PMID- 11231910 OWN - NLM STAT- MEDLINE DCOM- 20010517 LR - 20190831 IS - 1524-4636 (Electronic) IS - 1079-5642 (Linking) VI - 21 IP - 3 DP - 2001 Mar TI - Elevated circulating levels of monocyte chemoattractant protein-1 in patients with restenosis after coronary angioplasty. PG - 327-34 AB - 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. FAU - Cipollone, F AU - Cipollone F AD - Department of Medicine and Aging, University of Chieti "G D'Annunzio" School of Medicine, Chieti, Italy. FAU - Marini, M AU - Marini M FAU - Fazia, M AU - Fazia M FAU - Pini, B AU - Pini B FAU - Iezzi, A AU - Iezzi A FAU - Reale, M AU - Reale M FAU - Paloscia, L AU - Paloscia L FAU - Materazzo, G AU - Materazzo G FAU - D'Annunzio, E AU - D'Annunzio E FAU - Conti, P AU - Conti P FAU - Chiarelli, F AU - Chiarelli F FAU - Cuccurullo, F AU - Cuccurullo F FAU - Mezzetti, A AU - Mezzetti A LA - eng PT - Comparative Study PT - Journal Article PL - United States TA - Arterioscler Thromb Vasc Biol JT - Arteriosclerosis, thrombosis, and vascular biology JID - 9505803 RN - 0 (Chemokine CCL2) RN - 0 (Chemokine CCL5) RN - 0 (Interleukin-8) RN - 0 (Reactive Oxygen Species) RN - NI40JAQ945 (Tetradecanoylphorbol Acetate) SB - IM CIN - Arterioscler Thromb Vasc Biol. 2001 Mar;21(3):297-9. PMID: 11231906 CIN - Arterioscler Thromb Vasc Biol. 2001 Jun;21(6):1090-1. PMID: 11397725 MH - Aged MH - Analysis of Variance MH - *Angioplasty, Balloon, Coronary MH - Chemokine CCL2/*blood MH - Chemokine CCL5/blood MH - Coronary Disease/*blood/therapy MH - Female MH - Humans MH - Interleukin-8/blood MH - Male MH - Middle Aged MH - Monocytes/cytology/drug effects/metabolism MH - Reactive Oxygen Species/metabolism MH - Recurrence MH - Tetradecanoylphorbol Acetate/pharmacology MH - Time Factors EDAT- 2001/03/07 10:00 MHDA- 2001/05/22 10:01 CRDT- 2001/03/07 10:00 PHST- 2001/03/07 10:00 [pubmed] PHST- 2001/05/22 10:01 [medline] PHST- 2001/03/07 10:00 [entrez] AID - 10.1161/01.atv.21.3.327 [doi] PST - ppublish SO - Arterioscler Thromb Vasc Biol. 2001 Mar;21(3):327-34. doi: 10.1161/01.atv.21.3.327.