Arjen Lindenholz

147 Intracranial Atherosclerotic Burden and Cerebral Parenchymal Changes at 7T MRI 6 Discussion In the current study, an increased vessel wall lesion burden was associated with the presence of either small subcortical infarcts, lacunes of presumed vascular origin or deep grey matter infarcts, and with the presence of moderate to severe periventricular white matter hyperintensities. We did not find an association between intracranial vessel wall lesion burden and presence and number of large cortical infarcts and presence and number of infarcts when classified by type. In addition, the enhancing vessel wall lesion burden was only associated with the number of cortical microinfarcts. Several of the cerebral parenchymal changes we assessed in our study have been considered manifestations of SVD. 27 SVD is generally defined by cerebral parenchymal manifestations, as small vessel disease itself is difficult to quantify. 19,29-31 By contrast, large artery disease can be assessed directly using either lumenography techniques (stenosis) or intracranial vessel wall imaging (vessel wall lesions). 9 Many studies focus on either large vessel disease or SVD and ongoing effort has been committed to find differences or similarities between cerebral large artery disease and SVD. 32-39 Despite anatomical and pathophysiological differences between large and small intracranial vessels, the intracranial vasculature is interrelated as one vascular network. SVD has been recently described as a dynamic whole-brain disease that in some cases may share a similar etiology with large vessel disease. In this proposed ‘parent artery atheroma theory’ atherosclerotic plaques in the large cerebral arteries (e.g., MCA) cause an occlusion at the origin of smaller branching arteries, subsequently leading to cerebral parenchymal changes reflecting SVD. 21,39 The findings in our study can support this theory as we found an association between the presence of infarcts often related to SVD and the intracranial vessel wall lesion burden ( Table 2 ). Specific microbiota, proteases and immunoglobulins from atherosclerotic plaques can cause a cascade that harms the vessel wall endothelium, the blood brain barrier and consequently could lead to SVD. 22 This may be an alternative explanation of our findings that the co-occurrence of intracranial vessel wall lesions and parenchymal manifestations of SVD may suggest concomitant changes in both large and small intracranial vasculature. It remains unclear why an association was found between the enhancing vessel wall lesion burden and number of cortical microinfarcts, but not with presence of cortical microinfarcts nor with presence or number of any other type of infarct. Increasing evidence, including pooled data, show that vessel wall lesion enhancement may be associated with plaque vulnerability and consequently with higher risk of ischemic events. 40-42 Histopathological validation and especially follow-up studies with a larger sample size are necessary to investigate whether this applies to our study population.