MR Imaging–Detected Carotid Plaque Hemorrhage Is Stable for 2 Years and a Marker for Stenosis Progression

Simpson, Richard; Akwei, Solomon; Hosseini, Akram A.; MacSweeney, Shane; Auer, Dorothee P.; Altaf, Nishath

doi:10.3174/ajnr.a4267

Cited by 32 publications

(22 citation statements)

References 32 publications

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“…Thus, we cannot be sure whether the IPHs observed at follow-up were at the same location as those observed at baseline or if some of these may also represent newly developed IPH. In our visual assessment, however, we found that in 94% of the subjects, IPH remained present, which is in agreement with findings in two previous studies (6,24). Still, we may have underestimated the rate of new IPH development, as this would have been scored as growth of IPH with both community-dwelling subjects with atherosclerotic carotid plaques, male sex, hypertension, and current smoking were major risk factors for presence of IPH (12).…”

Section: Discussionsupporting

confidence: 80%

Change in Carotid Intraplaque Hemorrhage in Community-dwelling Subjects: A Follow-up Study Using Serial MR Imaging

Bouwhuijsen¹,

Selwaness²,

Tang³

et al. 2017

Radiology

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Purpose:To investigate intraplaque hemorrhage (IPH) development and change over time. Materials and Methods:Institutional review board approval and written informed consent from all participants were obtained. ; 95% CI: 7.1, 83.4; P = .020), and hypertension (subjects with hypertension vs those without hypertension, 32.5 mm 3 ; 95% CI: 7.7, 57.2; P = .010) were associated with IPH volume change. Conclusion:During 17 months of follow-up, both visual progression and regression of IPH volume occurs, whereas quantitatively IPH volume decreases. This suggests that IPH is a dynamic process with potential for either growth or resolution over time.q RSNA, 2016

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Section: Discussionsupporting

confidence: 80%

Change in Carotid Intraplaque Hemorrhage in Community-dwelling Subjects: A Follow-up Study Using Serial MR Imaging

Bouwhuijsen¹,

Selwaness²,

Tang³

et al. 2017

Radiology

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“…Although plaque features, such as HST1 and contrast enhancement, may persistent for months of ischemic stroke,24, 33, 34, 35 the short period (≤30 days) in our study contributed to the identification of meaningful associations of the features with culprit lesions. However, there is overlap in the studied features among groups.…”

Section: Discussionmentioning

confidence: 85%

Differential Features of Culprit Intracranial Atherosclerotic Lesions: A Whole‐Brain Vessel Wall Imaging Study in Patients With Acute Ischemic Stroke

Song

et al. 2018

JAHA

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BackgroundIntracranial atherosclerotic disease tends to affect multiple arterial segments. Using whole‐brain vessel wall imaging, we sought to study the differences in plaque features among various types of plaques in patients with a recent unilateral anterior circulation ischemic stroke.Methods and ResultsSixty‐one patients with unilateral anterior circulation ischemic stroke were referred to undergo whole‐brain vessel wall imaging (before and after contrast) within 1 month of symptom onset for intracranial atherosclerotic disease evaluations. Each plaque was classified as a culprit, probably culprit, or nonculprit lesion, according to its likelihood of causing the stroke. The associations between plaque features (thickening pattern, plaque‐wall contrast ratio, high signal on T1‐weighted images, plaque contrast enhancement ratio, enhancement grade, and enhancement pattern) and culprit lesions were estimated using mixed multivariable logistic regression after adjustment for maximum wall thickness. In 52 patients without motion corruption in whole‐brain vessel wall imaging, a total of 178 intracranial plaques in the anterior circulation were identified, including 52 culprit lesions (29.2%), 51 probably culprit lesions (28.7%), and 75 nonculprit lesions (42.1%). High signal on T1‐weighted images (adjusted odds ratio, 9.1; 95% confidence interval, 1.9–44.1; P=0.006), grade 2 (enhancement ratio of plaque ≥ enhancement ratio of pituitary) contrast enhancement (adjusted odds ratio, 17.4; 95% confidence interval, 1.8–164.9; P=0.013), and type 2 (≥50% cross‐sectional wall involvement) enhancement pattern (adjusted odds ratio, 10.1; 95% confidence interval, 1.3–82.2; P=0.030) were independently associated with culprit lesions.ConclusionsHigh signal on T1‐weighted images, grade 2 contrast enhancement, and type 2 enhancement pattern are associated with cerebrovascular ischemic events, which may provide valuable insights into risk stratification.

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“…As increasing evidence suggests that IPH is an undesirable pathologic event in the natural history of atherosclerosis, 1–5,11,12 understanding the pathogenesis and contributing factors of IPH becomes of pivotal importance. Approaches to detect and measure IPH are limited.…”

Section: Discussionmentioning

confidence: 99%

“…However, the role of IPH in atherothrombosis is becoming increasingly recognized through mechanistic prospective studies that are recently made possible by in vivo imaging. It has been recognized that IPH promotes plaque progression, 1–5 of which the pathways may involve iron-driven lipid oxidation, 6 cholesterol deposition from erythrocyte membrane, 7,8 blood-borne proteolytic activity, 9,10 and more. In accord with such an effect, IPH was shown in various clinical settings to predict subsequent clinical outcomes.…”

Section: Introductionmentioning

confidence: 99%

Blood Pressure Is a Major Modifiable Risk Factor Implicated in Pathogenesis of Intraplaque Hemorrhage

Sun

Cantón

Balu

et al. 2016

ATVB

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Objective Effective prevention and management strategies of intraplaque hemorrhage (IPH) remain elusive due to our limited knowledge regarding its etiology and contributing factors. This hypothesis-generating study aimed to investigate associations between cardiovascular risk factors and IPH for improved understanding of the pathogenesis of IPH. Approach and Results Asymptomatic subjects with 16–79% stenosis on ultrasound underwent carotid magnetic resonance imaging (MRI) using a large-coverage, three-dimensional MRI protocol. Individual plaques (maximum thickness>1.5 mm) in bilateral carotid arteries were identified and presence of IPH was determined. From 80 subjects, 176 de novo plaques were measured, of which 38 (21.6%) contained IPH. Blood pressure (BP), primarily low diastolic BP, was associated with IPH in multivariate analysis adjusted for age, sex, and plaque size (odds ratio [OR with 95% confidence interval] per 10 mmHg ↑: 0.51 [0.30–0.88]), which was little changed after adjusting for antihypertensive use and systemic atherosclerosis. Antiplatelet use was associated with IPH in age and sex-adjusted models (p=0.018), for which a trend remained after considering plaque size and past medical history (OR for aspirin alone vs. none: 3.1 [0.66–14.8]; OR for clopidogrel or dual therapy vs. none: 5.3 [0.80–35.0]; p=0.083). Conclusions Low diastolic BP was independently associated with IPH, which was unlikely due to treatment difference or BP changes from systemic atherosclerosis. Hemodynamic changes from lowering diastolic BP may be the pathophysiological link. Prospective serial studies are needed to assess whether BP and antiplatelet use are associated with the development of new or repeated IPH.

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MR Imaging–Detected Carotid Plaque Hemorrhage Is Stable for 2 Years and a Marker for Stenosis Progression

Cited by 32 publications

References 32 publications

Change in Carotid Intraplaque Hemorrhage in Community-dwelling Subjects: A Follow-up Study Using Serial MR Imaging

Change in Carotid Intraplaque Hemorrhage in Community-dwelling Subjects: A Follow-up Study Using Serial MR Imaging

Differential Features of Culprit Intracranial Atherosclerotic Lesions: A Whole‐Brain Vessel Wall Imaging Study in Patients With Acute Ischemic Stroke

Blood Pressure Is a Major Modifiable Risk Factor Implicated in Pathogenesis of Intraplaque Hemorrhage

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