Why the study?
Does sirolimus-eluting stent implantation reduce MCP-1 concentration and CCR2 expression compared to bare metal stents in patients with stable angina?
Does sirolimus-eluting stent implantation reduce MCP-1 concentration and CCR2 expression compared to bare metal stents in patients with stable angina?
Sirolimus-eluting stents suppress the inflammatory markers MCP-1 and CCR2 compared to bare metal stents, which correlates with reduced in-stent late lumen loss.
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SES blunt MCP-1 rise and correlate with less lumen loss versus BMS; confirms MCP-1's role in restenosis after coronary stenting.
BACKGROUND: Although restenosis after successful coronary stenting is associated with changes in adhesion molecules and chemokines, it is unclear whether the differential effects of these molecules between a bare metal stent (BMS) and sirolimus-eluting stent (SES) may help to prevent coronary restenosis. The aim of this clinical study was to compare the expression levels of those molecules after elective placement of either a BMS or SES. METHODS AND RESULTS: The subjects included 32 consecutive patients with stable angina who had undergone successful coronary stenting and who randomly received either a BMS (n=16) or SES (n=16). Quantitative angiographic analysis 6 months after stenting showed that the minimal lumen diameter was significantly greater in the SES as compared to the BMS group, while the percent diameter stenosis and in-stent lumen loss were significantly lower. Plasma monocyte chemotactic protein-1 (MCP-1) increased significantly after 14 days and 6 months and monocyte CCR2 expression increased 24 hr and 48 hr after stenting in the BMS but not the SES group. Changes in plasma MCP-1 (DeltaMCP-1) within 6 months after stenting correlated significantly with in-stent lumen loss. The DeltaMCP-1 (between 6 months and baseline) was significantly related only to the lumen loss (r=0.443, p=0.023), which suggests that the reduction of MCP-1 is the best contributor to decreased lumen loss. CONCLUSIONS: These data suggest that reduction in MCP-1 production by SES may be one mechanism to prevent restenosis after coronary stenting.
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Sako et al. (2008) studied this question.
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