Title
Vascular Function and Multiple Sclerosis
Document Type
Article
Publication Date
2012
Embargo Period
5-18-2017
Keywords
Inflammation, reactive hyperemia, FMD, physical activity
Abstract
Multiple sclerosis (MS) is a debilitating disease with an assumed autoimmune etiology which may lead to elevated oxidative stress, vascular dysfunction, and subsequent predisposition to cardiovascular disease. Therefore, the primary aim of this study was to evaluate vascular function and the potential role of oxidative stress in patients diagnosed with MS compared to healthy controls (C). Fourteen patients with relapsing-remitting MS (47 ± 3 years) and 13 age- and activity-matched controls (44 ± 5 years) underwent brachial artery flow-mediated dilation (FMD) and reactive hyperemia testing using ultrasound Doppler. Venous blood was analyzed for C-reactive protein (CRP), lipid hydroperoxides (LH), the ferric reducing ability of plasma (FRAP), superoxide dismutase (SOD), and catalase activity. CRP [1.8 ± 0.5 mg/L (MS), 1.0 ± 0.5 mg/L (C)] and LH [1.2 ± 0.2 μmol/L (MS), 1.1 ± 0.1 μmol/L (C)] were not different between MS patients and controls. FMD [8.0 ± 1.2% (MS) and 9.2 ± 1.6% (C)] and reactive hyperemia [380 ± 61 mL (MS) and 402 ± 69 mL (C)] were also not different between groups. Vascular function, as assessed by both FMD and reactive hyperemia, was not impaired in patients with MS compared to controls. Further, there was no evidence of elevated systemic inflammation or oxidative stress in these patients, who were currently all in remission. These findings suggest that impaired vascular function, elevated inflammation and oxidative stress are not an obligatory accompaniment to MS.
Published In
Journal of Neurology
Volume
258
Issue
11
Pages
2036-2042
Recommended Citation
Fjeldstad AS, McDaniel J, Witman MA, Ives SJ, Zhao J, Rose JW, Hannon J, Wray DW, Richardson RS. Vascular function and multiple sclerosis. J Neurol. 2011 Nov;258(11):2036-42. doi: 10.1007/s00415-011-6065-2. Epub 2011 May 5. PubMed PMID: 21544565.
DOI
10.1007/s00415-011-6065-2