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. AIM OF THE STUDY: 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). CONCLUSION: 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.

Acetylcysteine, coronary procedure and prevention of contrast-induced worsening of renal function: which benefit for which patient?

OBJECTIVES: This study was designed to determine whether acetylcysteine could provide a protective effect on renal function in a population of patients with normal renal function or mild to moderate chronic renal failure, usually referred for a coronary procedure. BACKGROUND: Contrast-induced nephropathy is a well-recognized complication of coronary angiography. Recent studies suggest that saline hydration and acetylcysteine reduce the incidence of contrast-induced worsening of renal function in patients with pre-existing chronic renal failure who are undergoing computed tomography examinations. METHODS: One hundred eight patients were blindly and randomly assigned to receive either acetylcysteine or placebo before and after administration of contrast agent in association with a moderate hydration protocol. Serum creatinine and urea nitrogen were measured before and 24 hours after coronary procedure. RESULTS: The mean serum creatinine concentration remained unchanged 24 hours after contrast agent administration in both groups: from 1.04 +/- 0.26 to 1.03 +/- 0.29 mg/dl in the acetylcysteine group and from 1.16 +/- 1.1 to 1.06 +/- 0.41 mg/dl in the control group (p = 0.29, for the comparison between two groups, NS). We divided the population into 3 subgroups according to their creatinine clearance: no significant change of serum creatinine concentration was observed in patients with normal renal function nor in patients with pre-existing mild to moderate chronic renal failure in both groups. There was no significant difference for the incidence of contrast-induced nephropathy between both groups (2 of the 53 patients in the acetylcysteine group and 3 of the 51 patients in the placebo group, p = 0.98, NS). CONCLUSIONS: Our data do not support the systematic use of acetylcysteine before a coronary procedure in patients with normal renal function or mild to moderate chronic renal failure, to prevent contrast-induced nephropathy.