The Effect Of Cardiovascular Risk Factors On Lesion Burden And Brain Atrophy In Multiple Sclerosis (S54.006)

2014 
Objectives: To investigate the association between cardiovascular (CV) risk factors and MRI disease severity in a large cohort of multiple sclerosis (MS) patients. Background: CV risks including smoking, obesity, hyperlipidemia, hypertension, and heart problems have been associated with changes in clinical outcomes in patients with MS. However, possible associations between CV risks and MRI outcomes were not explored in MS. Methods: 326 relapsing-remitting (RR) MS patients, 163 patients with progressive MS, 61 patients with clinically isolated syndrome and 175 age- and sex- matched healthy controls (HC) were screened for CV risks and scanned on a 3T MRI scanner. Participants were grouped based on disease status and disease course. The collected CV risks included hypertension, heart problems, smoking and body mass index (BMI). MRI measures assessed brain volumes and lesion volumes (LVs). Effect of single or combination of multiple CV risks on MRI outcomes was examined by analysis of covariance adjusted for age, sex and treatment status and supplemented by a binary logistic regression. Results: MS patients showed increased prevalence of smoking (51.7% vs. 36.5%, p=0.001) and hypertension (33.9% vs. 24.7%, p=0.035) compared to HCs. 49.9% of MS patients and 36% of HC showed 蠅2 CV risks (p<0.05), while the prevalence of 蠅3 CV risks was 18.8% in MS and 8.6% in HC groups (p<0.05). Significantly increased T2-LV was found among the RRMS patients who had hypertension, heart disease and obesity (p=0.028). Increased T2-LV was found among RRMS patients who were hypertensive, smoked, and had heart problems (p= 0.031). Those RRMS patients with hypertension and heart problems also had increased T2-LV (p=0.039). Having at least 2 cardiovascular risks was associated with more advanced grey matter (GM) atrophy among the RRMS patients (p<0.05). Conclusion: RRMS patients with more than one CV risks showed increased T2 lesion burden and more advanced GM atrophy. Disclosure: Dr. Kappus has nothing to disclose. Dr. Weinstock-Guttman has received personal compensation for activities with Biogen Idec, Teva Neuroscience, EMD Serono, Pfizer, Novartis, Genzyme, Sanofi-Aventis Pharmaceuticals, Inc., Mylan, and Acorda Therapeutics. Dr. Weinstock-Guttman has received research support from Biogen Idec, Teva Neuroscience, EMD Serono, Pfizer Inc, Novartis, Acorda, ITN, Questcor, Shire, Genzyme, Sanofi-Aventis Pharmaceuticals, Inc., National Multiple Sclerosis Society, the National Institutes of Health and Aspreva-Roche. Dr. Hagemeier has nothing to disclose. Dr. Kennedy has nothing to disclose. Dr. Melia has nothing to disclose. Dr. Carl has nothing to disclose. Dr. Ramasamy has nothing to disclose. Dr. Cherneva has nothing to disclose. Dr. Durfee has nothing to disclose. Dr. Bergsland has nothing to disclose. Dr. Dwyer has received personal compensation for activities with EMD Serono and Claret. Dr. Kolb has received personal compensation for activities with Teva Neuroscience, Biogen Idec and EMD Serono as a speaker and scientific advisory board member. Dr. Ramanathan has received personal compensation in an editorial capacity for The AAPS Journal. Dr. Zivadinov has received personal compensation for activities with Teva, Biogen Idec, EMD Serono, Novartis, Claret and Sanofi-Genzyme. Dr. Zivadinov has received research support from Biogen Idec, Teva Pharmaceuticals, Sanofi-Genzyme, Novartis and EMD Serono.
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