Abstract：
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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).
CONCLUSIONS: 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.
BACKGROUND: The PARISK study was registered on ClinicalTrials.gov with ID NCT01208025 on September 21, 2010 (https://clinicaltrials.gov/study/NCT01208025).
METHODS: 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.
RESULTS: 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).
CONCLUSIONS: 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.
BACKGROUND: The PARISK study was registered on ClinicalTrials.gov with ID NCT01208025 on September 21, 2010 (https://clinicaltrials.gov/study/NCT01208025).
摘要：
背景：危险斑块（PARISK）研究表明，颈动脉斑块伴斑块内出血（IPH）的患者发生同侧缺血性脑血管事件的风险增加。先前报道，有症状的IPH颈动脉斑块显示出比无症状斑块更高的IPH信号强度比（SIR）和更大的IPH体积。我们探讨了IPHSIR和IPH体积是否与IPH存在后的同侧缺血性脑血管事件相关。
方法：包括PARISK研究中的TIA和缺血性卒中患者，这些患者患有轻度至中度颈动脉狭窄和同侧IPH阳性颈动脉斑块（n=89）。临床终点是5年随访期间新的同侧缺血性脑血管事件，而基于成像的终点是2年后脑MRI上新出现的同侧脑梗塞(n=69)。训练有素的观察员划定IPH，与超T1加权MR图像上的周围肌肉组织相比，这是一个高强度区域。IPHSIR是IPH区域中的最大信号强度除以相邻肌肉组织的平均信号强度。使用Cox比例风险模型和逻辑回归研究IPHSIR或体积与临床和基于影像学的终点之间的关联。分别。
结果：在5.1（四分位距（IQR）：3.1-5.6）年的随访期间，共发现21例同侧脑血管缺血事件。在2年的神经MRI中发现了12个新的同侧脑梗塞。IPHSIR或IPH体积与临床终点无关联(HR:0.89[95%CI:0.67-1.10]和HR:0.91[0.69-1.19]每100μl增加,分别）与基于成像的终点（OR：1.04[0.75-1.45]和OR：1.21[0.87-1.68]每100μl增加，分别)。
结论：IPHSIR和IPH体积与未来的同侧缺血性脑血管事件无关。因此,IPH的定量评估似乎不能为卒中风险评估提供超出IPH存在的额外价值.试验注册PARISK研究于2010年9月21日在ClinicalTrials.gov上注册，ID为NCT01208025（https://clinicaltrials.gov/study/NCT01208025）。
方法：包括PARISK研究中的TIA和缺血性卒中患者，这些患者患有轻度至中度颈动脉狭窄和同侧IPH阳性颈动脉斑块（n=89）。临床终点是5年随访期间新的同侧缺血性脑血管事件，而基于成像的终点是2年后脑MRI上新出现的同侧脑梗塞(n=69)。训练有素的观察员划定IPH，与超T1加权MR图像上的周围肌肉组织相比，这是一个高强度区域。IPHSIR是IPH区域中的最大信号强度除以相邻肌肉组织的平均信号强度。使用Cox比例风险模型和逻辑回归研究IPHSIR或体积与临床和基于影像学的终点之间的关联。分别。
结果：在5.1（四分位距（IQR）：3.1-5.6）年的随访期间，共发现21例同侧脑血管缺血事件。在2年的神经MRI中发现了12个新的同侧脑梗塞。IPHSIR或IPH体积与临床终点无关联(HR:0.89[95%CI:0.67-1.10]和HR:0.91[0.69-1.19]每100μl增加,分别）与基于成像的终点（OR：1.04[0.75-1.45]和OR：1.21[0.87-1.68]每100μl增加，分别)。
结论：IPHSIR和IPH体积与未来的同侧缺血性脑血管事件无关。因此,IPH的定量评估似乎不能为卒中风险评估提供超出IPH存在的额外价值.试验注册PARISK研究于2010年9月21日在ClinicalTrials.gov上注册，ID为NCT01208025（https://clinicaltrials.gov/study/NCT01208025）。
