Author/Authors :
Huijgen، نويسنده , , Roeland and Boekholdt، نويسنده , , S. Matthijs and Arsenault، نويسنده , , Benoit J. and Bao، نويسنده , , Weihang and Davaine، نويسنده , , Jean-Michel and Tabet، نويسنده , , Fatiha and Petrides، نويسنده , , Francine and Rye، نويسنده , , Kerry-Anne and DeMicco، نويسنده , , David A. and Barter، نويسنده , , Philip J. and Kastelein، نويسنده , , John J.P. and Lambert، نويسنده , , G، نويسنده ,
Abstract :
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).
ives
rpose of this study was to investigate whether high levels of circulating proprotein convertase subtilisin kexin type 9 (PCSK9) would increase cardiovascular risk in statin-treated patients.
ound
s activate low-density lipoprotein (LDL) receptor gene expression, thus lowering plasma LDL levels. But statins also activate the expression of PCSK9, a secreted inhibitor of the LDL receptor, thereby limiting their beneficial effects.
s
e measured the plasma PCSK9 levels of 1,613 patients with stable coronary heart disease enrolled in the Treating to New Targets study, a randomized trial that compared the efficacy of high- versus low-dose atorvastatin. After a run-in period with atorvastatin 10 mg daily, patients were randomized to either continue with 10 mg or be up-titrated to 80 mg of atorvastatin, and followed during 5 years for major cardiovascular events (MCVEs).
s
ating PCSK9 levels measured at randomization were predictive of clinical outcomes in the group randomized to remain on atorvastatin 10 mg (p = 0.039), but not in the group that intensified atorvastatin treatment to 80 mg (p = 0.24). Further, PCSK9 levels measured 1 year post-randomization did not change upon increase of the statin dose.
sions
levels predict cardiovascular events in patients treated with low-dose atorvastatin. (A Study to Determine the Degree of Additional Reduction in CV Risk in Lowering LDL Below Minimum Target Levels [TNT]; NCT00327691)
