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Abstract Details

Comparative Performance of 7T and Conventional MRI for CAA Markers
Cerebrovascular Disease and Interventional Neurology
P4 - Poster Session 4 (8:00 AM-9:00 AM)
5-002

sensitivity of 7T MRI to detect imaging markers of CAA in comparison to conventional MRI

Cerebral amyloid angiopathy(CAA) is characterized by progressive amyloid-β deposition in cortical and leptomeningeal vessels, resulting in cognitive impairment, stroke, and intracranial hemorrhage. While definitive diagnosis requires histopathology, clinical diagnoses are primarily based on clinical and magnetic resonance imaging(MRI) findings. MRI diagnosis is influenced by imaging sequences and magnet strength. 7 Tesla (7T) MRI may improve visualization of hemorrhagic markers of CAA such as cortical microbleeds (CMBs), cortical superficial siderosis (CSS), and intragyral hemorrhage (IGH). 

We reviewed patients who underwent 7T brain MRI for evaluation of CAA at our institution. Eligible patients also had a conventional (1.5-3.0 Tesla) MRI for comparison.Radiographic findings were independently reviewed by two neuroradiologists and any disagreements were resolved through consensus. T2* and SWI sequences were reviewed for the presence (yes/no) of CMBs, CSS, and IGH. Results are reported descriptively.

Of the 70 patients who underwent 7T MRI for evaluation of CAA, 40 had conventional MRI for comparison. The cohort’s mean age was: 76.5(±10.2)years; 70% female;82/5%white, and 87.5% 1.5T, 12.5% 3.0T MRI. All 40 7T MRI scans included T2* and SWI sequences.Of the 40 conventional MRI scans, 14(35%) included SWI and 26 (65%) included T2*.On 7T T2*, the incidence of any CMBs, CSS, or IGH was 69.23%, 34.62%, 15.38% compared to 23.8%, 11.54%, 0 with conventional MRI. On 7T SWI, the incidence of any CMBs, CSS, or IGH was 57.14%,57.14%, 50% versus 50%, 50%, 7.14% with conventional MRI SWI.The “number needed to scan” to detect one additional patient with CMBs was 3,14 ; CSS was 5,14 ; and IGH was 7,3 for 7T T2* and SWI sequences, respectively.

7T MRI increased the likelihood of detecting hemorrhagic markers of CAA. The clinical implications of these findings requires further study.

Authors/Disclosures
Rojin Ahmadi, MD
PRESENTER
Dr. Ahmadi has nothing to disclose.
CAN Ozutemiz (University of minnesota) CAN Ozutemiz has nothing to disclose.
Kompal Kumar, Undergraduate Student Miss Kumar has nothing to disclose.
Carl-Lewis Valcinord, MD Dr. Valcinord has nothing to disclose.
Abbey Staugaitis Abbey Staugaitis has nothing to disclose.
Mark Folkertsma, MD Dr. Folkertsma has nothing to disclose.
Christopher Streib, MD (Department of Neurology) Dr. Streib has nothing to disclose.