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.
OBJECTIVE
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.


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 (10-80mg) to target low-density lipoprotein (LDL)<100mgdl(-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).


CONCLUSIONS
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.
Kadoglou
N P E
NP
First Department of Internal Medicine, Hippokratio General Hospital of Thessaloniki, Thessaloniki, Greece. nikoskad@yahoo.com
Gerasimidis
T
T
Kapelouzou
A
A
Moumtzouoglou
A
A
Avgerinos
E D
ED
Kakisis
J D
JD
Karayannacos
P E
PE
Liapis
C D
CD
D000368:Aged; D017130:Angioplasty / Q000295:instrumentation*; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002114:Calcinosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000628:therapy*; D016893:Carotid Stenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000628:therapy*; D003131:Combined Modality Therapy; D015536:Down-Regulation; D005260:Female; D006115:Greece; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D053495:Osteopontin / Q000097:blood*; D053244:Osteoprotegerin / Q000097:blood*; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use*; D012720:Severity of Illness Index; D015607:Stents; D013997:Time Factors; D016896:Treatment Outcome; D018608:Ultrasonography, Doppler
D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D053244:Osteoprotegerin; D011758:Pyrroles; C506895:SPP1 protein, human; C506030:TNFRSF11B protein, human; D053495:Osteopontin; D002097:C-Reactive Protein; D000069059:Atorvastatin