Beneficial Changes of Serum Calcification Markers and Contralateral Carotid Plaques Echogenicity after Combined Carotid Artery Stenting Plus Intensive Lipid-lowering Therapy in Patients with Bilateral Carotid Stenosis

Abstract Objectives/design In symptomatic patients treated with ipsilateral carotid artery stenting (CAS) plus intensive lipid lowering, we assessed the changes of osteopontin (OPN), osteoprotegerin (OPG) and the Gray-Scale Median (GSM) score contralateral to symptomatic carotid stenosis. Materials/methods Forty-six symptomatic patients (group A) with significant carotid stenosis (North American Symptomatic Carotid Endarterectomy Trial (NASCET): >70%) underwent ipsilateral CAS. Those patients had simultaneously contralateral low-grade carotid stenosis (NASCET: 30–69%). Group B included 67 symptomatic patients with low-grade bilateral carotid stenosis (NASCET: 30–69%), but without indications for revascularisation. All patients were treated with atorvastatin (10–80 mg) to target low-density lipoprotein (LDL) < 100 mg dl−1 . Blood samples and plaques' GSM score contralateral to brain infarct were assayed at baseline and after 6 months. Results At baseline, there were no significant differences between groups ( p > 0.05). Six-month atorvastatin treatment equivalently improved lipid profile in both groups ( p < 0.05). The parameters hsCRP, OPN and OPG were significantly down-regulated within both groups, but to a greater extent in group A ( p < 0.05). Besides this, contralateral GSM score was significantly improved from baseline in both groups ( p < 0.01), but that increment was more pronounced in group A (vs. group B; p = 0.041). These changes were inversely correlated with changes in OPN ( p = 0.014), OPG ( p = 0.011) and LDL ( p = 0.041). Conclusion Ipsilateral CAS plus intensive lipid-lowering therapy was associated with enhanced contralateral carotid plaque stability and attenuated inflammatory burden and calcification inhibitors to a greater extent than atorvastatin therapy alone in patients with bilateral carotid stenosis.