Sodium Valproate, a Histone Deacetylase Inhibitor, Is Associated With Reduced Stroke Risk After Previous Ischemic Stroke or Transient Ischemic Attack

Wouldn't you want this available for stroke prevention? Well you are out of luck. Nothing will be done with this because we have NO stroke strategy and NO stroke leadership.
There was already this from August 2013.

Impact of trichostatin A and sodium valproate treatment on post-stroke neurogenesis and behavioral outcomes in immature mice

 The latest here:

Sodium Valproate, a Histone Deacetylase Inhibitor, Is Associated With Reduced Stroke Risk After Previous Ischemic Stroke or Transient Ischemic Attack 

Rebecca L. Brookes, Siobhan Crichton, Charles D.A. Wolfe, Qilong Yi, Linxin Li, Graeme J. Hankey, Peter M. Rothwell, Hugh S. Markus

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https://doi.org/10.1161/STROKEAHA.117.016674

Stroke. 2017;STROKEAHA.117.016674

Originally published December 15, 2017

Rebecca L. Brookes

From the Stroke Research Group, Clinical Neurosciences, University of Cambridge, United Kingdom (R.L.B., H.S.M.); Division of Health and Social Care Research, Faculty of Life Sciences and Medicine, King’s College London, United Kingdom (S.C., C.D.A.W.); National Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario (Q.Y.); School of Medicine and Pharmacology, The University of Western Australia, Perth (G.J.H.); Department of Neurology, Sir Charles Gairdner Hospital, Perth, Australia (G.J.H.); Western Australian Neuroscience Research Institute, Perth (G.J.H.); and Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom (L.L., P.M.R.).

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Siobhan Crichton

From the Stroke Research Group, Clinical Neurosciences, University of Cambridge, United Kingdom (R.L.B., H.S.M.); Division of Health and Social Care Research, Faculty of Life Sciences and Medicine, King’s College London, United Kingdom (S.C., C.D.A.W.); National Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario (Q.Y.); School of Medicine and Pharmacology, The University of Western Australia, Perth (G.J.H.); Department of Neurology, Sir Charles Gairdner Hospital, Perth, Australia (G.J.H.); Western Australian Neuroscience Research Institute, Perth (G.J.H.); and Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom (L.L., P.M.R.).

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Charles D.A. Wolfe

From the Stroke Research Group, Clinical Neurosciences, University of Cambridge, United Kingdom (R.L.B., H.S.M.); Division of Health and Social Care Research, Faculty of Life Sciences and Medicine, King’s College London, United Kingdom (S.C., C.D.A.W.); National Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario (Q.Y.); School of Medicine and Pharmacology, The University of Western Australia, Perth (G.J.H.); Department of Neurology, Sir Charles Gairdner Hospital, Perth, Australia (G.J.H.); Western Australian Neuroscience Research Institute, Perth (G.J.H.); and Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom (L.L., P.M.R.).

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Linxin Li

From the Stroke Research Group, Clinical Neurosciences, University of Cambridge, United Kingdom (R.L.B., H.S.M.); Division of Health and Social Care Research, Faculty of Life Sciences and Medicine, King’s College London, United Kingdom (S.C., C.D.A.W.); National Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario (Q.Y.); School of Medicine and Pharmacology, The University of Western Australia, Perth (G.J.H.); Department of Neurology, Sir Charles Gairdner Hospital, Perth, Australia (G.J.H.); Western Australian Neuroscience Research Institute, Perth (G.J.H.); and Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom (L.L., P.M.R.).

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Graeme J. Hankey

From the Stroke Research Group, Clinical Neurosciences, University of Cambridge, United Kingdom (R.L.B., H.S.M.); Division of Health and Social Care Research, Faculty of Life Sciences and Medicine, King’s College London, United Kingdom (S.C., C.D.A.W.); National Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario (Q.Y.); School of Medicine and Pharmacology, The University of Western Australia, Perth (G.J.H.); Department of Neurology, Sir Charles Gairdner Hospital, Perth, Australia (G.J.H.); Western Australian Neuroscience Research Institute, Perth (G.J.H.); and Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom (L.L., P.M.R.).

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Peter M. Rothwell

From the Stroke Research Group, Clinical Neurosciences, University of Cambridge, United Kingdom (R.L.B., H.S.M.); Division of Health and Social Care Research, Faculty of Life Sciences and Medicine, King’s College London, United Kingdom (S.C., C.D.A.W.); National Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario (Q.Y.); School of Medicine and Pharmacology, The University of Western Australia, Perth (G.J.H.); Department of Neurology, Sir Charles Gairdner Hospital, Perth, Australia (G.J.H.); Western Australian Neuroscience Research Institute, Perth (G.J.H.); and Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom (L.L., P.M.R.).

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Hugh S. Markus

From the Stroke Research Group, Clinical Neurosciences, University of Cambridge, United Kingdom (R.L.B., H.S.M.); Division of Health and Social Care Research, Faculty of Life Sciences and Medicine, King’s College London, United Kingdom (S.C., C.D.A.W.); National Epidemiology and Surveillance, Canadian Blood Services, Ottawa, Ontario (Q.Y.); School of Medicine and Pharmacology, The University of Western Australia, Perth (G.J.H.); Department of Neurology, Sir Charles Gairdner Hospital, Perth, Australia (G.J.H.); Western Australian Neuroscience Research Institute, Perth (G.J.H.); and Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom (L.L., P.M.R.).

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Abstract

Background and Purpose—A variant in the histone deacetylase 9 (HDAC9) gene is associated with large artery stroke. Therefore, inhibiting HDAC9 might offer a novel secondary preventative treatment for ischemic stroke. The antiepileptic drug sodium valproate (SVA) is a nonspecific inhibitor of HDAC9. We tested whether SVA therapy given after ischemic stroke was associated with reduced recurrent stroke rate.

Methods—Data were pooled from 3 prospective studies recruiting patients with previous stroke or transient ischemic attack and long-term follow-up: the South London Stroke Register, The Vitamins to Prevent Stroke Study, and the Oxford Vascular Study. Patients receiving SVA were compared with patients who received antiepileptic drugs other than SVA using survival analysis and Cox Regression.

Results—A total of 11 949 patients with confirmed ischemic event were included. Recurrent stroke rate was lower in patient taking SVA (17 of 168) than other antiepileptic drugs (105 of 530; log-rank survival analysis P=0.002). On Cox regression, controlling for potential cofounders, SVA remained associated with reduced stroke (hazard ratio=0.44; 95% confidence interval: 0.3–0.7; P=0.002). A similar result was obtained when patients taking SVA were compared with all cases not taking SVA (Cox regression, hazard ratio=0.47; 95% confidence interval: 0.29–0.77; P=0.003).

Conclusions—These results suggest that exposure to SVA, an inhibitor of HDAC, may be associated with a lower recurrent stroke risk although we cannot exclude residual confounding in this study design. This supports the hypothesis that HDAC9 is important in the ischemic stroke pathogenesis and that its inhibition, by SVA or a more specific HDAC9 inhibitor, is worthy of evaluation as a treatment to prevent recurrent ischemic stroke.