PURPOSE: Previous studies reporting relaxation times within atherosclerotic plaque have typically used dedicated small-bore high-field systems and small sample sizes. This study reports quantitative T(1), T(2) and T(2) relaxation times within plaque tissue at 1.5 T using spatially co-matched histology to determine tissue constituents. METHODS: Ten carotid endarterectomy specimens were removed from patients with advanced atherosclerosis. Imaging was performed on a 1.5-T whole-body scanner using a custom built 10-mm diameter receive-only solenoid coil. A protocol was defined to allow subsequent computation of T(1), T(2) and T(2) relaxation times using multi-flip angle spoiled gradient echo, multi-echo fast spin echo and multi-echo gradient echo sequences, respectively. The specimens were subsequently processed for histology and individually sectioned into 2-mm blocks to allow subsequent co-registration. Each imaging sequence was imported into in-house software and displayed alongside the digitized histology sections. Regions of interest were defined to demarcate fibrous cap, connective tissue and lipid/necrotic core at matched slice-locations. Relaxation times were calculated using Levenberg-Marquardt's least squares curve fitting algorithm. A linear-mixed effect model was applied to account for multiple measurements from the same patient and establish if there was a statistically significant difference between the plaque tissue constituents. RESULTS: T(2) and T(2) relaxation times were statistically different between all plaque tissues (P=.026 and P=.002 respectively) [T(2): lipid/necrotic core was lower 47 ± 13.7 ms than connective tissue (67 ± 22.5 ms) and fibrous cap (60 ± 13.2 ms); T(2): fibrous cap was higher (48 ± 15.5 ms) than connective tissue (19 ± 10.6 ms) and lipid/necrotic core (24 ± 8.2 ms)]. T(1) relaxation times were not significantly different (P=.287) [T(1): Fibrous cap: 933 ± 271.9 ms; connective tissue (1002 ± 272.9 ms) and lipid/necrotic core (1044 ± 304.0 ms)]. We were unable to demarcate hemorrhage and calcium following histology processing. CONCLUSIONS: This study demonstrates that there is a significant difference between qT(2) and qT(2) in plaque tissues types. Derivation of quantitative relaxation times shows promise for determining plaque tissue constituents.
PURPOSE: Previous studies reporting relaxation times within atherosclerotic plaque have typically used dedicated small-bore high-field systems and small sample sizes. This study reports quantitative T(1), T(2) and T(2) relaxation times within plaque tissue at 1.5 T using spatially co-matched histology to determine tissue constituents. METHODS: Ten carotid endarterectomy specimens were removed from patients with advanced atherosclerosis. Imaging was performed on a 1.5-T whole-body scanner using a custom built 10-mm diameter receive-only solenoid coil. A protocol was defined to allow subsequent computation of T(1), T(2) and T(2) relaxation times using multi-flip angle spoiled gradient echo, multi-echo fast spin echo and multi-echo gradient echo sequences, respectively. The specimens were subsequently processed for histology and individually sectioned into 2-mm blocks to allow subsequent co-registration. Each imaging sequence was imported into in-house software and displayed alongside the digitized histology sections. Regions of interest were defined to demarcate fibrous cap, connective tissue and lipid/necrotic core at matched slice-locations. Relaxation times were calculated using Levenberg-Marquardt's least squares curve fitting algorithm. A linear-mixed effect model was applied to account for multiple measurements from the same patient and establish if there was a statistically significant difference between the plaque tissue constituents. RESULTS: T(2) and T(2) relaxation times were statistically different between all plaque tissues (P=.026 and P=.002 respectively) [T(2): lipid/necrotic core was lower 47 ± 13.7 ms than connective tissue (67 ± 22.5 ms) and fibrous cap (60 ± 13.2 ms); T(2): fibrous cap was higher (48 ± 15.5 ms) than connective tissue (19 ± 10.6 ms) and lipid/necrotic core (24 ± 8.2 ms)]. T(1) relaxation times were not significantly different (P=.287) [T(1): Fibrous cap: 933 ± 271.9 ms; connective tissue (1002 ± 272.9 ms) and lipid/necrotic core (1044 ± 304.0 ms)]. We were unable to demarcate hemorrhage and calcium following histology processing. CONCLUSIONS: This study demonstrates that there is a significant difference between qT(2) and qT(2) in plaque tissues types. Derivation of quantitative relaxation times shows promise for determining plaque tissue constituents.
Authors: Luca Biasiolli; Alistair C Lindsay; Joshua T Chai; Robin P Choudhury; Matthew D Robson Journal: J Cardiovasc Magn Reson Date: 2013-08-16 Impact factor: 5.364
Authors: Bram F Coolen; Claudia Calcagno; Pim van Ooij; Zahi A Fayad; Gustav J Strijkers; Aart J Nederveen Journal: MAGMA Date: 2017-08-14 Impact factor: 2.310
Authors: My Truong; Finn Lennartsson; Adnan Bibic; Lena Sundius; Ana Persson; Roger Siemund; René In't Zandt; Isabel Goncalves; Johan Wassélius Journal: Eur J Radiol Open Date: 2021-01-21