PMID- 11281299 OWN - NLM STAT- MEDLINE DCOM- 20010719 LR - 20191025 IS - 0954-6928 (Print) IS - 0954-6928 (Linking) VI - 12 IP - 2 DP - 2001 Mar TI - Role of cytokines in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty. PG - 107-13 AB - BACKGROUND: Inflammatory cytokines play an important role in mediating inflammatory/proliferative responses including atherosclerosis. However, their role in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA) remains to be clarified. OBJECTIVE: To determine plasma levels of inflammatory cytokines as well as cytokine-generation capacities of monocytes before PTCA and after the follow-up period. METHODS: Plasma levels of cytokines in 34 consecutive patients before and 3-6 months after PTCA were measured by enzyme-linked immunosorbent assay. We measured the plasma levels of macrophage-colony-stimulating factor (MCSF) and transforming growth factor-beta. Cytokine-generation capacities of monocytes were also measured by a whole-blood induction method with lipopolysaccharide. The levels of cytokines measured for assessment of the capacities included those of interleukin-1alpha, interleukin-1beta, interleukin-6, granulocyte-colony-stimulating factor, tumor necrosis factor-alpha and interferon-gamma. RESULTS: Plasma levels of MCSF in patients without restenosis (n = 20) decreased significantly (from 1460+/-138 microg/ml before PTCA to 1039+/-125 microg/ml after the follow-up period, P < 0.01), whereas those in patients with restenosis (n = 14) increased significantly (from 1107+/-105 microg/ml before PTCA to 1039+/-125 microg/ml after the follow-up period, P < 0.05). We noted a positive correlation between the increase in plasma levels of MCSF and the extent of loss of lumen by restenosis. Cytokine-generation capacities of monocytes for interleukin-1alpha and interleukin-1beta of patients with restenosis significantly increased but those of patients without restenosis did not. Furthermore, plasma levels of C-reactive protein decreased significantly only in patients without restenosis after the follow-up period. CONCLUSIONS: These results suggest that inflammatory changes mediated by cytokines may be involved in the pathogenesis of restenosis after PTCA. FAU - Tashiro, H AU - Tashiro H AD - Division of Cardiology, St Mary's Hospital, Kurume, Japan. FAU - Shimokawa, H AU - Shimokawa H FAU - Sadamatsu, K AU - Sadamatsu K FAU - Aoki, T AU - Aoki T FAU - Yamamoto, K AU - Yamamoto K LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Coron Artery Dis JT - Coronary artery disease JID - 9011445 RN - 0 (Cytokines) RN - 0 (Transforming Growth Factor beta) RN - 81627-83-0 (Macrophage Colony-Stimulating Factor) RN - 9007-41-4 (C-Reactive Protein) SB - IM MH - Aged MH - *Angioplasty, Balloon, Coronary MH - C-Reactive Protein/metabolism MH - Coronary Disease/*etiology/*therapy MH - Cytokines/*physiology MH - Enzyme-Linked Immunosorbent Assay MH - Female MH - Follow-Up Studies MH - Humans MH - Macrophage Colony-Stimulating Factor/blood MH - Male MH - Monocytes/metabolism MH - Recurrence MH - Time Factors MH - Transforming Growth Factor beta/blood EDAT- 2001/04/03 10:00 MHDA- 2001/07/20 10:01 CRDT- 2001/04/03 10:00 PHST- 2001/04/03 10:00 [pubmed] PHST- 2001/07/20 10:01 [medline] PHST- 2001/04/03 10:00 [entrez] AID - 10.1097/00019501-200103000-00004 [doi] PST - ppublish SO - Coron Artery Dis. 2001 Mar;12(2):107-13. doi: 10.1097/00019501-200103000-00004.