A randomized trial in patients undergoing percutaneous coronary angioplasty: Roxithromycin does not reduce clinical restenosis but angioplasty increases antibody concentrations against Chlamydia pneumoniae - 21/08/11
, Antje Haar, MD a, Klaus-Peter Schaps, MD a, c, Andreas Gaede, MD a, c, Marion Carstensen, MD a, b, Ilka Schalwat, MD a, Ralf Koester, MD a, Rainer Laufs, MD a, b, Thomas Meinertz, MD a, Wolfram Terres, MD a, cRésumé |
Background |
Elevated antibodies against Chlamydia pneumoniae have been associated with coronary artery disease. In patients undergoing percutaneous coronary angioplasty, we therefore investigated the effect of roxithromycin on symptomatic restenosis and determined antichlamydial antibodies as well as inflammatory and immunological parameters.
Methods |
A total of 327 patients undergoing coronary angioplasty were randomized to roxithromycin or placebo and followed-up for 1 year. Antibodies were determined by microimmunofluorescence and enzyme-linked immunosorbent assay; C-reactive protein, interleukin-10, tumor necrosis factor-α (TNF-α), and eotaxin were determined by enzyme-linked immunosorbent assay.
Results |
Although the frequency of restenosis was not affected by roxithromycin (25 restenoses vs 32 in the control group), antichlamydial antibodies increased during follow-up (anti-CP IgG +12 ± 2%, P < .001). Concentrations of TNF-α and eotaxin increased as well (TNF-α +9 ± 1% and eotaxin +10 ± 2%) and correlated with antichlamydial antibody concentrations (TNF-α, r = 0.23, P = .02; eotaxin, r = 0.32, P = .002).
Conclusions |
Treatment with roxithromycin was not associated with a reduction of symptomatic restenoses. During follow-up, a marked increase in antichlamydial antibodies, TNF-α, and eotaxin was observed, suggesting that angioplasty-induced plaque rupture induces a specific immunological response without activation of inflammatory mechanisms as represented by C-reactive protein. Whether this mechanism occurs in all plaque ruptures remains to be determined.
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| The study was financially supported by Aventis Germany. |
Vol 150 - N° 5
P. 987-993 - novembre 2005 Retour au numéro
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