R J Simpson1, S Akwei2, A A Hosseini2, S T MacSweeney3, D P Auer2, N Altaf4. 1. From the Radiological Sciences Group (R.J.S., S.A., A.A.H., D.P.A., N.A.), Division of Clinical Neurosciences, University of Nottingham, Nottingham, United Kingdom Department of Vascular and Endovascular Surgery (R.J.S., S.T.M., N.A.), Nottingham University Hospitals National Health Service Trust, Nottingham, United Kingdom. msxrs@nottingham.ac.uk. 2. From the Radiological Sciences Group (R.J.S., S.A., A.A.H., D.P.A., N.A.), Division of Clinical Neurosciences, University of Nottingham, Nottingham, United Kingdom. 3. Department of Vascular and Endovascular Surgery (R.J.S., S.T.M., N.A.), Nottingham University Hospitals National Health Service Trust, Nottingham, United Kingdom. 4. From the Radiological Sciences Group (R.J.S., S.A., A.A.H., D.P.A., N.A.), Division of Clinical Neurosciences, University of Nottingham, Nottingham, United Kingdom Department of Vascular and Endovascular Surgery (R.J.S., S.T.M., N.A.), Nottingham University Hospitals National Health Service Trust, Nottingham, United Kingdom.
Abstract
BACKGROUND AND PURPOSE: MR imaging-detected carotid plaque hemorrhage is associated with an increased risk of recurrent ischemic cerebrovascular events and could be an indicator of disease progression; however, there are limited data regarding the dynamics of the MR imaging-detected carotid plaque hemorrhage signal. We assessed the temporal change of this signal and its impact on carotid disease progression. MATERIALS AND METHODS: Thirty-seven symptomatic patients with 54 carotid stenoses of >30% on sonography underwent serial MR imaging during 24 months. A signal-intensity ratio of >1.5 between the carotid plaque and adjacent muscle was defined as plaque hemorrhage, and a change in signal-intensity ratio of >0.31 between time points was considered significant. Sixteen patients underwent ≥2 carotid sonography scans to determine the peak systolic velocities and degree of stenosis with time. RESULTS: Of the 54 carotids, 28 had the presence of hyperintense signal on an MR imaging sequence (PH+) and 26 had the absence of hyperintense signal on an MR imaging sequence (PH-) at baseline. The signal-intensity ratio was stable in 33/54 carotid plaques, but 39% showed a change. Plaque hemorrhage classification did not change in 87% of carotid plaques, but 4 became PH+, and 3, PH-. As a group, PH+ carotids did not change significantly in signal-intensity ratio (P = .585), whereas PH- showed an increased signal-intensity ratio at 24.5 months (P = .02). In PH+ plaques, peak systolic velocities significantly increased by 22 ± 39.8 cm/s from baseline to last follow-up sonography (Z = 2.427, P = .013). CONCLUSIONS: During 2 years, MR imaging-detected carotid plaque hemorrhage status remained stable in most (87%) cases with 4 (7%) incident plaque hemorrhages. PH+ plaques were associated with increased flow velocity during the follow-up period.
BACKGROUND AND PURPOSE: MR imaging-detected carotid plaque hemorrhage is associated with an increased risk of recurrent ischemic cerebrovascular events and could be an indicator of disease progression; however, there are limited data regarding the dynamics of the MR imaging-detected carotid plaque hemorrhage signal. We assessed the temporal change of this signal and its impact on carotid disease progression. MATERIALS AND METHODS: Thirty-seven symptomatic patients with 54 carotid stenoses of >30% on sonography underwent serial MR imaging during 24 months. A signal-intensity ratio of >1.5 between the carotid plaque and adjacent muscle was defined as plaque hemorrhage, and a change in signal-intensity ratio of >0.31 between time points was considered significant. Sixteen patients underwent ≥2 carotid sonography scans to determine the peak systolic velocities and degree of stenosis with time. RESULTS: Of the 54 carotids, 28 had the presence of hyperintense signal on an MR imaging sequence (PH+) and 26 had the absence of hyperintense signal on an MR imaging sequence (PH-) at baseline. The signal-intensity ratio was stable in 33/54 carotid plaques, but 39% showed a change. Plaque hemorrhage classification did not change in 87% of carotid plaques, but 4 became PH+, and 3, PH-. As a group, PH+ carotids did not change significantly in signal-intensity ratio (P = .585), whereas PH- showed an increased signal-intensity ratio at 24.5 months (P = .02). In PH+ plaques, peak systolic velocities significantly increased by 22 ± 39.8 cm/s from baseline to last follow-up sonography (Z = 2.427, P = .013). CONCLUSIONS: During 2 years, MR imaging-detected carotid plaque hemorrhage status remained stable in most (87%) cases with 4 (7%) incident plaque hemorrhages. PH+ plaques were associated with increased flow velocity during the follow-up period.
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