Circadian Fluctuations of Plasminogen Activator Inhibitor and Tissue Plasminogen Activator Levels in Plasma of Patients with Unstable Coronary Artery Disease and Acute Myocardial Infarction

Kurt Huber; Danuta Rosc; Irene Resch; Ernst Schuster; Dietmar H Glogar; F Kaindl; Bernd R Binder

doi:10.1055/s-0038-1646974

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1988; 60(03): 372-376
DOI: 10.1055/s-0038-1646974

Original Article

Schattauer GmbH Stuttgart

Circadian Fluctuations of Plasminogen Activator Inhibitor and Tissue Plasminogen Activator Levels in Plasma of Patients with Unstable Coronary Artery Disease and Acute Myocardial Infarction

Kurt Huber

¹The Department of Cardiology, University of Vienna, Austria

²The Department of Clinical Experimental Physiology, University of Vienna, Austria

,

Danuta Rosc

²The Department of Clinical Experimental Physiology, University of Vienna, Austria

,

Irene Resch

²The Department of Clinical Experimental Physiology, University of Vienna, Austria

,

Ernst Schuster

³The Department of Medical Computer Sciences, University of Vienna, Austria

,

Dietmar H Glogar

¹The Department of Cardiology, University of Vienna, Austria

,

F Kaindl

¹The Department of Cardiology, University of Vienna, Austria

,

Bernd R Binder

²The Department of Clinical Experimental Physiology, University of Vienna, Austria

› Author Affiliations

Abstract

PDF Download

Summary

A decrease in the fibrinolytic potential, mainly due to an elevation of plasminogen activator inhibitor (PAI), has been described in patients with stable coronary artery disease and a previous myocardial infarction. We investigated plasma levels of PAI and tissue plasminogen activator (t-PA) and their possible circadian variations in patients with unstable coronary artery disease (CAD). Sixty-three patients were studied for at least 2 consecutive days during their stay at the coronary care unit (CCU). Diurnal plasma fluctuations in PAI and t-PA and onset of further myocardial ischemic episodes were monitored. As controls we used 22 age-matched patients submitted to the clinic because of non cardiac chest pain or valvular disease who revealed no evidence of CAD. PAI levels were significantly elevated in patients with unstable CAD (p < 0.0001) but were not influenced by the extent of underlying CAD, history of previous myocardial infarction, known risk factors for CAD, or by extent of myocardial damage. The circadian variation of PAI levels with peak values between midnight and 6 A. M. found in controls was still present in patients but at a higher level. Preservation of circadian pattern in PAI plasma levels despite myocardial ischemic attacks indicates that elevation of PAI is rather not caused by a reactive phenomenon. On the other hand, elevated PAI levels and episodes of severe myocardial ischemia exhibiting a median time of onset at 10 A. M. seem to be closely related.

Keywords

Circadian variation - Tissue plasminogen activator - Plasminogen activator inhibitor - Unstable coronary artery disease

PDF (1025 kb)

References

References
1 Muller JA, Stone PH, Turi ZG. et al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985; 313: 1315-1322
2 Muller JA, Ludmer PL, Willich SN. et al. Circadian variation in the frequency of sudden cardiac death. Circulation 1987; 75: 131-138
3 Rocco MB, Barry J, Campbell S. et al Circadian variation of transient myocardial ischemia in patients with coronary artery disease. Circulation 1987; 75: 375-400
4 De Wood MA, Spores J, Notske R. et al Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980; 303: 897-902
5 Holmes DR, Hartzler GO, Smith HC, Fuster V. Coronary artery thrombosis in patients with unstable angina. Br Heart J 1981; 45: 411-416
6 Ganz W, Geft I, Maddahi J. et al Nonsurgical reperfusion in evolving myocardial infarction. J Am Coll Cardiol 1983; 1: 1247-1253
7 Ganz W, Geft I, Shah P. et al Intravenous streptokinase in evolving acute myocardial infarction. Am J Cardiol 1984; 53: 1209-1216
8 Sobel BE, Geltman EM, Tiefenbrunn AJ. et al. Improvement of regional myocardial metabolism after coronary thrombolysis induced with tissue plasminogen activator or streptokinase. Circulation 1984; 69: 983-990
9 Davies MJ, Thomas A. Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic disease. N Engl J Med 1984; 310: 1137-1140
10 Stehbens WE. Relationship of coronary artery thrombosis to myocardial infarction. Lancet 1985; 2: 639-642
11 Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Circulation 1985; 71: 699-708
12 Gallino A, Haeberli A, Baur HR, Straub PW. Fibrin formation and platelet aggregation in patients with severe coronary artery disease, relationship with the degree of myocardial ischemia. Circulation 1985; 72: 27-30
13 Soria C, Soria J, Mirshahi MC. et al. Dynamic coronary fibrinolysis evaluation in patients with myocardial infarction and unstable angina by specific plasma fibrin degradation product determination. Thromb Res 1987; 45: 383-392
14 Maseri A, L’Abbate A, Baroldi G. et al Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of “preinfarction” angina. N Engl J Med 1978; 299: 1271-1277
15 Estelles A, Tormo G, Aznar J, Espana F, Tormo V. Reduced fibrinolytic activity in coronary heart disease in basal conditions and after exercise. Thromb Res 1985; 40: 373-383
16 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: 1557-1563
17 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
18 Hamsten A, Blomback M, Wiman B. et al Haemostatic function in myocardial infarction. Br Heart J 1986; 55: 58-66
19 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: 117-119
20 The Criteria Committee of the New York Heart Association. Inc. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis ed. 6. Little Brown; Boston: 1964
21 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
22 Korninger C, Speiser W, Wojta J, Binder BR. Sandwich ELISA for t-PA antigen employing a monoclonal antibody. Thromb Res 1986; 41: 527-535
23 Kruskal JB, Commerford PJ, Franks JJ, Kirsch RE. Fibrin and fibrinogen-related antigens in patients with stable and unstable coronary artery disease. N Engl J Med 1987; 317: 1361-1365
24 Fitzgerald DJ, Roy L, Catella F, Fitzgerald GA. Platelet activation in unstable coronary disease. N Engl J Med 1986; 315: 983-988
25 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: 1514-1518
26 Meade TW, Chakrabarti R, Haines AP. et al Haemostatic function and cardiovascular death: early results of a prospective study. Lancet 1980; 01: 1050-1054
27 Mombelli G, Hof I, Haeberli A, Straub PW. Effect of heparin on plasma fibrinopeptide A in patient with acute myocardial infarction. Circulation 1984; 69: 684-689
28 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
29 Eisenberg PR, Shorman LA, Schectmann K, Perez J, Sobel SE, Jaffe AS. Fibrinopeptide A: a marker of acute coronary thrombosis. Circulation 1985; 71: 912-917
30 Theroux P, Latour J-G, Leger-Gauthier C, De Lara J. Fibrinopeptide A and platelet factor levels in unstable angina pectoris. Circulation 1987; 75: 156-162
31 Vermylen JA, Chamone AF. The role of the fibrinolytic system in thromboembolism. Progr Cardiavasc Dis 1979; 21: 255-266
32 Nilsson IM, Ljungner H, Tengborn L. Two different mechanisms in patients with venous thrombosis and defective fibrinolysis: low concentration of plasminogen activator or increased concentration of plasminogen activator inhibitor. Br Med J 1985; 290: 1453-1455
33 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
34 Bachmann F. Fibrinolysis. In: Thrombosis and Haemostasis 1987 Verstraete M, Vermylen J, Lijnen R, Arnout J. (eds). Leuven University Press; Leuven: 1987: 227-265
35 Kluft C, Jie AF H, Allen RA. Behaviour and quantitation of extrinsic (tissue-type) plasminogen activator in human blood. Thromb Haemostas 1983; 50: 518-523
36 Allen RH, Kluft C, Brommer EJ P. Effect of chronic smoking on fibrinolysis. Atherosclerosis 1985; 5: 443-450
37 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: 263-268
38 Juhan-Vague I, Aillaud MF, DeCock 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. Vol. VII 146-149
39 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