Signal intensity and volume of carotid intraplaque hemorrhage on magnetic resonance imaging and the risk of ipsilateral cerebrovascular events: The Plaque At RISK (PARISK) study

Signal intensity and volume of carotid intraplaque hemorrhage on magnetic resonance imaging and the risk of ipsilateral cerebrovascular events: The Plaque At RISK (PARISK) study

The Plaque At RISK (PARISK) study demonstrated that patients with a carotid plaque with intraplaque hemorrhage (IPH) have an increased risk of recurrent ipsilateral ischemic cerebrovascular events. It was previously reported that symptomatic carotid plaques with IPH showed higher IPH signal intensit...

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Bibliographic Details
Published in:Journal of cardiovascular magnetic resonance Vol. 26; no. 2; p. 101049
Main Authors: Nies, Kelly P.H., Aizaz, Mueez, van Dam-Nolen, Dianne H.K., Goring, Timothy C.D., Schreuder, Tobien A.H.C.M.L., van Orshoven, Narender P., Postma, Alida A., Bos, Daniel, Hendrikse, Jeroen, Nederkoorn, Paul, van der Geest, Rob, van Oostenbrugge, Robert J., Mess, Werner H., Kooi, M. Eline
Format: Journal Article
Language:English
Published: England Elsevier Inc 13-06-2024
Subjects:
Atherosclerosis
Carotid artery
Intraplaque hemorrhage
MRI
Signal intensity
Stroke
IPH
IR-TFE
MRI
HR
Intraplaque hemorrhage
FSPGR
SD
Signal intensity
Atherosclerosis
LRNC
Carotid artery
Stroke
OR
NASCET
CI
TSE
ICC
CMR
IQR
TIA
ROI
CTA
3D
SIR
PARISK
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Summary:The Plaque At RISK (PARISK) study demonstrated that patients with a carotid plaque with intraplaque hemorrhage (IPH) have an increased risk of recurrent ipsilateral ischemic cerebrovascular events. It was previously reported that symptomatic carotid plaques with IPH showed higher IPH signal intensity ratios (SIR) and larger IPH volumes than asymptomatic plaques. We explored whether IPH SIR and IPH volume are associated with future ipsilateral ischemic cerebrovascular events beyond the presence of IPH. Transient ischemic attack and ischemic stroke patients with mild-to-moderate carotid stenosis and an ipsilateral IPH-positive carotid plaque (n = 89) from the PARISK study were included. The clinical endpoint was a new ipsilateral ischemic cerebrovascular event during 5 years of follow-up, while the imaging-based endpoint was a new ipsilateral brain infarct on brain magnetic resonance imaging (MRI) after 2 years (n = 69). Trained observers delineated IPH, a hyperintense region compared to surrounding muscle tissue on hyper T1-weighted magnetic resonance images. The IPH SIR was the maximal signal intensity in the IPH region divided by the mean signal intensity of adjacent muscle tissue. The associations between IPH SIR or volume and the clinical and imaging-based endpoint were investigated using Cox proportional hazard models and logistic regression, respectively. During 5.1 (interquartile range: 3.1–5.6) years of follow-up, 21 ipsilateral cerebrovascular ischemic events were identified. Twelve new ipsilateral brain infarcts were identified on the 2-year neuro MRI. There was no association for IPH SIR or IPH volume with the clinical endpoint (hazard ratio (HR): 0.89 [95% confidence interval: 0.67–1.10] and HR: 0.91 [0.69–1.19] per 100-µL increase, respectively) nor with the imaging-based endpoint (odds ratio (OR): 1.04 [0.75–1.45] and OR: 1.21 [0.87–1.68] per 100-µL increase, respectively). IPH SIR and IPH volume were not associated with future ipsilateral ischemic cerebrovascular events. Therefore, quantitative assessment of IPH of SIR and volume does not seem to provide additional value beyond the presence of IPH for stroke risk assessment. Trial registration: The PARISK study was registered on ClinicalTrials.gov with ID NCT01208025 on September 21, 2010 (https://clinicaltrials.gov/study/NCT01208025). [Display omitted]
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ISSN:1097-6647
1532-429X
1532-429X
DOI:10.1016/j.jocmr.2024.101049