Aim: It remains unclear whether the increase of LDL cholesterol (LDL-C) is a risk factor for cerebral vascular disease (CVD). To clarify the effects of hypercholesterolemia on cerebral small vessel… Click to show full abstract
Aim: It remains unclear whether the increase of LDL cholesterol (LDL-C) is a risk factor for cerebral vascular disease (CVD). To clarify the effects of hypercholesterolemia on cerebral small vessel disease (SVD), we investigate the characteristics of microvasculature including lenticulostriate arteries (LSA) using high resolution brain magnetic resonance imaging (MRI) in subjects with familial hypercholesterolemia (FH). Methods: Twenty-seven patients with FH and 25 patients with type2 diabetes (DM), 25 healthy controls underwent 7Tesla (7T) brain MRI. The prevalence of SVD and LSA structural changes, vessel wall plaque images were determined in each group. Results: The prevalence of SVD, including white matter hyperintensities and lacunar infarctions, significantly increased in DM compared with both FH and controls. In addition, the average numbers of stems of LSA were significantly smaller in DM than FH as well as controls. Interestingly, both SVD prevalence and LSA structural changes showed no difference between FH and controls. Next, we examined the vessel wall imaging analyses of middle cerebral arteries (MCA) and vertebral-basilar arteries (VA-BA). The prevalence of vessel wall plaque on both horizontal segment of MCA (FH vs. controls; 51.8% vs. 20.0%, p Conclusion: The prevalence of SVD and LSA structural impairment definitely increased in DM, suggesting that DM was strong risk for CVD compared to hypercholesterolemia. On the other hand, the prevalence of vessel wall plaque on MCA and VA-BA were significantly high in FH compared to controls. These results suggested long-term increase of LDL-C induced the plaque formation in cerebral microvasculature. Image analyses using 7T MRI enables us to investigate the characteristics of cerebral microvasculature prior to the development of SVD, leading to earlier interventions aimed at the prevention of atherosclerotic events. Disclosure Y. Todate: None. Y. Ishigaki: None.
               
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