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Effects of persistent platelet reactivity despite aspirin therapy on cardiac troponin I and creatine kinase-MB levels after elective percutaneous coronary interventions

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Abstract

Background

Creatinine kinase-MB (CK-MB) and cardiac troponin I (cTnI) elevations are highly specific for myonecrosis after percutaneous coronary intervention (PCI). Aspirin is used to prevent thrombotic complications. Several studies have shown that some individuals exhibit a reduced or completely missing antiplatelet response to aspirin. The aim of this study is to investigate the effects of platelet reactivity despite aspirin therapy on CK-MB and cTnI levels after elective percutaneous coronary interventions despite 600 mg loading dose of clopidogrel.

Methods

One hundred fourteen (mean age 61.2 ± 9.3 years, 78.1% male) patients receiving 300 mg daily enteric coated aspirin for at least 7 days with documented coronary artery disease were included in the study. Platelet reactivity despite aspirin was measured by platelet function analyzer (PFA)-100 collagen/epinephrine cartridge. Blood samples for CK-MB and cTnI were obtained before and at 6, 24, and 36 h after the PCI. Persistent platelet reactivity was defined when collagen/epinephrine closure time <165 s.

Results

A total of 87 (76.4%) patients were noted to have normal platelet reactivity (Group A), and 27 (23.6%) had persistent platelet reactivity (Group B). The elevations of CK-MB and cTnI levels were statistically significant within the groups (both P < 0.001). However, there were no significant differences in the CK-MB and cTnI levels of the groups at baseline and after PCI for all studied hours.

Conclusion

Persistent platelet reactivity was not associated with increased risk of CK-MB, cTnI elevations in low-to-intermediate risk PCI patients.

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References

  1. Abdelmeguid AE, Topol EJ (1996) The myth of the myocardial ‘infarctlet’ during percutaneous coronary revascularization procedures. Circulation 94:3369–3375

    PubMed  CAS  Google Scholar 

  2. Califf RM, Abdelmeguid AE, Kuntz RE et al (1998) Myonecrosis after revascularization procedures. J Am Coll Cardiol 31:241–251

    Article  PubMed  CAS  Google Scholar 

  3. Kanaparti PK, Brown DL (2000) Relation between coronary atherosclerotic plaque burden and cardiac enzyme elevation following percutaneous coronary intervention. Am J Cardiol 86:619–622

    Article  PubMed  CAS  Google Scholar 

  4. Garbatz E, Iung B, Lefevre G et al (1999) Frequency and prognostic value of cardiac troponin I elevation after coronary stenting. Am J Cardiol 34:663–671

    Article  Google Scholar 

  5. Mehta SR, Yusuf S, Peters RJ et al (2001) Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study. Lancet 358:527–533

    Article  PubMed  CAS  Google Scholar 

  6. Steinhubl SR, Berger PB, Mann JT 3rd et al (2002) Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial. JAMA 288:2411–2420

    Article  PubMed  CAS  Google Scholar 

  7. Popma JJ, Weitz J, Bittl JA et al (1998) Antithrombotic therapy in patients undergoing coronary angioplasty. Chest 114:728S–741S

    Article  PubMed  CAS  Google Scholar 

  8. Patrono C, Coller B, Dalen JE et al (2001) Platelet-active drugs : the relationships among dose, effectiveness, and side effects. Chest 119:39S–63S

    Article  PubMed  CAS  Google Scholar 

  9. Sanderson S, Emery J, Baglin T et al (2005) Narrative review: aspirin resistance and its clinical implications. Ann Intern Med 142:370–380

    PubMed  CAS  Google Scholar 

  10. Patrono C (2003) Aspirin resistance: definition, mechanisms and clinical read-outs. J Thromb Haemost 1:1710–1713

    Article  PubMed  CAS  Google Scholar 

  11. Mason PJ, Freedman JE, Jacobs AK (2004) Aspirin resistance: current concepts. Rev Cardiovasc Med 5:156–163

    Article  PubMed  Google Scholar 

  12. Mason PJ, Jacobs AK, Freedman JE (2005) Aspirin resistance and atherothrombotic disease. JACC 6:986–993

    Google Scholar 

  13. Tantry US, Bliden KP, Gurbel PA (2005) Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation. J Am Coll Cardiol 46:1705–1709

    Article  PubMed  CAS  Google Scholar 

  14. Hayward CPM, Harrison P, Cattaneo M, Ortel TL, Rao AK (2006) on behalf of the platelet physiology subcommittee of the scientific and standardization committee of the international society on thrombosis and haemostasis platelet function analyzer (PFA–100) closure time in the evaluation of platelet disorders and platelet function. J Thromb Haemost 4:312–319

    Article  PubMed  CAS  Google Scholar 

  15. Mammen EF, Comp PC, Gosselin R et al (1998) PFA-100 system: a new method for assessment of platelet dysfunction. Semin Thromb Hemost 24:195–202

    Article  PubMed  CAS  Google Scholar 

  16. Andersen K, Hurlen M, Arnesen H et al (2003) Aspirin non-responsiveness as measured by PFA-100 in patients with coronary artery disease. Thromb Res 108:37–42

    Article  CAS  Google Scholar 

  17. Homoncik M, Jilma B, Hergovich N et al (2000) Monitoring of aspirin (ASA) pharmacodynamics with the platelet function analyzer PFA-100. Thromb Haemost 83:316–321

    PubMed  CAS  Google Scholar 

  18. Chen WH, Lee PY, Ng W et al (2004) Aspirin resistance is associated with high incidence of myonecrosis after nonurgent percutaneous coronary intervention despite clopidogrel pretreatment. J Am Coll Cardiol 43:1122–1126

    Article  PubMed  CAS  Google Scholar 

  19. Coma-Canella I, Velasco A, Castano S (2005) Prevalence of aspirin resistance measured by PFA-100. Int J Cardiol 101:71–76

    Article  PubMed  Google Scholar 

  20. Harrison P, Robinson MS, Mackie IJ et al (1999) Performance of the platelet function analyzer PFA-100 in testing abnormalities of primary haemostasis. Blood Coagul Fibrinolysis 10:25–31

    Article  PubMed  CAS  Google Scholar 

  21. Heilmann EJ, Kundu SK, Sio R, Garcia C et al (1997) Comparison of four commercial citrate blood collection systems for platelet function analysis by the PFA-100 system. Thromb Res 87:159–164

    Article  PubMed  CAS  Google Scholar 

  22. Favaloro EJ (2002) Clinical application of the PFA-100. Curr Opin Hematol 9:407–415

    Article  PubMed  Google Scholar 

  23. Hochholzer W, Trenk D, Bestehorn HP et al (2006) Impact of the degree of peri-interventional platelet inhibition after loading with clopidogrel on early clinical outcome of elective coronary stent placement. JACC 48:1742–1750

    PubMed  CAS  Google Scholar 

  24. Gum PA, Koltke-Marchant K, Poggio ED et al (2001) Profile and prevalance of aspirin resistance in patients with cardiovascular disease. Am J Cardiol 88:230–235

    Article  PubMed  CAS  Google Scholar 

  25. Wang JC, Aucoin-Barry D, Manuelian D et al (2003) Incidence of aspirin nonresponsiveness using the Ultegra Rapid Platelet Function Assay-ASA. Am J Cardiol 92:1492–1494

    Article  PubMed  Google Scholar 

  26. Abacı A, Calıskan M, Bayram F et al (2006) A new definition of aspirin non-responsiveness by Paltelet Function analyzer-100TM and its predictors. Platelets 17:7–13

    Article  PubMed  CAS  Google Scholar 

  27. Nageh T, Sherwood RA, Harris BM et al (2003) Cardiac troponin T and I and creatine-kinase-MB as markers of myocardial injury and predictors of outcome following percutaneous coronary intervention. Int J Cardiol 92:285–293

    Article  PubMed  Google Scholar 

  28. Kini AS, Lee P, Marmur JD et al (2004) Correlation of postpercutaneous coronary intervention creatine-kinase-MB and troponin I elevation in predicting mid-term mortality. Am J Cardiol 93:18–23

    Article  PubMed  CAS  Google Scholar 

  29. Kini A, Marmur J, Kini S et al (1999) Creatine-kinase-MB elevation after coronary intervention correlates with diffuse atherosclerosis, and low-to-medium level elevation has a bening clinical course. J Am Coll Cardiol 34:663–671

    Article  PubMed  CAS  Google Scholar 

  30. Fuchs S, Kornowski R, Mehran R et al (2000) Prognostic value of cardiac troponin-I levels following catheter-based coronary interventions. Am J Cardiol 85:1077–1082

    Article  PubMed  CAS  Google Scholar 

  31. Adams JE, Bodor GS, Devile-Roman VG et al (1993) Cardiac Troponin I: a marker with high specificity for cardiac injury. Circulation 88:101–106

    PubMed  Google Scholar 

  32. Amsterdam EA, Lewis WR (1998) Identification of low risk patients with chest pain in emergency department: another look at cardiac troponins. J Am Coll Cardiol 32:15–16

    Article  PubMed  CAS  Google Scholar 

  33. Varani E, Balducelli M, Vecchi G et al (2005) Occurence of non-Q myocardial infarction following percutaneous coronary intervention in the stent era: systematic monitoring of the three markers of myocardial necrosis. J Interv Cardiol 18:243–248

    Article  PubMed  Google Scholar 

  34. Gurbel PA, Bliden KP, Zaman KA et al (2005) Clopidogrel loading with eptifibatide to arrest the reactivity of platelets: results of the clopidogrel loading with eptifibatide to arrest the reactivity of platelets (clear platelets) study. Circulation 111:1153–1159

    Article  PubMed  CAS  Google Scholar 

  35. Kastarati A, Mehilli J, Schühlen H et al (2004) A clinical trial of abciximab in elective percutaneous coronary intervention after pretreatment with clopidogrel. N Engl J Med 350:232–238

    Article  Google Scholar 

  36. Mehilli J, Kastrati A, Schühlen H et al (2004) Randomized clinical trial of abciximab in diabetic patients undergoing elective percutaneous coronary interventions after pretreatment with a high loading dose of clopidogrel. Circulation 110:3627–3635

    Article  PubMed  CAS  Google Scholar 

  37. Hankey GJ, Eikelboom JW (2006) Aspirin resistance. Lancet 367:606–617

    Article  PubMed  CAS  Google Scholar 

  38. Eikelboom JW, Hirsh J, Weitz JI, et al (2002) Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation 105:1650–1655

    Article  PubMed  CAS  Google Scholar 

  39. Gum PA, Kottke-Marchant K, Welsh PA et al (2003) A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease. J Am Coll Cardiol 41:961–965

    Article  PubMed  CAS  Google Scholar 

  40. Grotemeyer KH, Scharafinski HW, Husstedt IW (1993) Two-year follow-up of aspirin responder and aspirin non responder A pilot-study including 180 post-stroke patients. Thromb Res 71:397–403

    Article  PubMed  CAS  Google Scholar 

  41. Weber AA, Przytulski B, Schanz A, Hohlfeld T, Schror K (2002) Towards a definition of aspirin resistance: a typological approach. Platelets 13:37–40

    Article  PubMed  CAS  Google Scholar 

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Correspondence to Oyku Gulmez.

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Gulmez, O., Yildirir, A., Kaynar, G. et al. Effects of persistent platelet reactivity despite aspirin therapy on cardiac troponin I and creatine kinase-MB levels after elective percutaneous coronary interventions. J Thromb Thrombolysis 25, 239–246 (2008). https://doi.org/10.1007/s11239-007-0067-z

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  • DOI: https://doi.org/10.1007/s11239-007-0067-z

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