Arjen Lindenholz

145 Intracranial Atherosclerotic Burden and Cerebral Parenchymal Changes at 7T MRI 6 Table 4. Associations between the presence of parenchymal changes and the enhancing intracranial vessel wall lesion burden. Outcome as present/absent Unadjusted relative risk (±95%CI) P-value Adjusted relative risk (±95%CI) P-value Infarcts Any anterior circulation infarct 1.00 (0.92-1.09) 0.957 0.99 (0.90-1.08) 0.824 Cortical infarcts 1.04 (0.95-1.14) 0.394 1.05 (0.94-1.16) 0.387 Infarcts often caused by SVD 1.06 (0.90-1.26) 0.498 1.00 (0.83-1.22) 0.975 Small subcortical infarcts NA NA NA NA Lacunes of presumed vascular origin 1.07 (0.87-1.32) 0.537 1.00 (0.78-1.28) 0.986 Deep grey matter infarcts 0.90 (0.65-1.24) 0.508 0.83 (0.61-1.14) 0.256 Cortical microinfarcts 1.24 (0.95-1.60) 0.112 1.18 (0.93-1.49) 0.187 White matter hyperintensities (Fazekas grade) Periventricular (0/1 vs. 2/3) 1.19 (0.98-1.45) 0.077 1.02 (0.81-1.29) 0.858 Deep (0/1 vs 2/3) 1.12 (0.92-1.36) 0.273 0.99 (0.80-1.24) 0.948 Table 4 . Included for analysis, n = 76. Six of 82 patients did not receive contrast agent. The unadjusted and adjusted (for age and sex) relative risks including their 95% confidence interval (CI) for the presence of cerebral parenchymal changes with the total number of anterior enhancing vessel wall lesions as included variable. A p-value < 0.05 was considered to indicate a statistically significant difference. A log-binomial regression model was used with a robust variance estimator. White matter hyperintensity Fazekas grade is described as: 0 = absence or single punctate white matter hyperintensity, 1 = ‘caps’ or pencil-thin lining or multiple punctate lesions, 2 = smooth ‘halo’ or beginning confluency of lesions, 3 = large confluent lesions or irregular hyperintensities extending into the deep white matter. 28 CMI; cortical microinfarct, NA; not applicable (only 1 count), SVD; small vessel disease.