Elevated plasma levels of MCP-1 measured 15 days after PTCA independently predicted restenosis at 6-month follow-up (beta=0.688, P<0.0001).
Cohort (n=50)
Elevated plasma levels of MCP-1 after PTCA are independently associated with the development of angiographic restenosis at 6 months, suggesting a pathogenic role for inflammation and monocyte activation.
Effect estimate: beta 0.688
p-value: p=<0.0001
Inflammation plays a pathogenic role in the development of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Monocyte chemoattractant protein-1 (MCP-1) is a potent chemoattractant of monocytes; however, its role in the pathophysiology of restenosis is still unclear. We set out to investigate the role of MCP-1 in restenosis after PTCA. In addition, we tested the hypothesis that MCP-1 exerts its effect, at least in part, by inducing O(2)(-) generation in circulating monocytes. Plasma levels of MCP-1 were measured before and 1, 5, 15, and 180 days after PTCA in 50 patients (30 males and 20 females, aged 62+/-5 years) who underwent PTCA and who had repeated angiograms at 6-month follow-up. Restenosis occurred in 14 (28%) patients. The MCP-1 level was no different at baseline between patients with or without restenosis. However, after the procedure, restenotic patients, compared with nonrestenotic patients, had statistically significant (P<0.0001) elevated levels of MCP-1. In contrast, plasma levels of other chemokines, such as RANTES and interleukin-8, did not differ between the 2 groups after PTCA. Higher MCP-1 throughout the study was correlated with restenosis. Moreover, increased MCP-1 was significantly correlated with increased monocyte activity, as reflected by enhanced O(2)(-) generation. Finally, multivariate regression analysis showed that the MCP-1 plasma level measured 15 days after PTCA was the only statistically significant independent predictor of restenosis (beta=0.688, P<0.0001). This study suggests that MCP-1 production and macrophage accumulation in the balloon-injured vessel may play a pivotal role in restenosis after PTCA. MCP-1 may induce luminal renarrowing, at least in part, by inducing O(2)(-) release in monocytes. Further understanding of the mechanism(s) by which MCP-1 is produced and acts after arterial injury may provide insight into therapies to limit the progression of atherosclerosis and restenosis after balloon angioplasty.
Cipollone et al. (Thu,) conducted a cohort in Restenosis after coronary angioplasty (n=50). Elevated plasma levels of MCP-1 vs. Lower plasma levels of MCP-1 was evaluated on Restenosis (beta 0.688, p=<0.0001). Elevated plasma levels of MCP-1 measured 15 days after PTCA independently predicted restenosis at 6-month follow-up (beta=0.688, P<0.0001).