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Platelet Activity in the Early Stage of Acute Myocardial Infarction: Relation to Time of Presentation, Treatment with Either Tissue Plasminogen Activator or Streptokinase and Cyclooxygenase Inhibition

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Abstract

Background. Platelet activation after myocardial infarction and thrombolytic treatment has been documented; but its relationship with the onset of symptoms and with thrombolysis, and the influence of aspirin in this setting is not well defined. In this study we measured platelet activity in the early phase of myocardial infarction treated with either streptokinase or rt-PA and evaluated influence of aspirin in this framework.

Methods. 41 patients (age 57 ± 6 years) were treated with thrombolytic therapy during myocardial infarction; 21 patients with 1,5 million units of streptokinase (Group 1) and 20 patients with 100 mg of rt-PA (Group 2); 10 randomly selected patients in each group were given 500 mg aspirin i.v. prior to infusion of thrombolytic drug and, subsequently, 325 mg aspirin a day orally. Consecutive samples of beta-thromboglobulin (BTG), a marker of platelet activity, were collected at admission and after thrombolysis for the following 48 hours. Results. At admission, BTG plasma levels averaged 125 ± 31 IU/ml in Group 1 and 134 ± 35 IU/ml in Group 2 (p = 0.81). Thrombolysis was followed by a similar increase of platelet activity with maximal values reached at the 3rd hour in both groups (196 ± 43 IU/ml in Group 1 and 192 ± 39 in Group 2: p < 001 versus baseline and p NS between the groups). Higher levels of BTG were observed in streptokinase-treated group starting from the 24th hour (p < 0.05). Patients treated with aspirin showed lower levels of BTG only from the 48th hour after thrombolysis in both groups. An inverse correlation was found between time elapsed from onset of symptoms to admission and BTG value on admission (r = −0.86 p < 0.001); in patients admitted within two hours from the beginning of symptoms, with higher levels of BTG, thrombolysis not induced a significant increase of platelet activity; who was observed in patients admitted later. Conclusions. A marked platelet activation is more evident in the first hours of myocardial infarction and is differently influenced by thrombolytic treatment in relation with the delay of patient presentation. Both streptokinase and rt-PA induce a similar increase of platelet activity which is more persistent after streptokinase; cyclooxygenase inhibition seems to influence the platelet activity only from the second day.

Condensed abstract. Influence of aspirin on platelet activity during myocardial infarction treated with thrombolytic therapy is not well defined. Twenty-one patients treated with streptokinase (Group 1) and 20 patients treated with rt-PA (Group 2) were randomly selected to give 500 mg of aspirin i.v. prior thrombolysis and subsequently 325 mg a day orally. Platelet activity was evaluated through determination of beta-thromboglobulin plasma levels. Thrombolysis was followed by a similar increase of platelet activity in both groups with maximal values reached at the 3rd hour; higher levels of beta-thromboglobulin were observed in streptokinase-treated group starting from 24th hour. Treatment with aspirin reduced beta-thromboglobulin plasma levels only at 48th hour in both groups.

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References

  1. Vaughan DE, Van Houtte E, Declerck PJ, Collen D. Streptoby kinase-induced platelet aggregation. Prevalence and mechanot nism. Circulation 1991;84:84–91.

    Google Scholar 

  2. Schafer AI, Adelman B. Plasmin inhibition of platelet func-tion and of arachidonic acid metabolism. J Clin Invest 1985; 75:456–61.

    PubMed  CAS  Google Scholar 

  3. Luenc SY, Karlberg KE, Chen J, Hacherman I, Egberg N, Bergstrom K. Enhanced platelet function in acute myocar-dial infarction is attenuated by streptokinase treatment. J Intern Med 1992;231:595–600.

    Article  Google Scholar 

  4. Eisenberg PR, Sherman LA, Jaffe AS. Paradoxic elevation of Æbrinopeptide A after streptokinase. Evidence for contindent ued thrombosis despite intense Æbrinolysis. J Am Coll Cardiol 1987;10:527–9.

    PubMed  CAS  Google Scholar 

  5. Saldeen TGP, Saldeen P, Nichols WW, Lawson DL, Nicolina FA, Mheta JL. Increased production of thromboxane A2 by acticoronary arteries after thrombolysis. Am Heart J 1993;125: 277–84.

    Article  PubMed  CAS  Google Scholar 

  6. Fitzgerald DJ, Catella F, Roy L, FitzGerald G. Marked aspiplatelet activation in vivo after intravenous streptokinase in patients with acute myocardial infarction. Circulation 1988; 77:142–150.

    PubMed  CAS  Google Scholar 

  7. Husted SE, Kristensen SD, Vissinger H, Morn B, Schmidt EB, Nielsen HK. Intravenous acetylsalicylic acid dose retion lated effects on platelet function and Æbrinolysis in healthy males. Thromb Hemost 1992;68:226–9.

    CAS  Google Scholar 

  8. Fitzgerald DJ, Wright F, FitzGerald GA. Increased throm-boxane biosynthesis during coronary thrombolysis: evidence that platelet activation and thromboxane A2 modulate the remarked sponse to tissue-type plasminogen activator. Circ Res 1989; 65:83–94.

    PubMed  CAS  Google Scholar 

  9. Golino P, Ashton JH, Glas-Greenwalt P, Mcnatt J, Buja LM, Willerson JT. Mediation of reocclusion by thromboxane A2 and serotonin after thrombolysis with tissue-type plasmino-pagen activator in a canine preparation of coronary thrombosis. Circulation 1988;77:678–82.

    PubMed  CAS  Google Scholar 

  10. Walz DA. Platelet-released proteins as molecular markers for the activation process. Semin in Thromb and Hemost 1984;10:270–9.

    Article  CAS  Google Scholar 

  11. Bertolino G, Noris P, Previtali M, Gamba G, Ferrario M, Montani L, et al. Platelet function after in vivo and in vitro treatment with thrombolytic agents. Am J Cardiol 1992;69: 457–61.

    Article  PubMed  CAS  Google Scholar 

  12. Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis: characteristics of coromarked nary atherosclerotic plaques underling fatal occlusive thrombi. Br Heart J 1985;50:127–31.

    Google Scholar 

  13. Ambrose JA, Winters SL, Arora RR, Eng A, Riccio A, Gorlin R, et al. Angiographic evolution of coronary artery morphol-synogy in unstable angina. J Am Coll Cardiol 1986;7:472–8.

    PubMed  CAS  Google Scholar 

  14. Fitzgerald DJ, Roy L, Catella F, FitzGerald GA. Platelet ac-tivation in unstable coronary disease. N Engl J Med 1986; 315:983–9.

    Article  PubMed  CAS  Google Scholar 

  15. Folts JD, Gallagher K, Rowe GG. Blood flow reduction in stenosed coronary arteries: vasospasm or platelet aggregapersistent tion? Circulation 1985;65:248–255.

    Google Scholar 

  16. Fitzgerald DJ, FitzGerald GA. Antiplatelet and anticoagudrug lant therapy during coronary thrombolysis. Trends Cardiov Med 1990;108:29–35.

    Google Scholar 

  17. Rebuzzi AG, Natale A, Bianchi C, Albanese S, Lanz GA, Coppola E, et al. Importance of reperfusion on tromboxane A2 metabolite excretion after thrombolysis. Am Heart J 1992;123:560–6.

    Article  PubMed  CAS  Google Scholar 

  18. Udvardy M, Hasfalvi J, Boda Z, Rak K. Beta-thromboglo-bulin and increased platelet activation after streptokinase treatment of acute myocardial infarction. Am J Cardiol 1992; 70:837–8.

    Article  PubMed  CAS  Google Scholar 

  19. Loscalzo J, Vaughan DE. Tissue plasminogen activator pro-motes platelet disaggregation in plasma. J Clin Invest 1987; 79:1749–55.

    PubMed  CAS  Google Scholar 

  20. Kerins PM, Roy L, FitzGerald GA, Fitzgerald DJ. Platelet and vascular function during coronary thrombolysis with tis-sue-type plasminogen activator. Circulation 1989;80:1718–23.

    PubMed  CAS  Google Scholar 

  21. Salvioni A, Marenzi G, Lauri G, Giraldi F, Perego GB, Grazi S, et al. Beta-thromboglobulin plasma levels in the Ærst week after myocardial infarction: influence of thrombolytic therapy. Am Heart J 1994;128:472–6.

    Google Scholar 

  22. Gulba DC, Barthels M, Westhoff-Bleck M, Jost S, Rafflenbuel W, Daniel GW, et al. Increased thrombin levels during thrombolytic therapy in acute myocardial infarction. Circulation 1991;83:937–44.

    PubMed  CAS  Google Scholar 

  23. Eidt JF, Allison P, Noble J, Ashton J, Golino O, Mc Natt J, Buja CM, et al. Thrombin is an important mediator of plate-let aggregation in stenosed canine coronary arteries with endothelial injury. J Clin Invest 1989;84:18–27.

    Article  PubMed  CAS  Google Scholar 

  24. Sitko GR, Ramjh IT, Stabilito II, Lheman D, Lynch JJ, Vlasuk GP. Conjunctive enhancement of enzymatic thrombolysis and prevention of thrombotic reocclusion with the selective factor Xa inhibition; tick anticoagulant peptide. Circulation 1992;85:805–15.

    PubMed  CAS  Google Scholar 

  25. Yang IK, Gold HK, Ziskind AA, Leinbach RC, Fallon JT, Collen D. Prevention of platelet-rich arterial thrombosis by selective thrombin inhibition. Circulation 1990;81:219–25.

    Google Scholar 

  26. Eisenberg PR. Role of new anticoagulants as adjunctive therapy during thrombolysis. Am J Cardiol 1991;67:19A–24A.

    Article  PubMed  CAS  Google Scholar 

  27. Salvioni A, Perego GB, Marenzi G, Lauri F, Giraldi F, Grazi S, et al. Late activation of Æbrinolytic system in myocardial infarction treated with thrombolytic therapy: inØuence of the coronary anatomical substrate. Eur Heart J 1996;17:230–6.

    PubMed  CAS  Google Scholar 

  28. Yasuda T, Gold HK, Yaoita H, Leinbach RC, Guerrero JL, Jang IK, et al. Comparative effects of aspirin, a synthetic thrombin inhibitor and a monoclonal antiplatelet glycoprotein IIb/IIIa antibody on coronary artery reperfusion, reocclusion and bleeding with recombinant tissue type plasminogen activator in a canine preparation. J Am Coll Cardiol 1990;16:714–22.

    PubMed  CAS  Google Scholar 

  29. Prager NA, Torr-Brown SR, Sobel BE, Abendschein PR. Maintenance of patency after thrombolysis in stenotic arter-ies requires combined inhibition of thrombin and platelets. J Am Coll Cardiol 1993;22:85–92.

    Article  PubMed  CAS  Google Scholar 

  30. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomized trial of intravenous streptoki-nase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988;2: 349–60.

    Google Scholar 

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Salvioni, A., Perego, G.B., Marenzi, G. et al. Platelet Activity in the Early Stage of Acute Myocardial Infarction: Relation to Time of Presentation, Treatment with Either Tissue Plasminogen Activator or Streptokinase and Cyclooxygenase Inhibition. J Thromb Thrombolysis 5, 65–71 (1998). https://doi.org/10.1023/A:1008861707773

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