title: Efficiency of statin treatment on EPC recruitment depends on baseline EPC titer and does not improve angiographic outcome in coronary artery disease patients treated with the Genous stent.
abstract: The objective of this study was to assess the effect of high-dose atorvastatin treatment on endothelial progenitor cell (EPC) recruitment and angiographic and clinical outcome in coronary artery disease (CAD) patients treated with the Genous EPC-capturing stent. The HEALING IIB study was a multicenter, open-label, prospective trial that enrolled 100 patients. Patients were started on 80 mg atorvastatin qd, at least 2 weeks before the index procedure and continued for at least 4 weeks after the index procedure. Eighty-seven patients were included in this analysis. EPC levels significantly increased as early as 2 weeks after the start of atorvastatin. Remarkably, among this group, 31 patients proved to be nonresponders to atorvastatin treatment (i.e., no increase in EPC levels), while 56 patients were responders (i.e., rise in EPC count between week -2 and 0). Compared to responders, nonresponders had a significantly higher baseline EPC count (76 ± 10 vs. 41 ± 5, p < 0.01) with a lower late luminal loss (LLL) at 6- and 18-month follow-up (FU) (0.61 ± 0.07 vs. 0.88 ± 0.08, p < 0.05, and 0.50 ± 0.08 vs. 0.82 ± 0.08, p < 0.01 respectively). Furthermore, baseline EPC count was inversely correlated with LLL at 6-month FU (R = -0.42, p < 0.001). Patients with a higher EPC count at baseline showed no increase in EPC recruitment in response to statin treatment but had favorable LLL at 6- and 18-month FU, whereas patients with lower EPC count were responsive to statin therapy, but EPCs might be less functional as they had higher LLL at 6- and 18-month FU. These data imply that although statin treatment can enhance EPC titer in patients with low baseline levels, there is no indication for a possible beneficial clinical effect with EPC capture stents.
authors.affiliation: Thoraxcenter Rotterdam, Erasmus University Medical Center, Rotterdam, The Netherlands.
authors.forename: Wijnand K
authors.initials: WK
authors.lastname: den Dekker
authors.forename: Jaco H
authors.initials: JH
authors.lastname: Houtgraaf
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Rowland
authors.forename: Erik
authors.initials: E
authors.lastname: Ligtenberg
authors.forename: Sanneke P M
authors.initials: SP
authors.lastname: de Boer
authors.forename: Renate
authors.initials: R
authors.lastname: de Jong
authors.forename: Robbert J
authors.initials: RJ
authors.lastname: de Winter
authors.forename: Peter
authors.initials: P
authors.lastname: den Heijer
authors.forename: Felix
authors.initials: F
authors.lastname: Zijlstra
authors.forename: Patrick W
authors.initials: PW
authors.lastname: Serruys
authors.forename: Caroline
authors.initials: C
authors.lastname: Cheng
authors.forename: Henricus J
authors.initials: HJ
authors.lastname: Duckers
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000069059:Atorvastatin; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging* / Q000473:pathology*; D003710:Demography; D066026:Endothelial Progenitor Cells / Q000187:drug effects*; D005260:Female; D006538:Heptanoic Acids / Q000494:pharmacology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011758:Pyrroles / Q000494:pharmacology; D012044:Regression Analysis; D015607:Stents; D016896:Treatment Outcome
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; D000069059:Atorvastatin