Time course of release of inflammatory markers after coronary stenting: comparison between bare metal stent and sirolimus-eluting stent.
BACKGROUND
High levels of release of inflammatory markers after coronary angioplasty are predictors of late restenosis. Sirolimus-eluting stent reduces the risk of restenosis.


OBJECTIVE
To compare the release of inflammatory markers after coronary angioplasty with sirolimus-eluting stent and bare metal stent.


METHODS
Sixteen patients with a proximal left anterior descending coronery artery stenosis were randomly assigned to receive either bare metal stent (n = 8) or sirolimus-eluting stent (n = 8). We measured simultaneously aortic and coronary sinus concentrations of the von Willebrand factor antigen, tumor necrosis factor-alpha and interleukin-6 before, immediately and after 2 h after stenting. High-sensitivity C-reactive protein and troponin-I circulating levels were measured before and 6 and 24 h after coronary angioplasty.


RESULTS
Before stenting, all values were similar in both groups. The coronary sinus change of the von Willebrand factor antigen level between baseline and 2 h after stenting was + 20.1 +/- 26.9% in the bare metal stent group and -5.7 +/- 23.02% in the sirolimus-eluting stent group (P < 0.05). We observed a significant increase in the von Willebrand factor antigen (from 132.8+/-58.8 to 169 +/- 40.7%, P < 0.05) systemic concentrations 24 h after stenting in the bare metal stent group but not in the sirolimus-eluting stent group (from 140.6+/-84% to 136 +/- 39.5%), P = NS).


CONCLUSIONS
The present study shows that a difference in the release of inflammatory markers can be detected after coronary stenting with bare metal stent or sirolimus-eluting stent. The lower release of the von Willebrand factor antigen in the coronary sinus 2 h after the procedure and the lower systemic concentrations of the von Willebrand factor antigen 24 h after stenting in the sirolimus-eluting stent group are likely to reflect a reduced production of the von Willebrand factor antigen at the site of the vascular injury.
Kefer
Joëlle M
JM
Divisions of Cardiology Haemostasis, University of Louvain, Brussels, Belgium.
Galanti
Laurence M
LM
Desmet
Sandrine
S
Deneys
Véronique
V
Hanet
Claude E
CE
D000941:Antigens / Q000032:analysis*; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D023903:Coronary Restenosis / Q000175:diagnosis*; D023921:Coronary Stenosis / Q000601:surgery*; D003331:Coronary Vessels / Q000737:chemistry*; D005260:Female; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage; D007249:Inflammation / Q000175:diagnosis; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008670:Metals / Q000276:immunology; D008875:Middle Aged; D009204:Myocardial Revascularization / Q000379:methods*; D011379:Prognosis; D012850:Sinus of Valsalva / Q000737:chemistry; D020123:Sirolimus / Q000008:administration & dosage; D015607:Stents; D019210:Troponin I / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014841:von Willebrand Factor / Q000276:immunology
D000941:Antigens; D015415:Biomarkers; D007166:Immunosuppressive Agents; D015850:Interleukin-6; D008670:Metals; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; C029417:Von Willebrand antigen; D014841:von Willebrand Factor; D002097:C-Reactive Protein; D020123:Sirolimus