Valsartan prevents neointimal hyperplasia after carotid artery stenting by suppressing endothelial cell injuries. (January 2015)

• Record Type: Journal Article
• Authors: Suzuki, Hidenori; Sano, Takanori; Umeda, Yasuyuki; Yamamoto, Akitaka; Toma, Naoki; Sakaida, Hiroshi; Taki, Waro
• Is Part Of: Neurological research. Volume 37:Number 1(2015)
• Page Start: 35
• Page End: 42
• Publication Date: 2015-01
• Subjects: Neurology -- Periodicals; Neurosciences -- Periodicals; 616.8005
• DOI: 10.1179/1743132814Y.0000000408
• Languages: English
• ISSNs: 0161-6412

Abstract

<abstract> <title> <x content-type="archive" xml:space="preserve">Abstract</x> </title> <sec> <title>Objectives:</title> <p>Restenosis or neointimal hyperplasia remains an important complication after carotid artery stenting (CAS) for carotid artery stenosis. The purpose of this study was to examine if an anti-hypertensive drug, angiotensin receptor blocker (ARB), prevents post-CAS neointimal hyperplasia during the first 1-year period after CAS, and to clarify the possible mechanisms.</p> </sec> <sec> <title>Methods:</title> <p>Hypertension had been treated with a calcium channel blocker (CCB) and/or an ARB, valsartan, by the preference of the neurosurgeon in charge in our department. At admission to perform CAS, patients were assigned to normotensive, valsartan (hypertensive patients treated with valsartan with/without any kind of CCBs), and non-valsartan (hypertensive patients treated with any kind of CCBs without ARBs) groups. Post-CAS neointimal hyperplasia was evaluated by carotid duplex ultrasound imaging in terms of intima<bold>-</bold>media thickening (IMT), which was performed at pre-CAS and at 90, 180, 270, and 360 days post-CAS. Biomarkers of oxidative stress (8-hydroxy-2'-deoxyguanosine), inflammation (C-reactive protein, tenascin-C) and endothelial cell injury (von Willebrand factor [vWF] antigen) were measured at pre-CAS and at 1, 7, and 180 days post-CAS.</p> </sec> <sec> <title>Results:</title> <p>The non-valsartan group (<italic>n</italic> = 8) had a higher incidence of maximum in-stent IMT ≧ 1·1 mm compared with the normotensive group (<italic>n</italic> = 6). Valsartan (<italic>n</italic> = 9) significantly suppressed plasma vWF levels at 7 days post-CAS and decreased the incidence of maximum in-stent IMT ≧ 1·1 mm compared with the non-valsartan group, although clinical parameters were similar between the two groups. Other biomarkers were not significantly different among the three groups.</p> </sec> <sec> <title>Conclusions:</title> <p>These findings suggest that valsartan may prevent post-CAS neointimal hyperplasia possibly by suppressing endothelial cell injury.</p> </sec> </abstract>