Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:327-334
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© 2001 American Heart Association, Inc.
Vascular Biology |
Elevated Circulating Levels of Monocyte Chemoattractant Protein-1 in Patients With Restenosis After Coronary Angioplasty
From the Department of Medicine and Aging (F.C., M.M., M.F., B.P., A.I., F. Chiarelli, F. Cuccurullo, A.M.) and the Department of Biomedical Science (M.R., P.C.), University of Chieti "G D’Annunzio" School of Medicine, Chieti, Italy, and the Division of Cardiology (L.P., G.M., E.D.), "Spirito Santo" Hospital, Pescara, Italy.
Correspondence to Andrea Mezzetti, MD, Centro per la Prevenzione dell’Aterosclerosi, la Diagnosi e Terapia dell’lpertensione Arteriosa e delle Dislipidemie, Nuovo Policlinico SS. Annunziata, Via dei Vestini 66, 66013 Chieti, Italy. E-mail mezzetti{at}unich.it
Abstract—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 O2- 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 O2- 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 (ß=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 O2- 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.
Key Words: angioplasty • restenosis • monocyte chemoattractant protein-1 • superoxide anion • monocytes
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