Abstract
Small cerebral perforating arteries are essential for brain blood supply. Pathological changes in these arteries, known as small vessel disease (SVD), are strongly linked to stroke and dementia. Previously, studying these small arteries in vivo was not feasible, but advancements in 7T MRI now allow for detailed analysis of their
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function. This thesis investigates the relationship between cerebral perforating artery function and SVD by addressing three key questions: (1) How does their function relate to other components of the cardiovascular system? (2) How do vascular risk factors influence their function? (3) How does their function relate to SVD damage? how does cerebral perforating artery function relate to other functional measures along the cardiovascular tree? Our findings show a relation in the function between the more proximal arteries and perforating arteries in this extensive network of cerebral blood supply, indicating a complex interplay between different parts of the cardiovascular system. It teaches us that damping behavior, i.e. vascular response to a pulse wave measured in flow velocity and pulsatility, varies along the cardiovascular tree. It also varies among individuals and regions. Likewise that the more proximal regions are more prone to early damage than the distal regions. Furthermore, this thesis has shown that lower flow velocity occurs in the small perforating arteries of the CSO border zone areas in patients with COD, implying that these border zone areas are more vulnerable to changes. To sum up how vascular risk factors relate to cerebral perforating artery function, my answer in the setting where I explored this is that they are not directly related. Future research should focus on longitudinal studies, also in other, including population-based, cohorts, to observe how vascular risk factors and its management potentially impacts perforating artery function over time. Does the cerebral perforating artery function relate to SVD damage? Yes, in this thesis I conclude that small vessel function is altered in patients with structural manifestations of SVD and also relates to lesion burden. This finding provides new markers for SVD at the level of the perforating arteries themselves. The journey in understanding cerebral SVD is far from over, and while our findings have increased the existing knowledge on the mechanisms underlying cerebral SVD, establishing a causal relationship requires longitudinal studies to track disease progression over time and the path before us is not finished jet. In conclusion, this thesis has demonstrated that new MRI markers of cerebral perforating artery function can help to better understand SVD. Hopefully, this will pave the way to develop effective interventions that can prevent or even treat SVD.
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