Valsartan prevents neointimal hyperplasia after carotid artery stenting by suppressing endothelial cell injuries

Objectives: 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. Methods: 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-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. Results: The non-valsartan group (n = 8) had a higher incidence of maximum in-stent IMT >= 1.1 mm compared with the normotensive group (n = 6). Valsartan (n = 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. Conclusions: These findings suggest that valsartan may prevent post-CAS neointimal hyperplasia possibly by suppressing endothelial cell injury.