Ilana Spokoyny, MD

Yu JH, Kwak HS, Chung GH, Hwang SB, Park MS, and Park SH. Association of Intraplaque Hemorrhage and Acute Infarction in Patients With Basilar Artery Plaque. Stroke. 2015 

Atherosclerosis is a common cause of stroke, and while imaging has previously focused on the quantitative aspects (how stenotic is the vessel), we are now able to and thus interested in characterizing the more qualitative aspects of the plaque. In atherosclerotic plaques, intraplaque hemorrhage (IPH) is commonly seen and is thought to represent rupture of friable plaque vessels. In carotid plaques, IPH is associated with instability and rapid progression of plaque size and luminal stenosis. There has been recent research showing that IPH in the MCA (based on T-1 sequence hyperintensity) is associated with a risk of ipsilateral stroke. This has not yet been evaluated in basilar plaques, and is what the authors of this paper set out to do. 

The T-1 sequence MPRAGE (magnetization prepared rapid acquisition with gradiant-echo) has been shown to be more sensitive and specific for the identification of IPH than conventional T-1 or time-of-flight (TOF) MRA. In this study, to be considered “high signal” on MPRAGE, the area in question was required to be at least 150% of the signal intensity of the adjacent muscle.

Over a 3 year period, patients who had at least 50% basilar stenosis on TOF MRA and who consented to participate were enrolled in the study. These patients were identified either because of acute stroke code activation, or presentation with neurologic complaints such as dizziness, headache, giddiness, or vertigo. The High-Res MRI (including MPRAGE) was performed within two weeks of the initial qualifying MRI/MRA scan. To be considered “symptomatic”, the MRI had to show ischemic stroke (high DWI, low ADC signal) in the basilar artery territory (implying the stroke occurred within the last week). Those patients with > 50%stenosis in one or both vertebral arteries, less than 50% basilar stenosis, or non-atherosclerotic etiology (dissection, moyamoya) were excluded.

Of 73 patients, 45 were symptomatic and 28 were asymptomatic. MPRAGE demonstrated IPH in 54.5% of symptomatic patients, and only 20% of asymptomatic patients. Overall, 30 patients were MPRAGE positive (for IPH) and 43 were MPRAGE negative. The imaging-positive and imaging-negative patients did not differ on baseline characteristics, except for presence of symptomatic lesion (80 vs. 49%, RR 1.64, p<0.01) and degree of stenosis (73 vs. 62%, p<0.001). The sensitivity and specificity of IPH on MPRAGE for predicting stroke were 46.5% and 80%, respectively.

The prevalence of basilar IPH was higher than the prevalence reported in MCA plaques, maybe because the basilar is easier seen on axial imaging due to larger wall area, and maybe because the imaging technique was more sensitive (MPRAGE vs. standard T-1 MRI). The authors point out the limitation of not having a histologic gold standard; however, they reference a study which compared MRI imaging to histology and determined that MPRAGE was better than T-1 Fast Spin Echo or TOF at detecting and quantifying IPH.

My only concern is that the High-Res MRI (with MPRAGE) was done up to 2 weeks following the original MRI, and the original MRI may have been up to one week post-stroke in symptomatic patients. It would be very interesting to follow the asymptomatic patients (who still had >50% basilar stenosis) with serial MPRAGE MRIs, to determine if those with IPH versus those without had higher rates of stroke, whether a certain degree of IPH can predict cerebrovascular events, and whether IPH appears following a cerebrovascular event in previously imaging-negative patients.​