068). They were correlated in the symptomatic plaques (r=0.59; P=0.006) but not in the asymptomatic plaques (r=0.07; P=0.625; P=0.033 for difference in r). Neither target-to-background ratio nor K-trans was significantly higher in the symptomatic plaques, but both showed an inverse relationship with time since last neurological event (r=-0.94 and -0.69 for target-to-background ratio and K-trans, respectively). Conclusions-The correlation between F-18-fluorodeoxyglucose positron emission tomography and dynamic contrast-enhanced MRI measurements varied with clinical conditions, pointing to a complex interplay between macrophages and neovessels under different pathophysiological conditions. The moderate correlation shown only in symptomatic plaques indicates the presence of acute plaque inflammation with increased metabolic activity and cytokine production by inflammatory cells.
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