Advertisement

Circadian fluctuation of fibrinolytic factors in blood

Investigation, importance and clinical consequences
  • Felicita Andreotti
  • Alessandro Manzoli
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 170)

Abstract

The system in blood which dissolves fibrin can be viewed as a “potential” mechanism which exerts a major effect only at sites of fibrin accumulation. The breakdown of fibrin deposits is, in fact, triggered by fibrin itself, as fibrin attracts the active enzyme tissue-type plasminogen activator (t-PA) and the inactive pro-enzyme plasminogen onto its surface [1]. There t-PA converts or “activates” plasminogen to plasmin. Plasmin in turn breaks the solid fibrin strands into soluble fragments typically containing two D domains or D-dimers (Figure 1).

Keywords

Plasminogen Activator Circadian Rhythm Plasminogen Activator Inhibitor Fibrinolytic Activity Circadian Variation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Bachmann F. Fibrinolysis. In Verstraete M, Vermylen J, Leijnen L, Arnout J, editors. Thrombosis and Haemostasis. Leuven: Leuven University Press 1987; 227–65.Google Scholar
  2. 2.
    Sprengers ED, Kluft C. Plasminogen activator inhibitors. Blood 1987; 69: 381–7.PubMedGoogle Scholar
  3. 3.
    Andreotti F, Davies GJ, Hackett D et al. Circadian variation of fibrinolytic factors in normal human plasma. Fibrinolysis 1988; 2: 90–2.Google Scholar
  4. 4.
    Fearnley GR. Fibrinolysis. London: Edward Arnold Ltd 1965; 28–44.Google Scholar
  5. 5.
    Ranby M, Sundell B, Nilsson TK. Blood collection in strong acidic citrate anticoagulant used in a study of dietary influence on basal tPA activity. Thromb Haemost 1989; 62: 917–22.PubMedGoogle Scholar
  6. 6.
    Davidson JF, Walker ID. Assessment of the fibrinolytic system. In Bloom AL, Thomas DP, editors. Haemostasis and Thrombosis. Edinburgh: Churchill Livingstone 1987; 953–66.Google Scholar
  7. 7.
    Verheijen JH, Mullaart E, Chang GTG, Kluft C, Wijngaards G. A simple, sensitive spectrophotometric assay for extrinsic (tissue-type) plasminogen activator applicable to measurement in plasma. Thromb Haemost 1982; 48: 266–9.PubMedGoogle Scholar
  8. 8.
    Ranby M, Bergsdorf N, Nilsson T, Mellbring G, Winblad B, Bucht G. Age dependence of tissue plasminogen activator concentrations in plasma, as studied by an improved enzyme-linked immunosorbent assay. Clin Chem 1986; 32: 2160–5.PubMedGoogle Scholar
  9. 9.
    Erickson LA, Fici GJ, Lund JE, Boyle TP, Polites HG, Marotti KR. Development of venous occlusions in mice transgenic for the plasminogen activator inhibitor-1 gene. Nature 1990; 346: 74–6.PubMedGoogle Scholar
  10. 10.
    Carmeliet P, Stassen JM, Schoonjans L et al. Plasminogen activator inhibitor-1 gene-deficient mice. II. Effects on haemostasis, thrombosis, and thrombolysis. J Clin Invest 1993; 92: 2756–60.PubMedGoogle Scholar
  11. 11.
    Carmeliet P, Schoonjans L, Kieckens L et al. Physiological consequences of loss of plasminogen activator gene function in mice. Nature 1994; 368: 419–24.PubMedGoogle Scholar
  12. 12.
    Hamsten A, Eriksson P. Fibrinolysis and atherosclerosis: an update. Fibrinolysis 1994; 8(Suppl 1): 253–62.Google Scholar
  13. 13.
    Rocha E, Paramo JA. The relationship between impaired fibrinolysis and coronary heart disease: a role for PAI-1. Fibrinolysis 1994; 8(5): 294–303.Google Scholar
  14. 14.
    Meade TM, Ruddock V, Stirling Y, Chakrabarti R, Miller GJ. Fibrinolytic activity, clotting factors, and long-term incidence of ischaemic heart disease in the North wick Park Heart Study. Lancet 1993; 342: 1076–9.PubMedGoogle Scholar
  15. 15.
    Cortellaro M, Cofrancesco E, Boschetti C et al. for the PLAT Group. Increased fibrin turnover and high PAI-1 activity as predictors of ischemic events in atherosclerotic patients. A case-control study. Arterioscler Thromb 1993; 13: 1412–7.PubMedGoogle Scholar
  16. 16.
    Hamsten A, de Faire U, Walldius G et al. Plasminogen activator inhibitor in plasma: risk factor for recurrent myocardial infarction. Lancet 1987; ii: 3–9.Google Scholar
  17. 17.
    Gram J, Jespersen J. A selective depression of tissue plasminogen activator (t-PA) activity in euglobulins characterizes a risk group among survivors of acute myocardial infarction. Thromb Haemost 1987; 57: 137–9.PubMedGoogle Scholar
  18. 18.
    Munkvad S, Gram J, Jespersen J. A depression of active tissue plasminogen activator in plasma characterizes patients with unstable angina pectoris who develop myocardial infarction. Eur Heart J 1990; 11: 525–8.PubMedGoogle Scholar
  19. 19.
    Paramo JA, Colucci M, Collen D. Plasminogen activator inhibitor in the blood of patients with coronary artery disease. Br Med J 1985; 291: 573–4.Google Scholar
  20. 20.
    Olofsson BO, Dahlen G, Nilsson TK. Evidence of increased levels of plasminogen activator inhibitor and tissue plasminogen activator in plasma of patients with angiographically verified coronary artery disease. Eur Heart J 1989; 10: 77–82.PubMedGoogle Scholar
  21. 21.
    Hamsten A, Wiman B, de Faire U, Blomback M. Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction. N Engl J Med 1985; 313: 1557–63.PubMedGoogle Scholar
  22. 22.
    Verheugt FWA, ten Cate JW, Sturk A et al. Tissue plasminogen activator activity and inhibition in acute myocardial infarction and angiographically normal coronary arteries. Am J Cardiol 1987; 59: 1075–9.PubMedGoogle Scholar
  23. 23.
    Barbash GI, Hod H, Roth A et al. Correlation of baseline plasminogen activator inhibitor activity with patency of the infarct artery after thrombolytic therapy in acute myocardial infarction. Am J Cardiol 1989; 64: 1231–5.PubMedGoogle Scholar
  24. 24.
    Sane DC, Stump DC, Topol EJ et al. Correlation between baseline plasminogen activator inhibitor levels and clinical outcome during therapy with tissue plasminogen activator for acute myocardial infarction. Thromb Haemost 1991; 65: 275–9.PubMedGoogle Scholar
  25. 25.
    Huber K, Rosc D, Resch I et al. Circadian fluctuations of plasminogen activator inhibitor and tissue plasminogen activator levels in plasma of patients with unstable coronary artery disease and acute myocardial infarction. Thromb Haemost 1988; 60: 372–6.PubMedGoogle Scholar
  26. 26.
    Aimer L, Ohlin H. Elevated levels of the rapid inhibitor of plasminogen activator (t-PA) in acute myocardial infarction. Thromb Res 1987; 47: 335–9.Google Scholar
  27. 27.
    Sakata K, Hoshino T, Yoshida H et al. Circadian fluctuations of tissue plasminogen activator antigen and plasminogen activator inhibitor-1 antigen in vasospastic angina. Am Heart J 1992; 124: 854–60.PubMedGoogle Scholar
  28. 28.
    Masuda T, Ogawa H, Miyao Y et al. Circadian variation in fibrinolytic activity in patients with variant angina. Br Heart J 1994; 71: 156–61.PubMedGoogle Scholar
  29. 29.
    Landin K, Tengborn L, Smith U. Elevated fibrinogen and plasminogen activator inhibitor (PAI-1) in hypertension are related to metabolic risk factors for cardiovascular disease. J Intern Med 1990; 227: 273–8.PubMedGoogle Scholar
  30. 30.
    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.PubMedGoogle Scholar
  31. 31.
    Jansson JH, Johansson B, Boman K, Nilsson TK. Hypofibrinolysis in patients with hypertension and elevated cholesterol. J Intern Med 1991; 229: 309–16.PubMedGoogle Scholar
  32. 32.
    Allen RA, Kluft C, Brommer EJP. Effect of chronic smoking on fibrinolysis. Arteriosclerosis 1985; 5: 443–50.PubMedGoogle Scholar
  33. 33.
    Aillaud MF, Pignol F, Alessi MC et al. Increase in plasma concentration of plasminogen activator inhibitor, fibrinogen, von Willebrand factor, factor VIII:C and in erythrocyte sedimentation rate with age. Thromb Haemost 1986; 55: 330–2.PubMedGoogle Scholar
  34. 34.
    Sundell IB, Nilsson TK, Hallmans G, Hellsten G, Dahlen GH. Interrelationships between plasma levels of plasminogen activator inhibitor, tissue plasminogen activator, lipoprotein(a), and established cardiovascular risk factors in a North Swedish population. Atherosclerosis 1989; 80: 9–16.PubMedGoogle Scholar
  35. 35.
    Juhan-Vague I, Alessi MC, Joly P et al. Plasma plasminogen activator inhibitor-1 in angina pectoris. Influence of plasma insulin and acute-phase response. Arteriosclerosis 1989; 9: 362–7.PubMedGoogle Scholar
  36. 36.
    Phillips GB, Pinkernell BH, Jing TY. The association of hypotestosteronemia with coronary artery disease in men. Arterioscler Thromb 1994; 14: 701–6.PubMedGoogle Scholar
  37. 37.
    Caron P, Bennet A, Camare R, Louvet JP, Boneu S, Pie P. Plasminogen activator inhibitor in plasma is related to testosterone in men. Metabolism 1989; 38: 1010–5.PubMedGoogle Scholar
  38. 38.
    Hjermann I. The metabolic cardiovascular syndrome: syndrome X, Reaven’s syndrome, insulin resistance syndrome, atherothrombogenic syndrome. J Cardiovasc Pharmacol 1992; 20(Suppl 8): S5–S10.PubMedGoogle Scholar
  39. 39.
    Andreotti F, Davies GJ, Hackett DR et al. Major circadian fluctuations in fibrinolytic factors and possible relevance to time of onset of myocardial infarction, sudden cardian death and stroke. Am J Cardiol 1988; 62: 635–7.PubMedGoogle Scholar
  40. 40.
    Bogaty P, Waters DD. Circadian patterns in coronary disease: the mournfulness of morning. Can J Cardiol 1988; 4(1): 5–11.PubMedGoogle Scholar
  41. 41.
    Fearnley GR, Balmforth G, Fearnley E. Evidence of a diurnal fibrinolytic rhythm; with a simple method of measuring natural fibrinolysis. Clin Sci 1957; 16: 645–50.PubMedGoogle Scholar
  42. 42.
    Cepelak V, Barcal R, Lang N, Cepelakova H. Zum Tag- und Nachtrhythmus der Fibrino-lyse. Zschr Inn Med 1966; 21: 202–4.Google Scholar
  43. 43.
    Cepelak V, Barcal R. Fibrinolysis in twins and its variation in circadian rhythm. Plzen Lek Sborn 1959; 22: 129–31.Google Scholar
  44. 44.
    Rosing DR, Brakman P, Redwood DR et al. Blood fibrinolytic activity in man: diurnal variation and the response to varying intensities of exercise. Circ Res 1970; 27: 171–84.PubMedGoogle Scholar
  45. 45.
    Billimoria JD, Drysdale J, James DCO, Maclagan NF. Determination of fibrinolytic activity of whole blood with special reference to the effects of exercise and fat feeding. Lancet 1959; ii: 471–5.Google Scholar
  46. 46.
    Rosing DR, Redwood DR, Brakman P, Astrup T, Epstein SE. Impairment of the diurnal fibrinolytic response in man: effects of aging, type IV hyperlipoproteinemia and coronary artery disease. Circ Res 1973; 32: 752–7.PubMedGoogle Scholar
  47. 47.
    Buckell M, Elliott FA. Diurnal fluctuation of plasma fibrinolytic activity in normal males. Lancet 1959; i: 660–2.Google Scholar
  48. 48.
    Mann RD. Effect of age, sex, and diurnal variation on the human fibrinolytic system. J Clin Path 1967; 20: 223–6.PubMedGoogle Scholar
  49. 49.
    Korsan-Bengtsen K, Wilhelmsen L, Tibblin G. Blood coagulation and fibrinolysis in relation to degree of physical activity during work and leisure time. Acta Med Scand 1973; 193: 73–7.PubMedGoogle Scholar
  50. 50.
    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 Haemost 1988; 59: 329–32.PubMedGoogle Scholar
  51. 51.
    Grimaudo V, Hauert J, Bachmann F, Kruithof EKO. Diurnal variation of the fibrinolytic system. Thromb Haemost 1988; 59: 495–9.PubMedGoogle Scholar
  52. 52.
    Neerstrand H, Ostergaard P, Bergqvist D, Matzsch T, Hedner MU. tPA inhibitor, tPA:Ag, plasminogen and alpha-2-antiplasmin after low molecular weight heparin or standard heparin. Fibrinolysis 1987; 1: 39–43.Google Scholar
  53. 53.
    Kluft C, Jie AFH, Allen AR. Behaviour and quantitation of extrinsic (tissue-type) plasminogen activator in human blood. Thromb Haemost 1983; 50: 518–23.PubMedGoogle Scholar
  54. 54.
    Marckmann P, Sandstrom B, Jespersen J. Dietary effects on circadian fluctuation in human blood coagulation factor VII and fibrinolysis. Atherosclerosis 1993; 101: 225–34.PubMedGoogle Scholar
  55. 55.
    Meijer P, Boon R, Jie AFH, Rosen S, Kluft C. Bioimmunoassay for tissue-type plasminogen activator (t-PA) in human plasma: effect of blood sampling and handling procedures and comparison with other t-PA activity methods. Fibrinolysis 1992; 6(Suppl 2): 90–2.Google Scholar
  56. 56.
    Lindahl TL, Ohlsson OJ, Wiman B. On the mechanism of the reaction between human PAI-1 and tPA. Biochem J 1990; 265: 109–13.PubMedGoogle Scholar
  57. 57.
    Johansen LG, Gram J, Kluft C, Jespersen J. Chronobiology of coronary risk markers in Greenland Eskimos — a comparative study with Caucasians residing in the same Arctic area. Chronobiol Intern 1991; 8: 400–5.Google Scholar
  58. 58.
    Angleton P, Chandler WL, Schmer G. Diurnal variation of tissue-type plasminogen activator and its rapid inhibitor (PAI-1). Circulation 1989; 79: 101–6.PubMedGoogle Scholar
  59. 59.
    Bridges AB, McLaren M, Scott NA, Pringle TH, McNeill GP, Belch JJF. Circadian variation of tissue plasminogen activator and its inhibitor, von Willebrand factor antigen, and prostacyclin stimulating factor in men with ischaemic heart disease. Br Heart J 1993; 69: 121–4.PubMedGoogle Scholar
  60. 60.
    Hendriks HF, Veenstra J, Velthuiste Wierik EJM, Schaafsma G, Kluft C. Effect of moderate dose of alcohol with evening meal on fibrinolytic factors. Br Med J 1994; 308: 1003–6.Google Scholar
  61. 61.
    Kruithof EKO, Tran-Thang C, Ransijn A, Bachmann F. Demonstration of a fast-acting inhibitor of plasminogen activators in human plasma. Blood 1984; 64: 907–11.PubMedGoogle Scholar
  62. 62.
    Booth NA, Simpson AJ, Croll A, Bennet B, MacGregor IR. Plasminogen activator inhibitor (PAI-1) in plasma and platelets. Br J Haematol 1988; 70: 327–33.PubMedGoogle Scholar
  63. 63.
    Loskutoff DJ. Regulation of PAI-1 gene expression. Fibrinolysis 1991; 5: 197–206.Google Scholar
  64. 64.
    Dawson S, Henney A. The status of PAI-1 as a risk factor for arterial and thrombotic disease. Atherosclerosis 1992; 95: 105–17.PubMedGoogle Scholar
  65. 65.
    Dawson S, Hamsten A, Wiman B, Henney A, Humphries S. Genetic variation at the plasminogen activator inhibitor-1 locus is associated with altered levels of plasma plasminogen activator inhibitor-1 activity. Arterioscler Thromb 1991; 11: 183–90.PubMedGoogle Scholar
  66. 66.
    Dawson SJ, Wiman B, Hamsten A, Green F, Humphries S, Henney AM. The two allele sequences of a common polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene respond differently to interleukin-1 in HepG2 cells. J Biol Chem 1993; 268: 10739–45.PubMedGoogle Scholar
  67. 67.
    Huber K, Kirchheimer JC, Korninger C, Binder BR. Hepatic synthesis and clearance of components of the fibrinolytic system in healthy volunteers and in patients with different stages of liver cirrhosis. Thromb Res 1991; 62: 491–500.PubMedGoogle Scholar
  68. 68.
    Colucci M, Paramo JA, Collen D. Generation in plasma of a fast-acting inhibitor of plasminogen activator in response to endotoxin stimulation. J Clin Invest 1985; 75: 818–24.PubMedGoogle Scholar
  69. 69.
    Wiman B, Almquist A, Sigurdardottir O, Lindahl T. Plasminogen activator inhibitor 1 (PAI) is bound to vitronectin in plasma. FEBS Lett 1988; 242: 125–8.PubMedGoogle Scholar
  70. 70.
    van Leeuwen RTJ, Kol A, Andreotti F, Kluft C, Maseri A, Sperti G. Angiotensin II increases plasminogen activator inhibitor type 1 and tissue-type plasminogen activator messenger RNA in cultured rat aortic smooth muscle cells. Circulation 1994; 90: 362–8.PubMedGoogle Scholar
  71. 71.
    Suffredini AF, Harpel PC, Parrillo JE. Promotion and subsequent inhibition of plasminogen activation after administration of intravenous endotoxin to normal subjects. N Engl J Med 1989; 320: 1165–71.PubMedGoogle Scholar
  72. 72.
    Emeis JJ, Kooistra T. Interleukin 1 and lipopolysaccharide induce an inhibitor of tissue plasminogen activator in vivo and in cultured endothelial cells. J Exp Med 1986; 163: 1260–6.PubMedGoogle Scholar
  73. 73.
    Ridker PM, Gaboury CL, Conlin PR, Seely EW, Williams GH, Vaughan DE. Stimulation of plasminogen activator inhibitor in vivo by infusion of angiotensin II. Evidence of a potential interaction between the renin-angiotensin system and fibrinolytic function. Circulation 1993; 87: 1969–73.PubMedGoogle Scholar
  74. 74.
    Medvescek M, Keber D, Stegnar M, Borovnicar A. PAI-1 response to a carbohydrate meal in obese subjects. Fibrinolysis 1990; 4(Suppl 2): 89–91.Google Scholar
  75. 75.
    Verheijen JH, Rijken DC, Chang GTG, Preston FE, Kluft C. Modulation of rapid plasminogen activator inhibitor in plasma by stanozolol. Thromb Haemost 1984; 51: 396–7.PubMedGoogle Scholar
  76. 76.
    Jespersen J. The diurnal increase in euglobulin fibrinolytic activity in women using oral contraceptives and in normal women, and the generation of extrinsic fibrinolytic activity. Thromb Haemost 1988; 567: 183–8.Google Scholar
  77. 77.
    Kluft C, Verheijen JH, Jie AFH et al. The postoperative fibrinolytic shutdown: a rapidly reverting acute phase pattern for the fast-acting inhibitor of tissue-type plasminogen activator after trauma. Scand J Clin Lab Invest 1985; 45: 605–10.PubMedGoogle Scholar
  78. 78.
    Johansen LG, Gram J, Kluft C, Jespersen J. Circadian variations of extrinsic fibrinolytic components in blood from Eskimos. Fibrinolysis 1990; 4(1): 35–9.Google Scholar
  79. 79.
    Fujii S, Lucore CL, Hopkins WE, Billadello JJ, Sobel BE. Induction of synthesis of plasminogen activator inhibitor type-1 by tissue-type plasminogen activator in human hepatic and endothelial cells. Thromb Haemost 1990; 64: 412–9.PubMedGoogle Scholar
  80. 80.
    Bosma PJ, van den Berg EA, Kooistra T, Siemieniak DR, Slightom JL. Human plasminogen activator inhibitor-1 gene. Promoter and structural gene nucleotide sequences. J Biol Chem 1988; 263: 9129–41.PubMedGoogle Scholar
  81. 81.
    Schleef RR, Bevilacqua MP, Sawdey M, Gimbrone 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: 5797–803.PubMedGoogle Scholar
  82. 82.
    Peternel P, Mozina H, Stegnar M, Keber D, Vene N. Reduced diurnal rhythm of fibrinolytic activity in patients with pace-maker. Fibrinolysis 1988; 2(Suppl 1): 7–9.Google Scholar
  83. 83.
    Lemmer B, Nold G. Circadian changes in estimated hepatic blood flow in healthy subjects. Br J Clin Pharmac 1991; 32: 627–9.Google Scholar
  84. 84.
    Menon SI, Smith PA, White RWB, Dewar HA. Diurnal variations of fibrinolytic activity and plasma- 11-hydroxycorticosteroid levels. Lancet 1967; ii: 531–3.Google Scholar
  85. 85.
    Chandler WL, Mornin D, Whitten RO et al. Insulin, Cortisol and catecholamines do not regulate circadian variations in fibrinolytic activity. Thromb Res 1990; 58: 1–12.PubMedGoogle Scholar
  86. 86.
    Grant PJ, Kruithof EKO, Felley CP, Felber JP, Bachmann F. Short-term infusions of insulin, triacylglycerol and glucose do not cause acute increases in plasminogen activator inhibitor-1 concentrations in man. Clin Sci 1990; 79: 513–7.PubMedGoogle Scholar
  87. 87.
    Harenberg J, Weber E, Spohr U, Mori H. Is the diurnal increase of fibrinolytic activity influenced by alpha- or beta-adrenergic blockade? Blut 1980; 41: 455–8.PubMedGoogle Scholar
  88. 88.
    Andreotti F, Kluft C, Davies GJ, Huisman LGM, de Bart ACW, Maseri A. Effect of propranolol (long-acting) on the circadian fluctuation of tissue-plasminogen activator and plasminogen activator inhibitor-1. Am J Cardiol 1991; 68: 1295–9.PubMedGoogle Scholar
  89. 89.
    de Fouw NJ, van Hinsbergh VWM, de Jong YF, Haverkate F, Bertina RM. The interaction of activated protein C and thrombin with the plasminogen activator inhibitor released from human endothelial cells. Thromb Haemost 1987; 57: 176–82.PubMedGoogle Scholar
  90. 90.
    Okajima K, Koga S, Kaji M et al. Effect of protein C and activated protein C on coagulation and fibrinolysis in normal human subjects. Thromb Haemost 1990; 63: 48–53.PubMedGoogle Scholar
  91. 91.
    DeWood 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.PubMedGoogle Scholar
  92. 92.
    Becker RC, Corrao JM, Baker SP, Gore JM, Alpert JS. Circadian variation in thrombolytic response to rt-PA in acute myocardial infarction. J Appl Cardiol 1988; 3: 213–21.Google Scholar
  93. 93.
    Kurnik PB. Circadian variation in the efficacy of t-PA. Circulation 1995; 91: 1341–6.PubMedGoogle Scholar
  94. 94.
    Huber K, Beckmann R, Probst P, Rauscha F, Kaindl F, Binder BR. Influence of cardiac output on peak t-PA plasma levels in patients receiving thrombolytic therapy with recombinant t-PA — correlation with patency rates. Thromb Haemost 1993; 69: 45–9.PubMedGoogle Scholar
  95. 95.
    Astrup T. Fibrinolysis in the organism. Blood 1956; 11: 781–806.PubMedGoogle Scholar
  96. 96.
    Lowe GDO, Wood DA, Douglas JT et al. Relationships of plasma viscosity, coagulation and fibrinolysis to coronary risk factors and angina. Thromb Haemost 1991; 65: 339–43.PubMedGoogle Scholar
  97. 97.
    WHO International Study Group. Myocardial infarction community registers: Public Health in Europe. Copenhagen: Regional Office for Europe (WHO) 1976; 5 (annex II): 188–91.Google Scholar
  98. 98.
    Muller JE, Ludmer PL, Willich SN et al. Circadian variation in the frequency of sudden cardiac death. Circulation 1987; 75: 131–8.PubMedGoogle Scholar
  99. 99.
    Marshall J. Diurnal variation in occurrence of strokes. Stroke 1977; 88: 230–1.Google Scholar
  100. 100.
    Kluft C, Andreotti F. Consequences of the circadian fluctuation in plasminogen activator inhibitor 1 (PAI-1) for studies on blood fibrinolysis. Fibrinolysis 1988; 2(Suppl 2): 93–5.Google Scholar
  101. 101.
    Simpson HCR, Mann JI, Meade TW, Chakrabarti R, Stirling Y, Woolf L. Hypertriglyceri-daemia and hypercoagulability. Lancet 1983; i: 786–90.Google Scholar
  102. 102.
    Keegan AL, Holland CD, Jayson MIV. Loss of diurnal variation in fibrinolytic activity in systemic sclerosis. Br J Rheumat 1985; 24: 211.Google Scholar
  103. 103.
    Knutsson A, Akerstedt T, Jonsson BG, Orth-Gomer K. Increased risk of ischaemic heart disease in shift workers. Lancet 1986; ii: 89–91.Google Scholar
  104. 104.
    Peternel P, Stegnar U, Salobir B, Salobir D, Keber D, Vene N. Shift work and circadian rhythm of blood fibrinolytic parameters. Fibrinolysis 1990; 4: 113–5.Google Scholar
  105. 105.
    Mackworth-Young CG, Andreotti F, Harmer I et al. Endothelium-derived haemostatic factors and the antiphospholipid syndrome. Br J Rheumat 1995; 34: 201–6.Google Scholar

Copyright information

© Kluwer Academic Publishers 1996

Authors and Affiliations

  • Felicita Andreotti
  • Alessandro Manzoli

There are no affiliations available

Personalised recommendations