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Thromb Haemost 1990; 63(03): 336-339
DOI: 10.1055/s-0038-1645042
Original Article
Schattauer GmbH Stuttgart

Plasminogen Activator Inhibitor-1 Levels in Patients with Chronic Angina Pectoris with or without Angiographic Evidence of Coronary Sclerosis

K Huber
1   The Department of Cardiology, University of Vienna, Vienna, Austria
2   The Laboratory for Clinical and Experimental Physiology, Department of Medical Physiology, University of Vienna, Vienna, Austria
,
I Resch
2   The Laboratory for Clinical and Experimental Physiology, Department of Medical Physiology, University of Vienna, Vienna, Austria
,
Th Stefenelli
1   The Department of Cardiology, University of Vienna, Vienna, Austria
,
I Lang
1   The Department of Cardiology, University of Vienna, Vienna, Austria
,
P Probst
1   The Department of Cardiology, University of Vienna, Vienna, Austria
,
F Kaindl
1   The Department of Cardiology, University of Vienna, Vienna, Austria
,
B R Binder
2   The Laboratory for Clinical and Experimental Physiology, Department of Medical Physiology, University of Vienna, Vienna, Austria
› Institutsangaben
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Publikationsverlauf

Received 12. Juni 1989

Accepted after revision 08. Januar 1990

Publikationsdatum:
30. Juni 2018 (online)

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Summary

Increased plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been shown to exist in 40 to 60% of patients with stable coronary artery disease and have been suggested to be responsible for the development of coronary thrombotic complications. However, it is also discussed whether PAI-1 elevation might mainly be due to variables like increased age or to reactive mechanisms caused e.g. by the chest pain itself. To exclude age dependent ui pain related influences, age-matched patients with stable angina pectoris (NHYA II) and angiographically proven coronary artery disease (CAD, n = 16) or without evidence for coronary sclerosis (variant angina, n = 10; angina-like syndrome with normal coronary angiogram, n = 5; non-CAD, n = 15) have been investigated for their plasma PAI-1 activity and t-PA antigen levels. The mean PAI activity in CAD patients (17.5 U/ml) was significantly higher than in non-CAD patients (9.6 U/ml) (p <0.0001). In the CAD patients no significant variation in plasma PAI-1 values could be demonstrated when related to the extent of the disease or to a history of previous myocardial infarction t-PA antigen was also elevated m CAD patients as compared to the non-CAD group (p <0.02). The results suggest therefore a strong correlation between coronary artery disease itself and elevated levels of components of the plasma fibrinolytic system.

 

  • References

  • 1 Hamsten A, Wiman B, De Faire U, Blomback M. Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivers of myocardial infarction. N Engl J Med 1985; 313: 1557-63
    CrossrefPubMedGoogle Scholar
  • 2 Hamsten A, Blomback M, Wiman B. Haemostatic function in myocardial infarction. Br Heart J 1986; 55: 58-66
    CrossrefPubMedGoogle Scholar
  • 3 Paramo JA, Colucci M, Collen D. Plasminogen activator inhibitor in the blood of patients with coronary artery disease. Br Med J 1985; 291: 574-5
    PubMedGoogle Scholar
  • 4 Mehta J, Mehta P, Lawson D, Saldeen T. Plasma tissue plasminogen activator inhibitor levels in coronary artery disease: correlation with age and serum triglyceride concentrations. J Am Coll Cardiol 1987; 9: 263-8
    CrossrefPubMedGoogle Scholar
  • 5 Hashimoto Y, Kobayashi A, Yamazaki N, Sugawara Y, Takada Y, Takada A. Relationship between age and plasma t-PA, PA inhibitor and PA activity. Thromb Res 1987; 46: 625-33
    CrossrefPubMedGoogle Scholar
  • 6 Huber K, Resch I, Rose D, Schuster E, Glogar DH, Binder BR. Circadian fluctuations of plasminogen activator inhibitor and tissue plasminogen activator in plasma of patients with unstable coronary artery disease and acute myocardial infarction. Thromb Haemostas 1988; 60: 372-6
    PubMedGoogle Scholar
  • 7 Huber K, Binder BR. Die Bedeutung des Plasminogenaktivator-Inhibitors bei stabiler und instabiler Angina pectoris. CorVas 1988; 3: 131-5
    PubMedGoogle Scholar
  • 8 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: 817-21
    PubMedGoogle Scholar
  • 9 Juhan-Vague I, Aillaud MF, De Cock F, Philip-Joet C, Arnaud C, Serradimigni A, Collen D. The fast-acting inhibitor of tissue-type plasminogen activator is an acute phase reactant protein. In: Progress in Fibrinolysis Davidson JF, Donati MB, Coccheri S. eds. Churchill Livingstone: Edinburgh; 1985. VII 146-9
  • 10 The Criteria Committee of New York Heart Association. In: Diseases of the Heart and Blood Vessels; Nomenclature and Criteria for Diagnosis Ed 6. Little Brown; New York: 1963
    Google Scholar
  • 11 Schroder JS, Bolen JL, Quint RA, Clark DA, Hayden WG, Higgins CB, Wexler L. Provocations of coronary spasm with ergonovin maleate test with results in 57 patients undergoing arteriography. Am J Cardiol 1977; 40: 487-93
    CrossrefPubMedGoogle Scholar
  • 12 Heupler FA, Proudfit WL, Razavi M, Shirey EK, Greenstreet R, Sheldon WC. Ergonovine maleate provocative test for coronary arterial spasm. Am J Cardiol 1978; 41: 631-40
    CrossrefPubMedGoogle Scholar
  • 13 Pasternak RC, Thibault GE, Savoia M, De Sanctis RW, Hutter AM. Jr. Chest pain with angiographically insignificant coronary arterial obstruction. Clinical presentation and long-term follow up. Am J Med 1980; 68: 813-9
    CrossrefPubMedGoogle Scholar
  • 14 Haglund O, Wibell L, Saldeen T. Plasminogen activators and inhibitors of plasminogen activators in patients with deep venous thrombosis (DVT). Diurnal variation of the inhibitor. Thromb Haemostas 1985; 54: 271
    PubMedGoogle Scholar
  • 15 Kluft C, Verheijen JH, Rijken DC, Chang GT G, Jie AF H, Onkelinx C. Diurnal fluctuations in the activity of the fast-acting t-PA inhibitor. In: Progress in Fibrinolysis VII Davidson JF, Donati MB, Coccheri S. (eds). Churchill Livingstone: Edinburgh; 1985: 117-9
  • 16 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: 41-3
    PubMedGoogle Scholar
  • 17 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: 718-24
    PubMedGoogle Scholar
  • 18 Korninger C, Speiser W, Wojta J, Binder BR. Sandwich ELISA for t-PA antigen employing a monoclonal antibody. Thromb Res 1986; 41: 527-35
    CrossrefPubMedGoogle Scholar
  • 19 Holmes RD, Hartzler GO, Smith HC, Fuster V. Coronary artery thrombosis in patients with unstable angina. Br Heart J 1981; 45: 411-6
    CrossrefPubMedGoogle Scholar
  • 20 Fuster V, Badimon L, Ambrose JA, Turitto V, Badimon JJ, Adams PC, Chesebro JH. Pathogenetic and angiographic features in unstable angina and other coronary syndromes. Thromb Haemostas 1987; 58: 246
    PubMedGoogle Scholar
  • 21 Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Circulation 1985; 71: 699-708
    CrossrefPubMedGoogle Scholar
  • 22 De Wood MA, Spores J, Notske R, Mouser LT, Burroughs R, Golden MS, Lang HT. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980; 303: 897-902
    CrossrefPubMedGoogle Scholar
  • 23 Ganz W, Geft I, Maddahi J. Nonsurgical reperfusion in evolving myocardial infarction. J Am Coll Cardiol 1983; 1: 1247-53
    CrossrefPubMedGoogle Scholar
  • 24 Davis MJ, Thomas A. Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic disease. N Engl J Med 1984; 310: 1137-40
    CrossrefPubMedGoogle Scholar
  • 25 Stehbens WE. Relationship of coronary artery thrombosis to myocardial infarction. Lancet 1985; 2: 639-42
    PubMedGoogle Scholar
  • 26 FitzGerald DJ, Roy L, Catella F, FitzGerald GA. Platelet activation in unstable coronary disease. N Engl J Med 1986; 315: 983-8
    CrossrefPubMedGoogle Scholar
  • 27 Tofler GH, Brezinski D, Schafer AI, Czeisler CA, Rutherford JD, Willich SN, Glaeson RE, Williams GH, Muller JE. Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden death. N Engl J Med 1987; 316: 1514-8
    CrossrefPubMedGoogle Scholar
  • 28 Meade TW, Chakrabarti R, Haines AP. Haemostatic function and cardiovascular death: early results of a prospective study. Lancet 1980; I: 1050-4
    PubMedGoogle Scholar
  • 29 Mombelli G, Hof I, Haeberli A, Straub PW. Effect of heparin on plasma fibrinopeptide A in patient with acute myocardial infarction. Circulation 1984; 69: 684-9
    CrossrefPubMedGoogle Scholar
  • 30 Van Hulsteijn H, Kolff J, Briet E, van der Laarse A, Bertina R. Fibrinopeptide A and beta-thromboglobulin in patients with angina pectoris and acute myocardial infarction. Am Heart J 1984; 107: 39-43
    CrossrefPubMedGoogle Scholar
  • 31 Eisenberg PR, Shorman LA, Schectmann K, Perez J, Sobel SE, Jaffe AS. Fibrinopeptide A: a marker of acute coronary thrombosis. Circulation 1985; 71: 912-7
    CrossrefPubMedGoogle Scholar
  • 32 Theroux P, Latour J-G, Leger-Gauthier C, De Lara J. Fibrinopeptide A and platelet factor levels in unstable angina pectoris. Circulation 1987; 75: 156-62
    CrossrefPubMedGoogle Scholar
  • 33 Vermylen JA, Chamone AF. The role of the fibrinolytic system in thromboembolism. Progr Cardiovasc Dis 1979; 21: 255-66
    CrossrefPubMedGoogle Scholar
  • 34 Nilsson IM, Ljungner H, Tengborn L. Two different mechanisms in patients with venous thrombosis and defective fibrinolysis: low concentrations of plasminogen activator or increased concentration of plasminogen activator inhibitor. Br Med J 1985; 290: 1453-5
    CrossrefPubMedGoogle Scholar
  • 35 Juhan-Vague I, Valadier J, Alessi MC, Aillaud MF, Ansaldi J, Philip-Joet C, Holvoet P, Serradimigni A, Collen D. Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis. Thromb Haemostas 1987; 57: 67-72
    PubMedGoogle Scholar
  • 36 Bachmann F. Fibrinolysis. In: Thrombosis and Haemostasis 1987 Verstraete M, Vermylen J, Lijnen R, Arnout J. (eds). Leuven University Press; Leuven: 1987: 227-52
  • 37 Francis Jr RB, Kawanishix D, Baruch T, Mahrer P, Rahimtoola S, Feinstein ID. Impaired fibrinolysis in coronary artery disease. Am Heart J 1988; 115: 776-80
    CrossrefPubMedGoogle Scholar
  • 38 Oseroff A, Krishnamurti C, Hasset A, Tang D, Alving B. Plasminogen activator inhibitor activities in men with coronary artery disease. J Lab Clin Med 1989; 113: 88-93
    PubMedGoogle Scholar
  • 39 Hammouda MW, Moroz LA. Aspirin and venous occlusion: effects on blood fibrinolytic activity and tissue-type plasminogen activator levels. Thromb Res 1986; 42: 73-82
    CrossrefPubMedGoogle Scholar
  • 40 Krishnamurti C, Tang DB, Bart CF, Alving BM. Plasminogen activator and plasminogen activator inhibitor activities in a reference population. Am J Clin Pathol 1988; 898: 747-52
    PubMedGoogle Scholar
  • 41 Duguid JB. Thrombosis as a factor in the pathogenesis of coronary atherosclerosis. J Pathol Bacteriol 1946; 58: 207-17
    CrossrefPubMedGoogle Scholar
  • 42 Huber K, Lang I, Jorg 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: 59-67
    CrossrefGoogle Scholar