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. 2006 Dec 5;28(11):512–518. doi: 10.1002/clc.4960281105

Preinterventional peak monocyte count and in‐stent intimal hyperplasia after coronary stent implantation in human coronary arteries

Young Joon Hong 1, Myung Ho Jeong 1,✉, Sang Yup Lim 1, Sang Rok Lee 1, Kye Hun Kim 1, Il Suk Sohn 1, Hyung Wookpark 1, Ju Han Kim 1, Weon Kim 1, Youngkeun Ahn 1, Jeong Gwan Cho 1, Jong Chun Park 1, Jung Chaee Kang 1
PMCID: PMC6653908  PMID: 16450794

Abstract

Background: The mechanism of restenosis after stent implantation principally is neointimal hyperplasia. There is evidence that monocytes play a important role in in‐stent restenosis (ISR) after stent implantation.

Hypothesis: This study assessed the relationship between preinterventional peak monocyte count and neointimal growth after successful stent implantation.

Methods: We performed coronary stent implantation in 85 patients (85 de novo lesions). Peripheral blood sample was obtained in all patients every 12 h before coronary angiography for measurement of peripheral monocytes. All patients received angiographic and intravascular ultrasound (IVUS) follow‐up at 6 months after stenting.

Results: The preinterventional circulating monocyte count was significantly higher in the ISR group than that in the group without ISR (654 ± 62/vs. 461 ± 222/mm3, p < 0.001) and was significantly higher in the reintervention group than that in the no‐reintervention group (660 ± 72/ vs. 470 ± 216/mm3, p < 0.001). The incidence of ISR and repeat intervention associated with preinterventional monocyte count was highest among the patients in the highest tertile, who were at a 2.64‐fold increased risk of ISR and 3.22‐fold increased risk of repeat intervention compared with the patients in the lowest tertile. A significant positive correlation was found between preinterventional peak monocyte count and preinterventional plaque and media cross‐sectional area and follow‐up neointima area (r = 0.311, p = 0.007, r = 0.465, p<0.001, respectively). The neointima area associated with preinterventional monocyte count was largest among the patients in the highest tertile, that is, 2‐fold larger than that of the patients in the lowest tertile (p < 0.001) and 1.44‐fold larger than that of the patients in the middle tertile (p = 0.001).

Conclusion: Our results suggest that circulating preinterventional monocytes play a principal role in the process of in‐stent neointimal growth after successful stent implantation.

Keywords: stents, coronary artery disease, restenosis, inflammation

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References

  • 1. Serruys PW, de Jaegere P, Kiemeneij F, Macaya C, Rutsch W, Heyndrickx G, Emanuelsson H, Marco J, Legrand V, Materne P: The BENESTENT Study Group: A comparison of balloon‐expandable‐stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994; 331: 489–495 [DOI] [PubMed] [Google Scholar]
  • 2. Fischman DL, Leon MB, Baim DS, Schatz RA, Savage MP, Penn I, Detre K, Veltri L, Ricci D, Nobuyoshi M: The Stent Restenosis Study Investigators: A randomized comparison of coronary‐stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med 1994; 331: 496–501 [DOI] [PubMed] [Google Scholar]
  • 3. Popma JJ, Califf RM, Topol EJ: Clincal trials of restenosis after coronary angioplasty. Circulation 1991; 84: 1426–1436 [DOI] [PubMed] [Google Scholar]
  • 4. Hoffmann R, Mintz GS, Dussaillant GR, Popma JJ, Pichard AD, Satler LF, Kent KM, Griffin J, Leon MB: Patterns and mechanisms of in‐stent restenosis: A serial intravascular ultrasound study. Circulation 1996; 94: 1247–1254 [DOI] [PubMed] [Google Scholar]
  • 5. Grewe PH, Deneke T, Machraoui A, Barmeyer J, Muller KM: Acute and chronic tissue response to coronary stent implantation: Pathologic findings in human specimens. J Am Coll Cardiol 2000; 35: 157–163 [DOI] [PubMed] [Google Scholar]
  • 6. Ross R: Atherosclerosis—an inflammatory disease. N Engl J Med 1999; 340: 115–126 [DOI] [PubMed] [Google Scholar]
  • 7. Fuster V, Badimon L, Badimon JJ, Chesebro J: The pathogenesis of coronary artery disease and acute coronary syndromes. N Engl J Med 1992; 326: 242–250 [DOI] [PubMed] [Google Scholar]
  • 8. Kornowski R, Hong MK, Tio FO, Bramwell O, Wu H, Leon MB: In‐stent restenosis: Contributions of inflammatory responses and arterial injury to neointimal hyperplasia. J Am Coll Cardiol 1998; 31: 224–230 [DOI] [PubMed] [Google Scholar]
  • 9. Rogers C, Welt FG, Karnovsky MJ, Edelman ER: Monocyte recruitment and neointimal hyperplasia in rabbits: Coupled inhibitory effects of heparin. Arterioscler Thromb Vasc Biol 1996; 16: 1312–1318 [DOI] [PubMed] [Google Scholar]
  • 10. Rogers C, Edelman ER, Simon DI: AmAbtothebeta2‐leukocyteintegrin Mac‐1 (CD11b/CD18) reduces intimal thickening after angioplasty or stent implantation in rabbits. Proc Natl Acad Sci USA 1998; 95: 10134–10139 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11. Egashira K, Zhao Q, Kataoka C, Ohtani K, Usui M, Charo IF, Nishida K, Inoue S, Katoh M, Ichiki T, Takeshita A: Importance of monocyte chemoattractant protein‐1 pathway in neointimal hyperplasia after periarterial injury in mice and monkeys. Circ Res 2002; 90: 1167–1172 [DOI] [PubMed] [Google Scholar]
  • 12. Moreno PR, Bernardi VH, Lopez‐Cuellar J, Newell JB, McMellon C, Gold HK, Palacios IF, Fuster V, Fallon JT: Macrophage infiltration predicts restenosis after coronary intervention in patients with unstable angina. Circulation 1996; 94: 3098–3102 [DOI] [PubMed] [Google Scholar]
  • 13. Assoian RK, Fleurdelys BE, Stevenson HC, Miller PJ, Madtes DK, Raines EW, Ross R, Sporn MB: Expression and secretion of type beta transforming factor by activated human macrophages. Proc Natl Acad Sci USA 1987; 84: 6020–6024 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14. Languino LR, Duperray A, Joganic KJ, Fornaro M, Thornton GB, Altieri DC: Regulation of leukocyte‐endothelium interaction and leukocyte transendothelial migration by intercellular adhesion molecule 1‐fibrinogen recognition. Proc Natl Acad Sci USA 1995; 92: 1505–1509 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15. Sukhova GK, Shi GP, Simon DI, Chapman HA, Libby P: Expression of the elastolytic cathepsins S and K in human atheroma and regulation of their production in smooth muscle cells. J Clin Invest 1998; 102: 576–583 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16. Walter DH, Schachinger V, Elsner M, Dimmeler S, Zeiher AM: Platelet glycoprotein IIIa polymorphism and risk of coronary stent thrombosis. Lancet 1997; 350: 1217–1219 [DOI] [PubMed] [Google Scholar]
  • 17. Nissen SE, Yock P: Intravascular ultrasound: Novel pathophysiological insights and current clinical applications. Circulation 2001; 103: 604–616 [DOI] [PubMed] [Google Scholar]
  • 18. Sangiorgi G, Holmes DR Jr, Schwartz RS: Restenosis: Etiologies and prevention In Evidence‐Based Cardiology (Eds. Yusuf S, Camm AJ, Fallen EL, Gersh BJ.), pp. 371–394. London, U. K: British Medical Journal, 2003. [Google Scholar]
  • 19. Sangiorgi G, Taylor AJ, Farb A, Carter AJ, Edwards WD, Holmes DR, Schwartz RS, Virmani R: Histopathology of postpercutaneous transluminal coronary angioplasty remodeling in human coronary arteries. Am Heart J 1999; 138: 681–687 [DOI] [PubMed] [Google Scholar]
  • 20. Li C, Cantor WJ, Nili N, Robinson R, Fenkell L, Tran YL, Whittingham HA, Tsui W, Cheema AN, Sparkes JD, Pritzker K, Levy DE, Strauss BH: Arterial repair after stenting and the effects of GM6001, a matrix metallo‐proteinase inhibitor. J Am Coll Cardiol 2002; 39: 1852–1858 [DOI] [PubMed] [Google Scholar]
  • 21. Bellas RE, Lee JS, Sonenshein GE: Expression of a constrictive NF‐κB‐like activity is essential for proliferation of cultured bovine vascular smooth muscle cells. J Clin Invest 1995; 96: 2521–2527 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22. Welt FGP, Rogers C: Inflammation and restenosis in the stent era. Arterioscler Thromb Vasc Biol 2002; 22: 1769–1776 [DOI] [PubMed] [Google Scholar]
  • 23. Liuzzo G, Buffon A, Biasucci LM, Gallimore JR, Caligiuri G, Vitelli A, Altamura S, Ciliberto G, Rebuzzi AG, Crea F, Pepys MB, Maseri A: Enhanced inflammatory response to coronary angioplasty in patients with severe unstable angina. Circulation 1998; 98: 2370–2376 [DOI] [PubMed] [Google Scholar]
  • 24. Fukuda D, Shimada K, Tanaka A, Kawarabayashi T, Yoshiyama M, Yoshikawa J: Circulating monocytes and in‐stent neointima after coronary stent implantation. J Am Coll Cardiol 2004; 43: 18–23 [DOI] [PubMed] [Google Scholar]
  • 25. Libby P: Inflammation in atherosclerosis. Nature 2002; 420: 868–874 [DOI] [PubMed] [Google Scholar]
  • 26. Falk E, Shah PK, Fuster V: Coronary plaque disruption. Circulation 1995; 92: 657–671 [DOI] [PubMed] [Google Scholar]
  • 27. van der Wal AC, Becker AE, van der Loos CM, Das PK: Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994; 89: 36–44 [DOI] [PubMed] [Google Scholar]
  • 28. Ridker PM: Clinical application of C‐reactive protein for cardiovascular disease detection and prevention. Circulation 2003; 107: 363–369 [DOI] [PubMed] [Google Scholar]
  • 29. Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL, Rebuzzi AG, Pepys MB, Maseri A: The prognostic value of C‐reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med 1994; 331: 417–424 [DOI] [PubMed] [Google Scholar]

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