M Hassan Pervaiz1, Sridevi Durga1, Abed Janoudi1, Kevin Berger2, George S Abela3,4,5. 1. Division of Cardiology, Department of Medicine, Michigan State University, East Lansing, MI, USA. 2. Department of Radiology, Michigan State University, East Lansing, MI, USA. 3. Division of Cardiology, Department of Medicine, Michigan State University, East Lansing, MI, USA. george.abela@ht.msu.edu. 4. Division of Pathology, Department of Physiology, Michigan State University, East Lansing, MI, USA. george.abela@ht.msu.edu. 5. Michigan State University, B208 Clinical Center, East Lansing, MI, 48824, USA. george.abela@ht.msu.edu.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: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.
Authors: Bruno Paun; Daniel García Leon; Alex Claveria Cabello; Roso Mares Pages; Elena de la Calle Vargas; Paola Contreras Muñoz; Vanessa Venegas Garcia; Joan Castell-Conesa; Mario Marotta Baleriola; Jose Raul Herance Camacho Journal: Eur Radiol Exp Date: 2020-06-03