Increased circulating platelet-derived microparticles are associated with stent-induced vascular inflammation

Inflammation as well as platelet activation at the site of local vessel-wall injury plays an essential role in the mechanism of restenosis after Percutaneous coronary intervention (PCI). Platelet-derived microparticles (PDMPs) released from activated platelets are thought to play a role in the inflammatory process, possibly interacting with leukocyte integrin Mac-1. We serially measured circulating PDMPs, high-sensitive C-reactive protein (hs-CRP) and activated Mac-1 on the surface of neutrophils in 61 patients undergoing coronary stenting. PDMPs, hs-CRP and Mac-1 increased after coronary stenting in a time-dependent manner with the maximum response at 48 h in coronary sinus blood (PDMPs: 10.3 ± 8.9–32.8 ± 13.8 U/ml; P < 0.001, hs-CRP: 0.27 ± 0.23–1.46 ± 0.99 mg/dl; P < 0.001, activated Mac-1, 134 ± 19% relative increase, P < 0.001). PDMPs were correlated with hs-CRP (R = 0.58, P < 0.001) and the relative increase in Mac-1 (R = 0.69, P < 0.001) 48 h after coronary stenting. Multiple regression analysis showed that each of PDMPs (R = 0.40, P < 0.05), hs-CRP (R = 0.33, P < 0.05) and Mac-1 (R = 0.48, P < 0.01) was an independent predictor of the late lumen loss. Coronary stenting enhanced circulating PDMPs in association with an inflammatory response in the injured vessel wall. PDMPs may be a useful marker for evaluation of stent-induced inflammatory status and a powerful predictor of restenosis equivalent to activated Mac-1.