Skip to main content
Clinical Cardiology logoLink to Clinical Cardiology
. 2006 Dec 5;26(3):153–157. doi: 10.1002/clc.4960260311

Accelerated plasminogen activator inhibitor may prevent late restenosis after coronary stenting in acute myocardial infarction

Teruo Inoue 1,, Isao Yaguchi 1, Keiichi Mizoguchi 1, Toshihiko Uchida 1, Kan Takayanagi 1, Terumi Hayashi 1, Shigenori Morooka 1, Yutaka Eguchi 2
PMCID: PMC6654356  PMID: 12685623

Abstract

Background: Although acceleration of plasma plasminogen activator inhibitor‐1 (PAI‐1) level after emergent coronary angioplasty in acute myocardial infarction (AMI) has been documented, its pathophysiologic role is still unknown.

Hypothesis: This study was designed to elucidate the role of PAI‐1 in the development of restenosis after primary coronary stenting in AMI.

Methods: We selected for this study 66 patients with AMI, who underwent primary coronary stenting for infarct‐related coronary artery lesions in an emergent situation. In all patients, plasma PAI‐1 level was measured at admission, and at 3 h, 24 h, 48 h, and 1 month after coronary stenting.

Results: At admission, the PAI‐1 level was equivalent in 24 patients who experienced restenosis and in 42 patients without restenosis (28 ± 4 vs. 29 ± 4 ng/ml). In patients with restenosis, the levels did not change during the course after coronary stenting. In patients without restenosis, however, the level significantly increased at 3 h (48 ± 9 ng/ml, p < 0.001), 24 h (42 ± 9, p < 0.01), and 48 h (38 ± 7, p < 0.05) after coronary stenting, and was restored to the level equivalent to that at admission (27 ± 2 ng/ml) 1 month after coronary stenting. The PAI‐1 level at 3 h after coronary stenting in patients without restenosis was significantly higher (p < 0.05) than the level (33 ± 6 ng/ml) in patients with restenosis. Multiple logistic regression analysis indicated that the PAI‐1 level 3 h after coronary stenting was an independent predictor of restenosis (Wald x2 = 3.826, p = 0.019, odds ratio 0.921, 95% confidence interval 0.866‐0.961).

Conclusion: Accelerated PAI‐1 after coronary stenting in patients with AMI may protect against the development of late restenosis.

Keywords: acute myocardial infarction, plasminogen activator inhibitor‐1, coronary stent, restenosis

Full Text

The Full Text of this article is available as a PDF (100.0 KB).

References

  • 1. Schwartz RS, Huber KC, Murphy JC, Edwards WD, Camrud AR, Vliestra RE, Holmes DR: Restenosis and the proportional neointimal response to coronary artery injury: Results in a porcine model. J Am Coll Cardiol 1992; 19: 267–274 [DOI] [PubMed] [Google Scholar]
  • 2. Schwartz RS, Murphy JC, Edwards WD, Camrud AR, Vliestra RE, Holmes DR: Restenosis after balloon angioplasty: A practical proliferative model in porcine coronary arteries. Circulation 1990; 82: 2190–2200 [DOI] [PubMed] [Google Scholar]
  • 3. Saksela O, Rifkin D: Cell‐associated plasminogen activation: Regulation and physiological function. Ann Rev Cell Biol 1988; 4: 93–126 [DOI] [PubMed] [Google Scholar]
  • 4. Hirashima O, Ogawa H, Oshima S, Sakamoto T, Honda Y, Sakata S, Masuda T, Miyao Y, Yasue H: Serial changes of plasma plasminogen activator inhibitor activity in acute myocardial infarction: Difference between thrombolytic therapy and direct coronary angioplasty. Am Heart J 1995; 130: 933–939 [DOI] [PubMed] [Google Scholar]
  • 5. Paganelli F, Alessi MC, Morange P, Maixent JM, Lévy S, Vague IJ: Relationship of plasminogen activator inhibitor‐1 levels following thrombolytic therapy with rt‐PA as compared to streptokinase and patency of in‐farct related coronary artery. Thromb Haemost 1999; 82: 104–108 [PubMed] [Google Scholar]
  • 6. Kohno H: High sensitive latex photometric immunoassay in clinical chemistry In Progress in Clinical Chemistry (Eds. Miyai K, Kanno T, Ishikawa E.), p. 225–229. Oxford, UK: Elsevier Science, 1992. [Google Scholar]
  • 7. Ono T, Ogura M, Furusaki F, Watanabe F, Sakata Y: The ratio of plasmin‐α2‐plasmin inhibitor complex to plasminogen activator inhibitor‐1 reflects the fibrinolytic potential in plasma. Fibrinolysis Proteol 2000; 14; (suppl 1): 72 [Google Scholar]
  • 8. Brack MJ, More RS, Pringle S, Gershlick AH: Absence of a prothrombotic state in restenotic patients? Coron Artery Dis 1994; 5: 501–506 [PubMed] [Google Scholar]
  • 9. Montalescot G, Ankri A, Vicaut E, Drobinski G, Grosgogeat Y, Thomas D: Fibrinogen after coronary angioplasty as a risk factor for restenosis. Circulation 1995; 92: 31–38 [DOI] [PubMed] [Google Scholar]
  • 10. Benchimol D, Bonnet J, Benchimol H, Drouillet F, Duplaa C, Couffinhal T, Desgranges C, Bricaud H: Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty. Int J Cardiol 1993; 38: 7–18 [DOI] [PubMed] [Google Scholar]
  • 11. Sakata K, Miura F, Sugino H, Shinobe M, Shirotani M, Yoshida H, Mori N, Hoshino T, Takada A: Impaired fibrinolysis early after percutaneous transluminal coronary angioplasty is associated with restenosis. Am Heart J 1996; 131: 1–6 [DOI] [PubMed] [Google Scholar]
  • 12. Huber K, Jorg M, Probst P, Schuster E, Lang I, Kaindl F, Binder BR: A decrease in plasminogen activator inhibitor‐1 activity after successful percutaneous transluminal coronary angioplasty is associated with a significantly reduced risk for coronary restenosis. Thromb Haemost 1992; 67: 209–213 [PubMed] [Google Scholar]
  • 13. Ishiwata S, Tukada T, Nakanishi S, Nishiyama S, Seki A: Postangioplasty restenosis: Platelet activation and the coagulation‐fibrinolysis system as possible factors in the pathogenesis of restenosis. Am Heart J 1997; 133: 387–392 [DOI] [PubMed] [Google Scholar]
  • 14. Shah PK, Amin J: Low high‐density lipoprotein level is associated with increased restenosis rate after coronary angioplasty. Circulation 1992; 85: 1279–1285 [DOI] [PubMed] [Google Scholar]
  • 15. Strauss BH, Lau HK, Bowman KA, Sparkes J, Chisholm RJ, Garvey MB, Fenkell LL, Natarajan MK, Singh I, Teitel JM: Plasma urokinase antigen and plasminogen activator inhibitor‐1 antigen levels predict angiographic coronary restenosis. Circulation 1999; 100: 1616–1622 [DOI] [PubMed] [Google Scholar]
  • 16. Schneiderman J, Sawdey MS, Keeton MR, Bordin GM, Bernstein EF, Dilley RB, Loskutoff DJ: Increased type 1 plasminogen activator inhibitor gene expression in atherosclerotic human arteries. Proc Natl Acad Sci USA 1992; 89: 6998–7002 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17. Lupu F, Bergonzelli GE, Heim DA, Cousin E, Genton CY, Bachmann F, Kruithof EK: Localization and production of plasminogen activator inhibitor‐1 in human healthy and atherosclerotic arteries. Arterioscler Thromb 1993; 13: 1090–1100 [DOI] [PubMed] [Google Scholar]
  • 18. Carmeliet P, Moons L, Lijnen R, Janssens S, Lupu F, Collen D, Gerard RD: Inhibitory role of plasminogen activator inhibitor‐1 in arterial wound healing and neointima formation: A gene targeting and gene transfer study in mice. Circulation 1997; 96: 3180–3191 [DOI] [PubMed] [Google Scholar]
  • 19. He CS, Wilhelm SM, Pentland AP, Marmer BL, Grant GA, Eisen AZ, Goldberg GI: Tissue cooperation in a proteolytic cascade activating human interstitial collagenase. Proc Natl Acad Sci USA 1989; 86: 2632–2636 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20. Tkachuk V, Stepanova V, Little PJ, Bobik A: Regulation and role of urokinase plasminogen activator in vascular remodelling. Clin Exp PHARmacol Physiol 1996; 23: 759–765 [DOI] [PubMed] [Google Scholar]

Articles from Clinical Cardiology are provided here courtesy of Wiley

RESOURCES