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 .
Effects of ezetimibe on markers of synthesis and absorption of cholesterol in high-risk patients with elevated C-reactive protein.
AIMS High-risk subjects with elevated C-reactive protein ( CRP ) are at high risk for cardiovascular events and frequently require potent statins or combined lipid-lowering therapy to achieve lipid targets and decrease inflammation . Our study aim ed at evaluating the effects of three lipid-modifying therapies on LDL-cholesterol , CRP levels and markers of cholesterol absorption and synthesis . MAIN METHODS A prospect i ve intervention study was performed in high cardiovascular risk individuals receiving atorvastatin 10 mg daily for four weeks . Those with CRP≥2.0mg/L were r and omized to another four-week treatment period with atorvastatin 40 mg , ezetimibe 10 mg or the combination of atorvastatin 40 mg / ezetimibe 10 mg  . Lipids , markers of cholesterol absorption ( campesterol and β-sitosterol ) , and synthesis ( desmosterol ) , as well as CRP were quantified at baseline and end of study . KEY FINDINGS One hundred and twenty two individuals were included .  Atorvastatin alone or combined with ezetimibe  reduced both LDL-cholesterol and CRP ( P<0.002 vs. baseline ; Wilcoxon ) ; ezetimibe did not modify CRP . Ezetimibe-based therapies  reduced absorption markers and their ratios to cholesterol ( P<0.0001 vs. baseline , for all ; Wilcoxon ) , whereas atorvastatin alone increased campesterol/cholesterol and β-sitosterol/cholesterol ratios ( P<0.05 vs. baseline ; Wilcoxon ) . In addition , ezetimibe also increased desmosterol and desmosterol/cholesterol ratio ( P<0.0001 vs. baseline ; Wilcoxon ) . SIGNIFICANCE These results contribute to underst and ing the link between cellular cholesterol homeostasis , inflammation and lipid-modifying therapies . Our findings highlight the broader benefit of combined therapy with a potent statin and ezetimibe  decreasing inflammation , and preventing increase in cholesterol bio synthesis , an effect not observed with ezetimibe alone
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 .