Similar trends were observed for changes in total cholesterol .
Implication sGiven the available data , the addition of ezetimibe to ongoing simvastatin , atorvastatin , or rosuvastatin monotherapy offers greater reduction in LDL-C among patients at high risk of CVD compared to doubling the initial statin dose
Purpose While statins are used as first-line treatments for high-risk patients with hypercholesterolemia , statin monotherapy is often insufficient to achieve target low-density lipoprotein cholesterol ( LDL-C ) levels .
Second-line treatment options include up-titration of statin dose , switching to a more potent statin , or combination therapy , e.g. , with ezetimibe .
The aim of this study was to evaluate the efficacy of adding ezetimibe to simvastatin , atorvastatin , or rosuvastatin monotherapy versus doubling the dosage or switching to a higher-potency statin in a population of patients with hypocholesterolemia at high risk of cardiovascular disease ( CVD ) and who had been previously treated with a statin .
Pleiotropic effects of ezetimibe/simvastatin vs. high dose simvastatin.
BACKGROUND In the setting of stable coronary artery disease ( CAD ) , it is not known if the pleiotropic effects of cholesterol reduction differ between combined ezetimibe/simvastatin and high-dose simvastatin alone . OBJECTIVE We sought to compare the anti-inflammatory and antiplatelet effects of ezetimibe 10mg/simvastatin 20 mg ( E10/S20 ) with simvastatin 80 mg ( S80 ) . METHODS AND RESULTS CAD patients ( n=83 , 63 ± 9 years , 57 % men ) receiving S20 , were r and omly allocated to receive E10/S20 or S80 , for 6 weeks . Lipids , inflammatory markers ( C-reactive protein , interleukin-6 , monocyte chemoattractant protein-1 , soluble CD40 lig and and oxidized LDL ) , and platelet aggregation ( platelet function analyzer [PFA]-100 ) changes were determined . Baseline lipids , inflammatory markers and PFA-100 were similar between groups . After treatment , E10/S20 and S80 patients presented , respectively : ( 1 ) similar reduction in LDL-C ( 29 ± 13 % vs. 28 ± 30 % , p=0.46 ) , apo-B ( 18 ± 17 % vs. 22 ± 15 % , p=0.22 ) and oxidized LDL ( 15 ± 33 % vs. 18 ± 47 % , p=0.30 ) ; ( 2 ) no changes in inflammatory markers ; and , ( 3 ) a higher increase of the PFA-100 with E10/S20 than with S80 ( 27 ± 43 % vs. 8 ± 33 % , p=0.02 ) . CONCLUSIONS These data suggest that among stable CAD patients treated with S20 , ( 1 ) both E10/S20 and S80 were equally effective in further reducing LDL-C ; ( 2 ) neither treatment had any further significant anti-inflammatory effects ; and ( 3 ) E10/S20 was more effective than S80 in inhibiting platelet aggregation . Thus , despite similar lipid lowering and doses 4 × less of simvastatin , E10/S20 induced a greater platelet inhibitory effect than S80
Similar trends were observed for changes in total cholesterol .
Implication sGiven the available data , the addition of ezetimibe to ongoing simvastatin , atorvastatin , or rosuvastatin monotherapy offers greater reduction in LDL-C among patients at high risk of CVD compared to doubling the initial statin dose
Purpose While statins are used as first-line treatments for high-risk patients with hypercholesterolemia , statin monotherapy is often insufficient to achieve target low-density lipoprotein cholesterol ( LDL-C ) levels .
Second-line treatment options include up-titration of statin dose , switching to a more potent statin , or combination therapy , e.g. , with ezetimibe .
The aim of this study was to evaluate the efficacy of adding ezetimibe to simvastatin , atorvastatin , or rosuvastatin monotherapy versus doubling the dosage or switching to a higher-potency statin in a population of patients with hypocholesterolemia at high risk of cardiovascular disease ( CVD ) and who had been previously treated with a statin .