Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Predictors of coronary artery reocclusion following fibrinolysis (thrombolysis)

C Michael Gibson, MS, MD
Sabina A Murphy, MPH
Section Editor
Freek Verheugt, MD, FACC, FESC
Deputy Editor
Gordon M Saperia, MD, FACC


Reocclusion of the infarct-related artery following successful reperfusion with fibrinolysis in patients with ST-elevation myocardial infarction remains a major limitation. Despite adjunctive pharmacologic therapy with antiplatelet and anticoagulant therapy, early thrombotic reocclusion occurs in 5 to 10 percent of patients before hospital discharge and in up to 25 percent by three months in studies prior to the use of dual antiplatelet therapy [1-5]. Early reinfarction occurs in 3 to 5 percent [6-8]. Reocclusion is clinically silent in over 50 percent of cases.

Whether symptomatic or silent, reocclusion is associated with significant morbidity and mortality in both the short and long term. Among 810 patients evaluated by the TAMI study group, the in-hospital mortality rate was significantly higher in those with reocclusion (11 versus 4 percent with a patent coronary artery) [1]. In a study of 20,101 patients enrolled in the TIMI trials, the increase in mortality with early reocclusion persisted at two years (19.6 versus 10.1 percent) [5].

Thus, percutaneous coronary intervention is often recommended even in clinically stable patients after fibrinolysis. (See "Acute ST elevation myocardial infarction: Selecting a reperfusion strategy", section on 'Fibrinolysis followed by PCI'.)

This topic will review the predictors of coronary artery reocclusion following fibrinolysis. The role of coronary artery patency in outcome after myocardial infarction and the general principals of the clinical use of fibrinolytic therapy are discussed elsewhere. (See "Coronary artery patency and outcome after myocardial infarction" and "Fibrinolysis for acute ST elevation myocardial infarction: Initiation of therapy".)


Demographic and clinical variables have not proven very helpful in predicting which patients will develop reocclusion [1,2]. However, one large series did find that clinical predictors of reinfarction included advanced age, shorter time to fibrinolysis, nonsmoking status, prior infarction or angina, female sex, anterior infarction, and lower systolic blood pressure [6].

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: Sep 09, 2016.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Ohman EM, Califf RM, Topol EJ, et al. Consequences of reocclusion after successful reperfusion therapy in acute myocardial infarction. TAMI Study Group. Circulation 1990; 82:781.
  2. Ellis SG, Topol EJ, George BS, et al. Recurrent ischemia without warning. Analysis of risk factors for in-hospital ischemic events following successful thrombolysis with intravenous tissue plasminogen activator. Circulation 1989; 80:1159.
  3. GUSTO Angiographic Investigators. The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med 1993; 329:1615.
  4. Meijer A, Verheugt FW, Werter CJ, et al. Aspirin versus coumadin in the prevention of reocclusion and recurrent ischemia after successful thrombolysis: a prospective placebo-controlled angiographic study. Results of the APRICOT Study. Circulation 1993; 87:1524.
  5. Gibson CM, Karha J, Murphy SA, et al. Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials. J Am Coll Cardiol 2003; 42:7.
  6. Hudson MP, Granger CB, Topol EJ, et al. Early reinfarction after fibrinolysis: experience from the global utilization of streptokinase and tissue plasminogen activator (alteplase) for occluded coronary arteries (GUSTO I) and global use of strategies to open occluded coronary arteries (GUSTO III) trials. Circulation 2001; 104:1229.
  7. Birnbaum Y, Herz I, Sclarovsky S, et al. Admission clinical and electrocardiographic characteristics predicting an increased risk for early reinfarction after thrombolytic therapy. Am Heart J 1998; 135:805.
  8. Becker RC. Reocclusion following successful thrombolysis. Emerging concepts. Cardiology 1993; 82:265.
  9. Ott I, Malcouvier V, Schömig A, Neumann FJ. Proteolysis of tissue factor pathway inhibitor-1 by thrombolysis in acute myocardial infarction. Circulation 2002; 105:279.
  10. Gibson CM, Cannon CP, Piana RN, et al. Angiographic predictors of reocclusion after thrombolysis: results from the Thrombolysis in Myocardial Infarction (TIMI) 4 trial. J Am Coll Cardiol 1995; 25:582.
  11. Serruys PW, Wijns W, van den Brand M, et al. Is transluminal coronary angioplasty mandatory after successful thrombolysis? Quantitative coronary angiographic study. Br Heart J 1983; 50:257.
  12. Gash AK, Spann JF, Sherry S, et al. Factors influencing reocclusion after coronary thrombolysis for acute myocardial infarction. Am J Cardiol 1986; 57:175.
  13. Harrison DG, Ferguson DW, Collins SM, et al. Rethrombosis after reperfusion with streptokinase: importance of geometry of residual lesions. Circulation 1984; 69:991.
  14. Badger RS, Brown BG, Kennedy JW, et al. Usefulness of recanalization to luminal diameter of 0.6 millimeter or more with intracoronary streptokinase during acute myocardial infarction in predicting "normal" perfusion status, continued arterial patency and survival at one year. Am J Cardiol 1987; 59:519.
  15. Veen G, Meyer A, Verheugt FW, et al. Culprit lesion morphology and stenosis severity in the prediction of reocclusion after coronary thrombolysis: angiographic results of the APRICOT study. Antithrombotics in the Prevention of Reocclusion in Coronary Thrombolysis. J Am Coll Cardiol 1993; 22:1755.
  16. Davies SW, Marchant B, Lyons JP, et al. Irregular coronary lesion morphology after thrombolysis predicts early clinical instability. J Am Coll Cardiol 1991; 18:669.
  17. Grines CL, Topol EJ, Bates ER, et al. Infarct vessel status after intravenous tissue plasminogen activator and acute coronary angioplasty: prediction of clinical outcome. Am Heart J 1988; 115:1.
  18. Alison HW, Russell RO Jr, Mantle JA, et al. Coronary anatomy and arteriography in patients with unstable angina pectoris. Am J Cardiol 1978; 41:204.
  19. Ambrose JA, Winters SL, Arora RR, et al. Angiographic evolution of coronary artery morphology in unstable angina. J Am Coll Cardiol 1986; 7:472.
  20. Wilson RF, Holida MD, White CW. Quantitative angiographic morphology of coronary stenoses leading to myocardial infarction or unstable angina. Circulation 1986; 73:286.
  21. Bresnahan DR, Davis JL, Holmes DR Jr, Smith HC. Angiographic occurrence and clinical correlates of intraluminal coronary artery thrombus: role of unstable angina. J Am Coll Cardiol 1985; 6:285.
  22. McMahon MM, Brown BG, Cukingnan R, et al. Quantitative coronary angiography: measurement of the "critical" stenosis in patients with unstable angina and single-vessel disease without collaterals. Circulation 1979; 60:106.
  23. Wall TC, Mark DB, Califf RM, et al. Prediction of early recurrent myocardial ischemia and coronary reocclusion after successful thrombolysis: a qualitative and quantitative angiographic study. Am J Cardiol 1989; 63:423.
  24. Reiner JS, Lundergan CF, van den Brand M, et al. Early angiography cannot predict postthrombolytic coronary reocclusion: observations from the GUSTO angiographic study. Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries. J Am Coll Cardiol 1994; 24:1439.
  25. Freeman MR, Williams AE, Chisholm RJ, Armstrong PW. Intracoronary thrombus and complex morphology in unstable angina. Relation to timing of angiography and in-hospital cardiac events. Circulation 1989; 80:17.
  26. Sansa M, Cernigliaro C, Bolognese L, et al. Angiographic morphology and response to therapy in unstable angina. Clin Cardiol 1988; 11:121.
  27. Bugiardini R, Pozzati A, Borghi A, et al. Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome. Am J Cardiol 1991; 67:460.
  28. van den Berg EK, Schmitz JM, Benedict CR, et al. Transcardiac serotonin concentration is increased in selected patients with limiting angina and complex coronary lesion morphology. Circulation 1989; 79:116.
  29. Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion. Circulation 1985; 71:699.
  30. Davies MJ, Thomas AC, Knapman PA, Hangartner JR. Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. Circulation 1986; 73:418.
  31. Chesebro JH, Knatterud G, Roberts R, et al. Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. Circulation 1987; 76:142.
  32. Karagounis L, Sorensen SG, Menlove RL, et al. Does thrombolysis in myocardial infarction (TIMI) perfusion grade 2 represent a mostly patent artery or a mostly occluded artery? Enzymatic and electrocardiographic evidence from the TEAM-2 study. Second Multicenter Thrombolysis Trial of Eminase in Acute Myocardial Infarction. J Am Coll Cardiol 1992; 19:1.
  33. Anderson JL, Karagounis LA, Becker LC, et al. TIMI perfusion grade 3 but not grade 2 results in improved outcome after thrombolysis for myocardial infarction. Ventriculographic, enzymatic, and electrocardiographic evidence from the TEAM-3 Study. Circulation 1993; 87:1829.
  34. Vogt A, von Essen R, Tebbe U, et al. Impact of early perfusion status of the infarct-related artery on short-term mortality after thrombolysis for acute myocardial infarction: retrospective analysis of four German multicenter studies. J Am Coll Cardiol 1993; 21:1391.
  35. Van Belle E, Lablanche JM, Bauters C, et al. Coronary angioscopic findings in the infarct-related vessel within 1 month of acute myocardial infarction: natural history and the effect of thrombolysis. Circulation 1998; 97:26.
  36. Cannon CP, McCabe CH, Henry TD, et al. A pilot trial of recombinant desulfatohirudin compared with heparin in conjunction with tissue-type plasminogen activator and aspirin for acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 5 trial. J Am Coll Cardiol 1994; 23:993.
  37. von Essen R, Zeymer U, Tebbe U, et al. HBW 023 (recombinant hirudin) for the acceleration of thrombolysis and prevention of coronary reocclusion in acute myocardial infarction: results of a dose-finding study (HIT-II) by the Arbeitsgemeinschaft Leitender Kardiologischer Krankenhausärzte. Coron Artery Dis 1998; 9:265.
  38. Johns JA, Gold HK, Leinbach RC, et al. Prevention of coronary artery reocclusion and reduction in late coronary artery stenosis after thrombolytic therapy in patients with acute myocardial infarction. A randomized study of maintenance infusion of recombinant human tissue-type plasminogen activator. Circulation 1988; 78:546.
  39. Serruys PW, Arnold AE, Brower RW, et al. Effect of continued rt-PA administration on the residual stenosis after initially successful recanalization in acute myocardial infarction--a quantitative coronary angiography study of a randomized trial. Eur Heart J 1987; 8:1172.
  40. Arnout J, Simoons M, de Bono D, et al. Correlation between level of heparinization and patency of the infarct-related coronary artery after treatment of acute myocardial infarction with alteplase (rt-PA). J Am Coll Cardiol 1992; 20:513.
  41. Kleiman NS, Ohman EM, Califf RM, et al. Profound inhibition of platelet aggregation with monoclonal antibody 7E3 Fab after thrombolytic therapy. Results of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) 8 Pilot Study. J Am Coll Cardiol 1993; 22:381.