Download PDF
Thromb Haemost 1992; 67(02): 209-213
DOI: 10.1055/s-0038-1648414
Original Articles
Schattauer GmbH Stuttgart

A Decrease in Plasminogen Activator Inhibitor-1 Activity after Successful Percutaneous Transluminal Coronary Angioplasty Is Associated with a Significantly Reduced Risk for Coronary Restenosis

Kurt Huber
1   The Department of Cardiology, University of Vienna, Austria
2   Laboratory for Clinical Experimental Physiology, University of Vienna, Austria
,
Maria Jörg
2   Laboratory for Clinical Experimental Physiology, University of Vienna, Austria
,
Peter Probst
1   The Department of Cardiology, University of Vienna, Austria
,
Ernst Schuster
3   Department of Medical Computer Sciences, University of Vienna, Austria
,
Irene Lang
1   The Department of Cardiology, University of Vienna, Austria
,
Fritz Kaindl
1   The Department of Cardiology, University of Vienna, Austria
,
Bernd R Binder
2   Laboratory for Clinical Experimental Physiology, University of Vienna, Austria
› Author Affiliations
Further Information

Publication History

Received 22 May 1991

Accepted after revision 09 September 1991

Publication Date:
02 July 2018 (online)

  PDF Download  Permissions and Reprints

Summary

To determine a possible relation of changes in plasma levels of plasminogen activator inhibitor 1 (PAI-1) and tissue plasminogen activator (t-PA) to the development of coronary restenosis after successful coronary angioplasty (PTC A), we followed 104 patients with a low grade residual stenosis after PTCA (less than 30%) for a period of 12 months. PAI-1 plasma levels (functional activity) and t-PA antigen were determined 1 day before PTCA and 3 days, 3 months and 6 months thereafter. Thirty-four patients (32.69%) developed angiographically proven coronary restenosis (group A) within a time range of 4-48 weeks (median 12.5 weeks) after PTCA while the remaining patients (group B) had neither clinical signs nor angiographic evidence of restenosis after 6 months. No significant differences could be demonstrated in t-PA antigen or PAI-1 activity (plasma levels between the two groups of patients the day before PTCA). During the whole observation period t-PA plasma levels were not significantly different between the two groups; however, PAI-1 plasma levels were significantly higher at 3 months and 6 months after PTCA in patients of group A (p <0.005). When the pattern of PAI-1 plasma levels over time (increase or decrease between two consecutive time points of blood collection) was used to discriminate between the two study groups only 3.5-18% of patients with a decrease in PAI-1 developed coronary restenosis within the following observation period in contrast to 25-58% of patients with an increase in PAI-1 plasma levels (p <0.05 to p <0.0005).

 

  • References

  • 1 Hamsten A, Wiman B, De Faire U, Blombaeck M. Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction. N Engl J Med 1985; 313: 1557-1563
    CrossrefPubMedGoogle Scholar
  • 2 Paramo JA, Colucci M, Collen D. Plasminogen activator inhibitor in the blood of patients with coronary artery disease. Br Med J 1985; 291: 574-575
    PubMedGoogle Scholar
  • 3 Hamsten A, Blombaeck M, Wiman B. Haemostatic function in myocardial infarction. Br Heart J 1986; 55: 58-66
    CrossrefPubMedGoogle Scholar
  • 4 Gram J, Kluft C, Jespersen J. Depression of tissue plasminogen activator (t-PA) activity and rise of t-PA inhibition and acute phase reactants in blood of patients with acute myocardial infarction (AMI). Thromb Haemostas 1987; 58: 817-821
    PubMedGoogle Scholar
  • 5 Huber K, Resch I, Rose D, Schuster E, Glogar DH, Binder BR. Circadian variations of plasminogen activator inhibitor and tissue plasminogen activator levels in plasma of patients with unstable coronary artery disease and acute myocardial infarction. Thromb Haemostas 1988; 60: 372-376
    PubMedGoogle Scholar
  • 6 Huber K, Lang I, Jörg M, Probst P, Binder BR. Plasminogen activator inhibitor-1 and transient myocardial ischemia. In: Predisposing Conditions for Acute Ischemic Syndromes. Von Arnim Th, Maseri A. (eds). Steinkopff-Verlag; Darmstadt: 1989. pp 59-69
    Google Scholar
  • 7 Huber K, Resch I, Stefenelli Th, Lang I, Probst P, Binder BR. Plasminogen activator inhibitor-1 levels in patients with chronic angina pectoris with or without angiographic evidence of coronary sclerosis. Thromb Haemostas 1990; 63: 336-339
    PubMedGoogle Scholar
  • 8 Ogawa H, Osahima S, Obata K. Tissue plasminogen activator inhibitor (PAI-1) levels in coronary sinus in coronary artery disease. Circulation 1989; 80 Suppl II 11-645 (abstract 2562)
    PubMedGoogle Scholar
  • 9 Grüntzig AR, Senning A, Siegenthaler WE. Non-operative dilatation of coronary artery stenosis: percutaneous transluminal angioplasty. N Engl J Med 1979; 301: 61-68
    CrossrefPubMedGoogle Scholar
  • 10 Kluft C, Jie AFH, Rijken DC, Verheijen JH. Daytime fluctuations in blood of tissue-type plasminogen activator (t-PA) and its fast-acting inhibitor (PAI-1). Thromb Haemostas 1988; 59: 329-332
    PubMedGoogle Scholar
  • 11 Huber K, Beckmann R, Lang I, Schuster E, Binder BR. Circadian fluctuations in plasma levels of tissue plasminogen activator antigen and plasminogen activator inhibitor activity. Fibrinolysis 1989; 3: 41-43
    PubMedGoogle Scholar
  • 12 Angleton P, Chandler WL, Schmer G. Diurnal variation of tissue-type plasminogen activator and its rapid inhibitor (PAI-1). Circulation 1989; 79: 101-106
    CrossrefPubMedGoogle Scholar
  • 13 Verheijen JH, Chang GTG, Kluft C. Evidence for the occurrence of a fast-acting inhibitor for tissue-type plasminogen activator in plasma. Thromb Haemostas 1984; 51: 392-395
    PubMedGoogle Scholar
  • 14 Korninger C, Wagner O, Binder BR. Tissue plasminogen activator inhibitor in human plasma: development of a functional assay system and demonstration of a correlating Mr 50,000 antiactivator. J Lab Clin Med 1985; 105: 718-724
    PubMedGoogle Scholar
  • 15 Korninger C, Speiser W, Wojta J, Binder BR. Sandwich ELISA for t-PA antigen employing a monoclonal antibody. Thromb Res 1986; 41: 527-535
    CrossrefPubMedGoogle Scholar
  • 16 King III SP. Percutaneous transluminal coronary angioplasty: the second decade. Am J Cardiol 1988; 62: 2K-6K
    CrossrefPubMedGoogle Scholar
  • 17 Blackshear JL, O’Callaghan WG, Califf RM. Medical approaches to prevention of restenosis after coronary angioplasty. J Am Coll Cardiol 1987; 9: 834-848
    CrossrefPubMedGoogle Scholar
  • 18 Lam JYT, Chesebro JH, Steele PM. et al Deep arterial injury during experimental angioplasty: relationship to a positive mindium-labeled platelet scintigram, quantitative platelet deposition, and mural thrombus. JACC 1986; 8: 1380-1386
    CrossrefPubMedGoogle Scholar
  • 19 Chesebro JH, Lam JYT, Badimon L, Fuster V. Restenosis after arterial angioplasty: a hemorrheologic response to injury. Am J Cardiol 1987; 60: 10B-16B
    PubMedGoogle Scholar
  • 20 Wilentz JR, Sanborn TA, Faxon DP. et al Platelet accumulation in experimental angioplasty: time course and relation to vascular injury. Circulation 1987; 75: 636-642
    CrossrefPubMedGoogle Scholar
  • 21 Ip JH, Fuster V, Badimon L, Badimon J, Taubmann MB, Chesebro JH. Syndromes of accelerated atherosclerosis: role of vascular injury and smooth muscle cell proliferation. Am J Coll Cardiol 1990; 15: 1667-1687
    CrossrefPubMedGoogle Scholar
  • 22 Goodnight JH. The new general linear model procedure. Proceedings of the First International SAS Users’ Meeting. SAS Institute Inc.; Cary, NC: 1976
  • 23 Wolinsky H. Insights into coronary angioplasty-induced restenosis from examination of atherogenesis. Am J Cardiol 1987; 60: 65B-67B
    CrossrefPubMedGoogle Scholar
  • 24 Liu MW, Roubin GS, King III SB. Restenosis after coronary angioplasty: potential biologic determinants and role of intimai hyperplasia. Circulation 1989; 79: 1374-1387
    CrossrefPubMedGoogle Scholar
  • 25 Leimgruber PP, Roubin GS, Hollman J. et al Restenosis after successful coronary angioplasty in patients with single vessel disease. Circulation 1986; 73: 710-717
    CrossrefPubMedGoogle Scholar
  • 26 Libby P, Hannson GK. Biology of disease. Involvement of the immune system in human atherogenesis: current knowledge and unanswered questions. Lab Invest 1991; 64: 5-15
    PubMedGoogle Scholar
  • 27 Schleef RR, Bevilacqua MP, Sawdey M, Gimbrone Jr MA, Loskutoff DJ. Cytokine activation of vascular endothelium. Effects on tissue-type plasminogen activator and type 1 plasminogen activator inhibitor. J Biol Chem 1988; 263: 5797-5803
    PubMedGoogle Scholar
  • 28 Shimowaka H, Aarhus LL, Vanhoutte PM. Porcine coronary arteries with regenerated endothelium have a reduced endothelium-dependent responsiveness to aggregating platelets and serotonin. Circ Res 1987; 61: 256-270
    CrossrefPubMedGoogle Scholar
  • 29 Weidinger FF, McLenachan JM, Cybulsky MI, Gordon JB, Rennke HG, Hollenberg NK, Fallon JT, Ganz P, Cooke JP. Persistent dysfunction of regenerated endothelium following balloon angioplasty of rabbit iliac artery. Circulation 1990; 81: 1667-1679
    CrossrefPubMedGoogle Scholar
  • 30 Forrester JS, Litvack F, Grundfest W, Hieckey A. A perspective of coronary disease seen through the arteries of living man. Circulation 1987; 75: 505-513
    CrossrefPubMedGoogle Scholar
  • 31 Mizuno K, Miyamoto A, Satomura K, Kurita A, Arai T, Sakurada M, Yanagida S, Nakamura H. Angioscopic coronary macromorphology in patients with acute coronary disorders. Lancet 1991; 337: 809-812
    CrossrefPubMedGoogle Scholar