Investigating the treatment of vascular risk with simvastatin in secondary progressive multiple sclerosis: analysis from the MS-STAT2 randomised controlled trial

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ID: 318657
2026
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Abstract
Abstract Vascular comorbidity is associated with more severe disability in multiple sclerosis. However, it is unknown whether treating vascular risk will lead to a disease modifying effect. Given the established role of simvastatin as a modifier of vascular risk, we aimed to investigate whether randomisation to simvastatin could mitigate the relationships between serum cholesterol profiles and disease worsening, compared to placebo, in the MS-STAT2 trial. MS-STAT2 (NCT03387670) recruited 964 patients with secondary progressive multiple sclerosis, who were randomised to simvastatin (80mg) or placebo for 3 years. 246 participants additionally underwent yearly magnetic resonance imaging (MRI). Vascular risks were systematically assessed at trial baseline. In this exploratory analysis, the relationships between cholesterol ratio (total cholesterol/high-density lipoprotein) and longitudinal clinical and MRI outcomes were assessed, comparing simvastatin to placebo groups. At baseline, median (IQR) age was 55 (50-60) years and median cholesterol ratio 3.4 (2.8 to 4.3). 73% were female, and 72% required a walking aid. Higher cholesterol ratio was associated with more severe baseline disability. No longitudinal relationships were observed between cholesterol ratio and clinical or brain atrophy outcomes. However, for each unit increase in cholesterol ratio, T2 lesion volume increased by +2.47% (95% CI: +0.03 to +4.97) from baseline in the placebo group. This relationship was significantly reduced in those randomised to simvastatin (-3.10% [-0.06 to -6.06]). Randomisation to simvastatin appeared to mitigate the relationship between higher cholesterol ratio and longitudinal increases in T2 lesion volume in patients with secondary progressive multiple sclerosis. Further multi-modal interventional studies targeting vascular risk in patients with multiple sclerosis are warranted.
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Authors Thomas Williams, Nicholas Magill, Nevin John, Alessia Bianchi, James Blackstone, Marie Braisher, Floriana De Angelis, Alberto Calvi, Sean Apap Mangion, Charles Wade, Marios Yiannakas, Jonathan Stutters, Antonio Ricciardi, Ferrán Prados, David MacManus, Claudia A. M. Gandini Wheeler‐Kingshott, Frederik Barkhof, Olga Ciccarelli, Jeremy Chataway, the MS-STAT2 investigators, Jeremy Chataway, Thomas Williams, Nevin John, Floriana De Angelis, Alberto Calvi, Alessia Bianchi, Sarah Wright, Madiha Shatila, Anisha Doshi, Sean Apap Mangion, Charles Wade, Wallace Brownlee, Claudia A M Gandini Wheeler-Kingshott, Frederik Barkhof, Olga Ciccarelli, Jonathan Stutters, Ferran Prados Carrasco, Antonio Ricciardi, Marios Yiannakas, David MacManus, Mariana Agiu, Vanessa Bassan, Tiggy Beyene, S.-J. Conway, Batoul Fneich, Alfredo H. Jimenez, Sarah Pullinger, Eirini Samdanidou, Megan Wynne, Marie Braisher, James Blackstone, Rachel Merry, Gil Barton, Leanne Crisp, Josephine Parker, Jennifer Flight, Liz Deane, Chris Frost, Jennifer Nicholas, Stuart Nixon, Judy Beveridge, Sue Pavitt, Siddharthan Chandran, Don Mahad, Peter Connick, Dawn Lyle, Ian Galea, Elisabeth Jarman, Carmen Jacob, Stefania Kaninia, Basil Sharrack, David Paling, Helen Ford, Linford Fernandes, Maruthi Vinjam, Owen Pearson, Gillian Ingram, Christopher Rickards, Marguerite Hill, Nikos Evangelou, Christopher Allen, Abdullah Shehu, Tarunya Arun, Mohamed Belhag, Gavin McDonnell, Fiona Magill, Stephen Ramsay, Ruth Geraldes, Matthew Craner, Daniel Cullen, H. Birmingham, Ana Cavey, Charles Hillier, Judith Dube, Michelle Davis, Jeban Ganesalingam, Leonora Fisniku, Julia Aram, Julie Newman, JC Hobart
Journal Brain communications
Year 2026
DOI
10.1093/braincomms/fcag240
URL
https://doi.org/10.1093/braincomms/fcag240
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