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European Heart Journal 2001 22(7):580-586; doi:10.1053/euhj.2000.2261
Copyright © 2001 by the European Society of Cardiology.
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Indirect evidence for a role of a subpopulation of activated neutrophils in the remodelling process after percutaneous coronary intervention

M.A Costaa,f1, L.E.A de Witb,f1, V de Valkc, P Serranoa, A.J Wardeha, P.W Serruysa,f2 and W Sluiterb

a Thoraxcenter, Dijkzigt University Hospital, Rotterdam, The Netherlands
b Department of Biochemistry, Cardiovascular Research Institute, Erasmus University, Rotterdam, The Netherlands
c Cardialysis BV, Rotterdam, The Netherlands

revised April 25, 2000; accepted April 26, 2000

Abstract

Aim Leukocytes have been implicated in restenosis following percutaneous transluminal coronary angioplasty. We investigated the link between the activated status of circulating neutrophils and restenosis after angioplasty.

Methods and Results The population of 108 patients with single, de novo lesions located in native coronary arteries were treated with elective balloon angioplasty (n=44) or stenting (n=64). Pre-, post-procedure and 6-month follow-up, angiograms were analysed by an independent core laboratory. Blood samples were collected immediately before treatment and the antigen CD66, which is specifically expressed by activated neutrophils, was measured. Overall, the average expression of CD66 was 6·4±3·6 of mean fluorescence intensity. In the stepwise linear regression model, which included biological, clinical and angiographic variables, absolute gain showed a direct association (P<0·001) with relative late loss (relative late loss=absolute late loss÷pre-procedure reference diameter), whereas CD66 expression was inversely associated with relative late loss (P=0·004). CD66 expression also showed an inverse association with relative late loss in the balloon angioplasty treated patients (P=0·002, ß=–0·49). In the stent subgroup, only reference vessel diameter and acute gain were independent predictors of relative late loss.

Conclusion Our results confirm the beneficial role of activated neutrophils pre-procedure in the restenotic process after balloon angioplasty. The lack of a relationship between CD66 expression by neutrophils and relative late loss after stenting suggests that this leukocyte may be involved in the remodelling process.

Key Words: Balloon angioplasty, stent, restenosis, leukocytes

f1 Equal contribution.

f2 Correspondence: P. W. Serruys MD, PhD, FACC, FESC Prof. of Interventional Cardiology, Erasmus University, Head of Interventional Dept., Heartcenter Rotterdam, Thoraxcenter, Bd. 418, University Hospital Dijkzigt, Dr. Molewaterplein 40,3015 GD Rotterdam, The Netherlands.

References

  1. Kakuta T, Currier JW, Haudenschild CC, Ryan TJ, Faxon DP. Differences in compensatory vessel enlargement, not intimal formation, account for restenosis after angioplasty in the hypercholesterolemic rabbit model. Circulation. 1994;89:2809–2815[Abstract/Free Full Text]
  2. Post MJ, Borst C, Kuntz RE. The relative importance of arterial remodeling compared with intimal hyperplasia in lumen renarrowing after balloon angioplasty. A study in the normal rabbit and the hypercholesterolemic Yucatan micropig. Circulation. 1994;89:2816–2821[Abstract/Free Full Text]
  3. Lafont A, Guzman L, Whitlow P, Cornhill JF, Chisolm G. Restenosis after angioplasty in a rabbit model of experimental atherosclerosis: intimal, medial, and adventitial changes associated with constrictive remodeling. Circ Res. 1995;76:996–1003[Abstract/Free Full Text]
  4. Di Mario C, Gil R, Camenzind. Quantitative assessment with intracoronary ultrasound of the mechanisms of restenosis after percutaneous transluminal coronary angioplasty and directional coronary atherectomy. Am J Cardiol. 1995;75:772–777[CrossRef][ISI][Medline]
  5. Pietersma A, Kofflard M, de Wit LEA. Late lumen loss after coronary angioplasty is associated with the activation status of circulating phagocytes before treatment. Circulation. 1995;91:1320–1325[Abstract/Free Full Text]
  6. Mickelson JK, Lakkis NM, Villarreal-Levy G, Hughes BJ, Smith CW. Leukocyte activation with platelet adhesion after coronary angioplasty: a mechanism for recurrent disease? J Am Coll Cardiol. 1996;28:345–353[Abstract]
  7. Inoue T, Sakai Y, Morooka S, Hayashi T, Takayanagi K, Takabatake Y. Expression of polymorphonuclear leukocyte adhesion molecules and its clinical significance in patients treated with percutaneous transluminal coronary angioplasty. J Am Coll Cardiol. 1996;28:1127–1133[Abstract]
  8. Inoue T, Sakai Y, Hoshi K, Yamaguchi I, Fujito T, Morooka S. Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty. Circulation. 1998;97:2511–2518[Abstract/Free Full Text]
  9. Van Put DJM, Van Osselaer N, De Meyer GRY. Role of polymorphonuclear leukocytes in collar-induced intimal thickening in the rabbit carotid artery. Arterioscler Thromb Biol. 1998;18:915–921[Abstract/Free Full Text]
  10. Rogers C, Edelman ER, Simon DI. A mAb to the ß2-leukocyte integrin Mac-1 (CD11b/CD18) reduces intimal thickening after angioplasty or stent implantation in rabbits. Proc Natl Acad Sci USA. 1998;95:10134–10139[Abstract/Free Full Text]
  11. Staab ME, Srivatsa SS, Lerman A. Arterial remodeling after experimental percutaneous injury is highly dependent on adventitial injury and histopathology. Int J Cardiol. 1996;58:31–40
  12. Schwartz RS, Topol EJ, Serruys PW, Sangiorgi G, Holmes DR Jr. Artery size, neointima, and remodeling: time for some standards. J Am Coll Cardiol. 1998;32:2087–2094[Free Full Text]
  13. Tetteroo PAT, Bos MJE, Visser FJ, von dem Borne AEGKR. Neutrophil activation detected by monoclonal antibodies. J Immunol. 1986;136:3427–3432[Abstract]
  14. Skubitz KM, Campbell KD, Ahmed K, Skubitz APN. CD66 family members are associated with tyrosine kinase activity in human neutrophils. J Immunol. 1995;155:5382–5390[Abstract]
  15. Skubitz KM, Campbell KD, Skubitz APN. CD66a, CD66b, CD66c, and CD66d each independently stimulate neutrophils. J Leukoc Biol. 1996;60:106–117[Abstract]
  16. Ducker TP, Skubitz KM. Subcellular localization of CD66, CD67, and NCA in human neutrophils. J Leukoc Biol. 1992;52:11–16[Abstract]
  17. Kuroki M, Yamanaka T, Matsuo Y, Oikawa S, Nakazato H, Matsuoka Y. Immunochemical analysis of carcinoembryonic antigen (CEA)-related antigens differentially localized in intracellular granules of human neutrophils. Immunol Invest. 1995;24:829–843[ISI][Medline]
  18. Kuroki M, Matsuo T, Kinugasa T, Matsuoka Y. Augmented expression and release of nonspecific cross-reacting antigens (NCAs), members of the CEA family, by human neutrophils during cell activation. J Leukoc Biol. 1992;52:551–557[Abstract]
  19. Stocks SC, Kerr MA, Haslett C, Dransfield I. CD66-dependent neutrophil activation: a possible mechanism for vascular selectin-mediated regulation of neutrophil adhesion. J Leukoc Biol. 1995;58:40–48[Abstract]
  20. Stocks SC, Ruchaud-Sparagano MH, Kerr MA, Grunert F, Haslett C, Dransfield I. CD66: role in the regulation of neutrophil effector function. Eur J Immunol. 1996;26:2924–2932[ISI][Medline]
  21. Ruchaud-Sparagano MH, Stocks SC, Turley H, Dransfield I. Activation of neutrophil function via CD66: differential effects upon ß2integrin mediated adhesion. Br J Haematol. 1997;98:612–620[CrossRef][ISI][Medline]
  22. Escaned J, Baptista J, Di Mario C. Significance of automated stenosis detection during quantitative angiography: insights gained from intracoronary ultrasound. Circulation. 1996;94:966–972[Abstract/Free Full Text]
  23. Serruys PW, Luijten HE, Beatt KJ. Incidence of restenosis after successful coronary angioplasty: a time related phenomenon. A quantitative angiographic study in 342 consecutive patients at 1,2,3, and 4 months. Circulation. 1988;77:361–371[Abstract/Free Full Text]
  24. Rensing BJ, Hermans WR, Deckers JW, de Feyter PJ, Serruys PW. Which angiographic variable best describes functional status 6 months after successful single-vessel coronary balloon angioplasty? J Am Coll Cardiol. 1993;21:317–324[Abstract]
  25. Kuijpers TW, Tool ATJ, van der Schoot CE. Membrane surface antigen expression on neutrophils: a reappraisal of the use of surface markers for neutrophil activation. Blood. 1991;78:1105–1111[Abstract/Free Full Text]
  26. Costa MA, Sabaté M, Kay IP. Three-dimensional intravascular ultrasonic volumetric quantification of stent recoil and neointimal formation of two new generation tubular stents. Am J Cardiol. 2000;85:135–139[CrossRef][ISI][Medline]
  27. Mintz GS, Popma JJ, Hong MK. Intravascular ultrasound discern device-specific effects and mechanisms of restenosis. Am J Cardiol. 1996;78:18–22[CrossRef][ISI][Medline]
  28. Faxon DP, Coats W, Currier J. Remodeling of the coronary artery after vascular injury. Progr Cardiovasc Dis. 1997;40:129–140[CrossRef][ISI][Medline]
  29. Schwartz JD, Monea S, Marcus SG. Soluble factor(s) released from neutrophils activates endothelial cell matrix metalloproteinase-2. J Surg Res. 1998;76:79–85[CrossRef][ISI][Medline]
  30. Hauck CR, Meyer TF, Lang F, Gulbins E. CD66-mediated phagocytosis of Opa52 Neisseria gonorrhoeae requires a Src-like tyrosine kinase- and Rac1-dependent signalling pathway. EMBO J. 1998;17:443–454[CrossRef][ISI][Medline]
  31. Gray-Owen SD, Dehio C, Haude A, Grunert F, Meyer TF. CD66 carcinoembryonic antigens mediate interactions between Opa-expressing Neisseria gonorrhoea and human polymorphonuclear phagocytes. EMBO J. 1997;16:3435–3445[CrossRef][ISI][Medline]
  32. Golino P, Ambrosio G, Ragni M. Inhibition of leukocyte and platelet adhesion reduces neointimal hyperplasia after arterial injury. Thromb Haemost. 1997;77:783–788[ISI][Medline]
  33. Rogers C, Welt FGP, Karnovsky MJ, Edelman ER. Monocyte recruitment and neointimal hyperplasia in rabbits. Coupled inhibitory effects of heparin. Arterioscler Throm Vasc Biol. 1996;16:1312–1318[Abstract/Free Full Text]
  34. Carlos TM, Harlan JM. Leukocyte-endothelial adhesion molecules. Blood. 1994;84:2068–2101[Abstract/Free Full Text]
  35. De Servi S, Mazzone A, Ricevuti G. Granulocyte activation after coronary angioplasty in humans. Circulation. 1990;82:140–146[Abstract/Free Full Text]
  36. Ikeda H, Nakayama H, Oda T. Neutrophil activation after percutaneous transluminal coronary angioplasty. Am Heart J. 1994;128:1091–1098[CrossRef][ISI][Medline]
  37. Neumann FJ, Ott I, Gawaz M, Puchner G, Schömig A. Neutrophil and platelet activation at balloon-injured coronary artery plaque in patients undergoing angioplasty. J Am Coll Cardiol. 1996;27:819–824[Abstract]
  38. Kling D, Fingerle J, Harlan JM. Inhibition of leukocyte extravasation with a monoclonal antibody to CD18 during formation of experimental intimal thickening in rabbit carotid arteries. Arterioscleroris and Thrombosis. 1992;12:997–1007
  39. Guzman LA, Forudi F, Villa AE, Topol EJ. Role of leukocytes in neointimal formation after balloon angioplasty in the rabbit atherosclerotic model. Cor Art Dis. 1995;6:693–701
  40. Adelman AG, Cohen EA, Kimball BP. A comparison of directional atherectomy with balloon angioplasty for lesions of the left anterior descending coronary artery. N Engl J Med. 1993;329:228–233[Abstract/Free Full Text]
  41. Schwartz RS, Huber KC, Murphy JG. Restenosis and the proportional neointimal response to coronary artery injury: results in a porcine model. J Am Coll Cardiol. 1992;19:267–274[Abstract]
  42. Serruys PW, Kay IP, Disco C, Deshpande NV, de Feyter PJ. Periprocedural quantitative coronary angiography after Palmaz-Schatz stent implantation predicts the restenosis rate at six moths: results of a meta-analysis of the BElgian NEtherlands Stent study (BENESTENT) I, BENESTENT II Pilot, BENESTENT II and MUSIC trials. Multicenter Ultrasound Stent In Coronaries. J Am Coll Cardiol. 1999;34:1067–1074[Abstract/Free Full Text]

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M. A. Costa and D. I. Simon
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