PET/CTA detection of muscle inflammation related to cholesterol crystal emboli without arterial obstruction
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PET/CTA was used to evaluate the effect of cholesterol crystal emboli (CCE) on muscle injury. Cholesterol crystals (CCs) released during plaque rupture travel downstream and lodge in muscle triggering inflammation and tissue injury.
Thigh muscles in three groups of rabbits (n = 22) were studied after intra-arterial injection of CCs, Group I (n = 10); polystyrene microspheres, Group II (n = 5); or normal saline, Group III (n = 7). After 48 hours, muscle inflammation and injury were measured by fluorodeoxy-glucose uptake using PET/CTA, serum tissue factor (TF), and creatinine phosphokinase (CPK). Macrophages were stained with RAM11 and CCs with Bodipy.
SUVmax of thigh muscles was greater for Group I vs Group II and III (0.40 ± 0.16 vs 0.21 ± 0.11, P = .038 and 0.23 ± 0.06, P = .036). CPK levels rose significantly in Group I vs Group II and III (6.7 ± 6.0 vs 0.6 ± 0.4, P = .007 and 0.9 ± 0.4 mg·dL−1, P = .023). No arterial thrombosis was detected by CTA or histology of embolized arteries and TF did not rise significantly. There were extensive macrophage infiltrates surrounding muscle necrosis in Group I only.
Cholesterol crystal emboli triggered muscle inflammation and necrosis with an intact circulation. PET/CTA may help in the early detection of inflammation caused by CCs.
KeywordsPET/CTA 18F-fluorodeoxyglucose (18FDG) cholesterol crystal emboli myositis inflammation
Cholesterol crystal embolization
Positron emission tomography and computed tomography angiography
Maximum standardized uptake values
Scanning electron microscopy
Serum tissue factor
The authors thank Ruiping Huang, Tracy Needham, Jeremy Williams, and Michelle Bengel for technical support. We also thank Melinda Frame, PhD, Center for Advanced Microscopy and Amy Porter, HT, QIHC, Investigative Histopathology Laboratory, Michigan State University, East Lansing, MI. Support was provided in part from Michigan State University and Edward W. Sparrow Hospital, Lansing, MI.
Dr. G.S. Abela is a recipient of grants from Merck and speaker for Amgen and Daiichi Sankyo. Dr. K. Berger is recipient of grants from Merck and Janssen. He is a speaker for Cardinal Health and Educational Symposia. For all remaining authors, conflict of interest is none declared.
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