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Thromb Haemost 1999; 81(06): 865-868
DOI: 10.1055/s-0037-1614589
Letters to the Editor
Schattauer GmbH

Elevated Levels of Plasmin-α2 Antiplasmin Complexes in Unstable Angina

Antoni Bayés-Genís
4   From the Department of Cardiology, Hospital de Sant Pau, Barcelona, Spain
,
Josep Guindo
4   From the Department of Cardiology, Hospital de Sant Pau, Barcelona, Spain
,
Artur Oliver
1   Hematology Unit, Fundació Puigvert, Barcelona, Spain
,
Lina Badimon
4   From the Department of Cardiology, Hospital de Sant Pau, Barcelona, Spain
,
Miquel Fiol
2   Department of Cardiology, Hospital Son Dureta, Palma de Mallorca, Spain
,
Jose Mateo
3   Hematology Department, Hospital de Sant Pau, Barcelona, Spain
,
Joan Carles Souto
3   Hematology Department, Hospital de Sant Pau, Barcelona, Spain
,
Jose M. Dominguez
4   From the Department of Cardiology, Hospital de Sant Pau, Barcelona, Spain
,
Jordi Fontcuberta
3   Hematology Department, Hospital de Sant Pau, Barcelona, Spain
,
Antoni Bayés de Luna
4   From the Department of Cardiology, Hospital de Sant Pau, Barcelona, Spain
› Author Affiliations
Further Information

Publication History

Received 27 May 1998

Accepted after resubmission 15 February 1999

Publication Date:
09 December 2017 (online)

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Summary

The evidence of elevated levels of several biochemical markers of prothrombotic state in patients with unstable angina suggests that thrombus formation and lysis play a pivotal role in acute coronary syndromes. The clinical syndrome of unstable angina encompasses a variety of clinical presentations of transient episodes of myocardial ischemia. This study was designed to assess plasmin generation in different settings of unstable angina. Evidence of plasmin generation in patients with unstable angina was measured by circulating plasmin-α2 antiplas-min complexes (PAP). A second objective was to identify whether PAP levels had a prognostic value to predict outcome. Eighty-five patients admitted to the coronary care unit for unstable angina were classified into three groups. Group A included 26 patients with postinfarction angina; group B comprised 26 patients with new onset angina; and group C included 33 patients with crescendo angina. Mean PAP levels were higher in the three groups compared to healthy controls. A significant correlation was found between levels of PAP and D-dimer, particularly in postinfarction angina (r = 0.6; p <0.0005). This trial adds new insights into the pathophysiology of unstable angina. It demonstrates that plasmin is generated in the different settings of unstable angina but particularly in postinfarction angina patients where a fibrin-rich thrombus is responsible of the symptoms. However, in this series PAP levels do not predict an uneventful outcome neither in the acute phase nor at long term (6 months).

Abbreviations and acronyms: CABG: coronary artery bypass graft; CCU: coronary care unit; ECG: electrocardiogram; IABP: intraaortic balloon pump; MI: myocardial infarction; PAP: plasmin-α2 antiplasmin complexes; PTCA: percutaneous transluminal coronary angioplasty

 

  • References

  • 1 Davies MJ, Thomas AC. Plaque fissuring: the cause of acute myocardial infarction, sudden death and crescendo angina. Br Heart J 1985; 53: 363-73.
    CrossrefPubMedSearch in Google Scholar
  • 2 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: 699-708.
    CrossrefPubMedSearch in Google Scholar
  • 3 Ambrose JA, Winters SL, Arora RR, Eng A, Riccio A, Gorlin R, Fuster V. Angiographic evolution of coronary artery morphology in unstable angina. J Am Coll Cardiol 1986; 7: 472-8.
    CrossrefPubMedSearch in Google Scholar
  • 4 Vetrovec GW, Leinbach RC, Gold HK, Cowley MJ.. Intracoronary thrombolysis in syndromes of unstable ischemia: angiographic and clinical results. Am Heart J 1982; 104: 946-52.
    CrossrefPubMedSearch in Google Scholar
  • 5 Mizuno K, Satomura K, Miyamoto A, Arakawa K, Shibuya T, Arai T, Kurita A, Nakamura H, Ambrose JA. Angioscopic evaluation of coronary artery thrombi in acute coronary syndromes. N Engl J Med 1992; 326: 287.
    CrossrefPubMedSearch in Google Scholar
  • 6 Braunwald E. Unstable Angina: A classification. Circulation 1989; 80: 410-4.
    CrossrefPubMedSearch in Google Scholar
  • 7 Willensky RL, Bourdillon PDV, Vix VA, Zeller JA. Intracoronary artery thrombus formation in unstable angina: a clinical, biochemical and angio-graphic correlation. J Am Coll Cardiol 1993; 21: 692-9.
    CrossrefPubMedSearch in Google Scholar
  • 8 Théroux P, Latour JG, Léger-Gauthier C, De Lara J. Fibrinopeptide A and platelet factor levels in unstable angina pectoris. Circulation 1987; 75: 156-62.
    CrossrefPubMedSearch in Google Scholar
  • 9 Kruskal JB, Commerford DJ, Franks JJ, Kirsh RE. Fibrin and fibrinogen-related antigens in patients with stable and unstable coronary artery disease. N Engl J Med 1987; 317: 1361-5.
    CrossrefPubMedSearch in Google Scholar
  • 10 Gurfinkel E, Bozovich G, Cerdá M, Mejaíl I, Oxilia A, Mautner B. The time significance of acute thrombotic reactant markers in patients with and without silent myocardial ischemia and overt unstabla angina pectoris. Am J Cardiol 1995; 76: 121-4.
    CrossrefPubMedSearch in Google Scholar
  • 11 Holvoet P, de Boer A, Verstreken M, Collen D. An Enzyme-linked immunosorbent assay (ELISA) for the measurement of plasmin-α2-antiplasmin complex in human plasma. Application to the detection of in vivo activation of the fibrinolytic system. Thromb Haemost 1986; 56: 124-7.
    Thieme ConnectPubMedSearch in Google Scholar
  • 12 Nieuwenhuizen W. Plasma assays for derivatives of fibrin and of fibrinogen, based on monoclonal antibodies. Fibrinolysis 1988; 2: 1-5.
    PubMedSearch in Google Scholar
  • 13 Pelzer H, Pilgrim A, Schwartz A, Merte D, Keuper H, Hock H. Determination of α2-antiplasmin-plasmin complex in human plasma with an enzyme-linked immunosorbent assay. Fibrinolysis 1993; 7: 69-74.
    PubMedSearch in Google Scholar
  • 14 Fuster V, Badimon L, Cohen M, Ambrose JA, Badimon JJ, Chesebro JH. Insights into the pathogenesis of acute ischemic syndromes. Circulation 1988; 77: 1213-20.
    CrossrefPubMedSearch in Google Scholar
  • 15 Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease in the acute coronary syndromes. N Engl J Med 1992; 326: 310-8.
    CrossrefPubMedSearch in Google Scholar
  • 16 Montes R, Páramo A, Angles-Cano E, Rocha E. Development and clinical application of a new ELISA assay to determine plasmin-α2-antiplasmin complexes in plasma. Br J Haematol 1996; 92: 979-85.
    CrossrefPubMedSearch in Google Scholar
  • 17 Vaziri ND, Kennedy SC, Kennedy D, Gonzales E. Coagulation, fibrinolytic, and inhibitory proteins in acute myocardial infarction and angina pectoris. Am J Med 1992; 93: 651-7.
    CrossrefPubMedSearch in Google Scholar
  • 18 Alexopoulos D, Ambrose JA, Stump D, Borrico S, Gorlin R, Deshmuckh P, Fisher EA. Thrombosis-related markers in unstable angina pectoris. J Am Coll Cardiol 1991; 17: 866-71.
    CrossrefPubMedSearch in Google Scholar
  • 19 Badimon L, Badimon JJ, Turitto VT, Vallabhajosula S, Fuster V. Platelet thrombus formation on collagen type I: a model of deep vessel injury: influence of blood rheology, von Willebrand factor, and blood coagulation. Circulation 1988; 78: 1432-42.
    PubMedSearch in Google Scholar
  • 20 Badimon L, Badimon JJ. Mechanism of arterial thrombosis in nonparallel streamlines: platelet thrombi grow at the apex of stenotic severely injured vessel wall: experimental study in the pig model. J Clin Invest 1989; 84: 1134-44.
    CrossrefPubMedSearch in Google Scholar
  • 21 Farb A, Burke AP, Tang AL, Liang Y, Mannan P, Smialek J, Virmani R. Coronary plaque erosion without rupture into a lipid core: a frequent cause of coronary thrombosis in sudden coronary death. Circulation 1996; 93: 1354-63.
    CrossrefPubMedSearch in Google Scholar
  • 22 Davies SW, Marchart B, Lyons JP, Timmis AD. Irregualr coronary lesion morphology after thrombosis predicts early clinical instability. J Am Coll Cardiol 1991; 18: 669-74.
    CrossrefPubMedSearch in Google Scholar
  • 23 Mailhac A, Badimon JJ, Fallon JT, Fernández-Ortiz A, Meyer B, Chesebro JH, Fuster V, Badimon L. Effect of an eccentric severe stenosis on fibrin (ogen) deposition on severely damaged vessel wall in arterial thrombosis. Relative contribution of fibrin(ogen) and platelets. Circulation 1994; 90: 988-96.
    CrossrefPubMedSearch in Google Scholar
  • 24 Meyer BJ, Badimon JJ, Mailhac A, Fernández Ortiz A, Chesebro JH, Fuster V, Badimon L. Inhibition of growth of thrombus on fresh mural thrombus. Targeting optimal therapy. Circulation 1994; 90: 2432-8.
    CrossrefPubMedSearch in Google Scholar
  • 25 Bresnahan DR, Davis JL, Holmes Jr DR, Hugh CS. Angiographic occurrence and clinical correlates of intraluminal coronary artery thrombus: role of unstable angina. J Am Coll Cardiol 1985; 6: 285-9.
    CrossrefPubMedSearch in Google Scholar
  • 26 Moise A, Lesperance J, Theroux P, Taeymans Y, Goulet C, Bourassa MG. Clinical and angiographic predictors of new total coronary occlusion in coronary artery disease: analysis of 313 nonoperated patients. Am J Cardiol 1984; 54: 1176-81.
    CrossrefPubMedSearch in Google Scholar
  • 27 Hangartner JRW, Charleston AJ, Davies MJ, Thomas AC. Morphological characteristics of clinically significant coronary artery stenosis in stable angina. Br Heart J 1986; 56: 501-8.
    CrossrefPubMedSearch in Google Scholar
  • 28 Luchi RJ, Scott SM, Deupree RH. Comparison of medical and surgical treatment for unstable angina pectoris. Results of a Veterans Administration Cooperative Study. N Engl J Med 1987; 316: 977-84.
    CrossrefPubMedSearch in Google Scholar