Plasma levels of C-reactive protein after coronary stent implantation

Citation
M. Gottsauner-wolf et al., Plasma levels of C-reactive protein after coronary stent implantation, EUR HEART J, 21(14), 2000, pp. 1152-1158
Citations number
33
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
EUROPEAN HEART JOURNAL
ISSN journal
0195668X → ACNP
Volume
21
Issue
14
Year of publication
2000
Pages
1152 - 1158
Database
ISI
SICI code
0195-668X(200007)21:14<1152:PLOCPA>2.0.ZU;2-L
Abstract
Aims This study was designed to investigate the role of inflammation on the occurrence of angiographic restenosis 6 months after coronary stent implan tation and the influence of different kinds of antithrombotic and antiplate let strategies on inflammation. Methods and Results In an open randomized trial, 40 consecutive patients we re treated with aspirin (100 mg . day(-1)) and either ticlopidine (2 x 250 mg . day(-1)) (n=17), or phenprocoumon (INR 2.0-3.0)and dipyridamole (3 x 1 60 mg . day(-1)) (n=23) after successful elective coronary stent implantati on. Plasma levels of C-reactive protein were determined one day before sten t implantation and serially thereafter twice daily up to 120 h. C-reactive protein plasma levels increased significantly (P<0.0001) after stent implan tation. Phenprocoumon and dipyridamole or ticlopidine had no effect on C-re active protein plasma levels (P=0.51) or the occurrence of angiographic res tenosis (P=0.48). C-reactive protein plasma levels were significantly highe r in patients with lesion type C compared to types A or B (P=0.035), respec tively. C-reactive protein plasma levels were significantly higher and mean shoulder levels occurred 48 h later in patients with restenosis compared t o patients without restenosis after 6 months (P=0.038). Conclusions Elevated C-reactive protein plasma levels still persisting 96 h after stent implantation might reflect a prolonged inflammatory reaction t o coronary stent implantation which might causally be involved in pathophys iological mechanisms leading to restenosis. (Eur Heart J 2000; 21: 1152-115 8) (C) 2000 The European Society of Cardiology.