Aspirin resistance and its clinical implications Review article
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Published:
Sep 30, 2007
Keywords:
aspirin, aspirin resistance, cardiovascular events
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Abstract
Aspirin resistance is the inability of aspirin to reduce platelet production of thromboxane A2 and thereby platelet activation and aggregation remain preserved. Aspirin resistance can be detected by laboratory tests of platelet thromboxane A2 production or platelet function that depend on platelet thromboxane production. Potential causes of aspirin resistance include inadequate dose, drug interactions, genetic polymorphisms of COX-1 and other genes involved in thromboxane biosynthesis, upregulation of non-platelet sources of thromboxane biosynthesis, and increased platelet turnover. Increasing degrees of aspirin resistance may correlate independently with increasing risk of cardiovascular events. Variable effects of aspirin among individuals might in part explain why the absolute risk of recurrent vascular events in patients receiving aspirin therapy remains relatively high.
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Postuła , M., & Kapłon , A. (2007). Aspirin resistance and its clinical implications. Cardiology in Practice, 1(3), 144-151. Retrieved from https://journalsmededu.pl/index.php/kwp/article/view/1708
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Copyright: © Medical Education sp. z o.o. This is an Open Access article distributed under the terms of the Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). License (https://creativecommons.org/licenses/by-nc/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Address reprint requests to: Medical Education, Marcin Kuźma (marcin.kuzma@mededu.pl)
References
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3. Patrono C., Aspirin resistance: definition, mechanism and clinical read-outs. J Thromb Haemost 2003, 1: 1710-1713.
4. Awtry E.H., Loscalzo J. Aspirin. Circulation 2000, 101: 1206-1218.
5. Vane J.R., Bakhle Y.S., Botting R.M.: Cyclooxygenases 1 and 2. Annu. Rev. Pharmacol. Toxicol. 1998, 38: 97-120.
6. Catella-Lawson F., Reilly M.P., Kapoor S.C. et al.: Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N. Engl. J. Med. 2001, 345: 1809-17.
7. Capone M.L., Sciulli M.G., Tacconelli S. et al.: Pharmacodynamic interaction of naproxen with low-dose aspirin in healthy subjects. J. Am. Coll. Cardiol. 2005, 45: 1295-301.
8. Pulcinelli F.M., Pignatelli P., Celestini A. et al.: Inhibition of platelet aggregation by aspirin progressively decreases in long-term treated patients. J. Am. Coll. Cardiol. 2004, 43: 979-84.
9. Santopinto J., Gurfinkel E.P., Torres V. et al.: Prior aspirin users with acute non-ST-elevation coronary syndromes are at increased risk of cardiac events and benefit from enoxaparin. Am. Heart J. 2001, 141: 566-72.
10. Macchi L., Christiaens L., Brabant S. et al.: Resistance to aspirin in vitro is associated with increased platelet sensitivity to adenosine diphosphate. Thromb. Res. 2002, 107: 45-49.
11. Kawasaki T., Ozeki Y., Igawa T., Kambayashi J.: Increased sensitivity to collagen in individuals resistant to low-dose aspirin. Stroke 2000, 31: 591-95.
12. Cipollone F., Ciabattoni G., Patrignani P. et al.: Oxidant stress and aspirin-insensitive thromboxane biosynthesis in severe unstable angina. Circulation 2000, 102: 1007-1013.
13. Maclouf J., Folco G., Patrono C.: Eicosanoids and iso-eicosanoids: constitutive, inducible and transcellular biosynthesis in vascular disease. Thromb. Haemost. 1998, 79: 691-705.
14. Cipollone F., Rocca B., Patrono C.: Cyclooxygenase-2 expression and inhibition in atherothrombosis. Arterioscler. Thromb. Vasc. Biol. 2004, 24: 246-55.
15. Valles J., Santos M.T., Aznar J. et al.: Erythrocyte promotion of platelet reactivity decreases the effectiveness of aspirin as an antithrombotic therapeutic modality: the effect of low-dose aspirin is less than optimal in patients with vascular disease due to prothrombotic effects of erythrocytes on platelet reactivity. Circulation 1998, 97: 350-5.
16. Hurlen M., Seljeflot I., Arnesen H.: Increased platelet aggregability during exercise in patients with previous myocardial infarction. Lack of inhibition by aspirin. Thromb. Res. 2000, 99: 487-94.
17. O’Donnell C.J., Larson M.G., Feng D. et al.: Genetic and environmental contributions to platelet aggregation: The Framingham Heart Study. Circulation 2001, 103: 3051-56.
18. Jefferson B.K., Foster J.H., McCarthy J.J. et al.: Aspirin resistance and a single gene. Am. J. Cardiol. 2005, 95: 805-808.
19. Hetherington S.L., Singh R.K., Lodwick D. et al.: Dimorphism in the P2Y1 ADP receptor gene is associated with increased platelet activation response to ADP. Arterioscler. Thromb. Vasc. Biol. 2005, 25: 252-257.
20. Schwartz K.A., Schwartz D.E., Ghosheh K. et al.: Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarction. Am. J. Cardiol. 2005, 95: 973-975.
21. Harisson P., Platelet function analysis. Blood Reviews 2005, 19: 111-123.
22. Hart R.G., Leonard A.D., Talbert R.L. et al.: Aspirin dosage and thromboxane synthesis in patients with vascular disease. Pharmacotherapy 2003, 23: 579-84.
23. Grotemeyer K.H., Scharafinski H.W., Husstedt I.W.: Two-year follow-up of aspirin responder and aspirin non responder. A pilotstudy including 180 post-stroke patients. Thromb. Res. 1993, 71: 397-403.
24. Grundmann K., Jaschonek K., Kleine B. et al.: Aspirin non-responder status in patients with recurrent cerebral ischemic attacks. J. Neurol. 2003, 250: 63-66.
25. Mueller M.R., Salat A., Stangl P. et al.: Variable platelet response to low-dose ASA and the risk of limb deterioration in patients submitted to peripheral arterial angioplasty. Thromb. Haemost. 1997, 78: 1003-1007.
26. Gum P.A., Kottke-Marchant K., Poggio E.D. et al.: Profile and prevalence of aspirin resistance in patients with cardiovascular disease. Am. J. Cardiol. 2001, 88: 230-235.
27. Gum P.A., Kottke-Marchant K., Welsh P.A. et al.: A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease. J. Am. Coll. Cardiol. 2003, 41: 961-965.
28. Pamukcu B., Oflaz H., Onur I. et al.: Clinical relevance of aspirin resistance in patients with stable coronary artery disease: a prospective follow-up study (PROSPECTAR). Blood Coagul. Fibrinolysis 2007, 18: 187-192.
29.Chen W.H., Cheng X., Lee P.Y. et al.: Aspirin resistance and adverse clinical events in patients with coronary artery disease. Am. J. Med. 2007, 120: 631-635.
30. Pamukcu B., Oflaz H., Oncul A. et al.: The role of aspirin resistance on outcome in patients with acute coronary syndrome and the effect of clopidogrel therapy in the prevention of major cardiovascular events. J. Thromb. Thrombolysis. 2006, 22: 103-110.
31.Eikelboom J.W., Hirsh J., Weitz J.I. et al.: Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation 2002, 105: 1650-1655.
32. Gianetti J., Parri M.S., Sbrana S. et al.: Platelet activation predicts recurrent ischemic events after percutaneous coronary angioplasty: a 6 months prospective study. Thromb. Res. 2006, 118: 487-493.
33. Fuchs I., Frossard M., Spiel A. et al.: Platelet function in patients with acute coronary syndrome (ACS) predicts recurrent ACS. J. Thromb. Haemost. 2006, 4: 2547-2552.
34. Frossard M., Fuchs I., Leitner J.M. et al.: Platelet function predicts myocardial damage in patients with acute myocardial infarction. Circulation 2004, 110: 1392-1397.
35. Chen W.H., Lee P.Y., Ng W. et al.: Aspirin resistance is associated with a high incidence of myonecrosis after non-urgent percutaneous coronary intervention despite clopidogrel pretreatment. J. Am. Coll. Cardiol. 2004; 43: 1122-1126.
36. Chen W.H., Lee P.Y., Ng W. et al.: Relation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary intervention. Am. J. Cardiol. 2005, 96: 760-763.
2. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002, 324: 71-86.
3. Patrono C., Aspirin resistance: definition, mechanism and clinical read-outs. J Thromb Haemost 2003, 1: 1710-1713.
4. Awtry E.H., Loscalzo J. Aspirin. Circulation 2000, 101: 1206-1218.
5. Vane J.R., Bakhle Y.S., Botting R.M.: Cyclooxygenases 1 and 2. Annu. Rev. Pharmacol. Toxicol. 1998, 38: 97-120.
6. Catella-Lawson F., Reilly M.P., Kapoor S.C. et al.: Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N. Engl. J. Med. 2001, 345: 1809-17.
7. Capone M.L., Sciulli M.G., Tacconelli S. et al.: Pharmacodynamic interaction of naproxen with low-dose aspirin in healthy subjects. J. Am. Coll. Cardiol. 2005, 45: 1295-301.
8. Pulcinelli F.M., Pignatelli P., Celestini A. et al.: Inhibition of platelet aggregation by aspirin progressively decreases in long-term treated patients. J. Am. Coll. Cardiol. 2004, 43: 979-84.
9. Santopinto J., Gurfinkel E.P., Torres V. et al.: Prior aspirin users with acute non-ST-elevation coronary syndromes are at increased risk of cardiac events and benefit from enoxaparin. Am. Heart J. 2001, 141: 566-72.
10. Macchi L., Christiaens L., Brabant S. et al.: Resistance to aspirin in vitro is associated with increased platelet sensitivity to adenosine diphosphate. Thromb. Res. 2002, 107: 45-49.
11. Kawasaki T., Ozeki Y., Igawa T., Kambayashi J.: Increased sensitivity to collagen in individuals resistant to low-dose aspirin. Stroke 2000, 31: 591-95.
12. Cipollone F., Ciabattoni G., Patrignani P. et al.: Oxidant stress and aspirin-insensitive thromboxane biosynthesis in severe unstable angina. Circulation 2000, 102: 1007-1013.
13. Maclouf J., Folco G., Patrono C.: Eicosanoids and iso-eicosanoids: constitutive, inducible and transcellular biosynthesis in vascular disease. Thromb. Haemost. 1998, 79: 691-705.
14. Cipollone F., Rocca B., Patrono C.: Cyclooxygenase-2 expression and inhibition in atherothrombosis. Arterioscler. Thromb. Vasc. Biol. 2004, 24: 246-55.
15. Valles J., Santos M.T., Aznar J. et al.: Erythrocyte promotion of platelet reactivity decreases the effectiveness of aspirin as an antithrombotic therapeutic modality: the effect of low-dose aspirin is less than optimal in patients with vascular disease due to prothrombotic effects of erythrocytes on platelet reactivity. Circulation 1998, 97: 350-5.
16. Hurlen M., Seljeflot I., Arnesen H.: Increased platelet aggregability during exercise in patients with previous myocardial infarction. Lack of inhibition by aspirin. Thromb. Res. 2000, 99: 487-94.
17. O’Donnell C.J., Larson M.G., Feng D. et al.: Genetic and environmental contributions to platelet aggregation: The Framingham Heart Study. Circulation 2001, 103: 3051-56.
18. Jefferson B.K., Foster J.H., McCarthy J.J. et al.: Aspirin resistance and a single gene. Am. J. Cardiol. 2005, 95: 805-808.
19. Hetherington S.L., Singh R.K., Lodwick D. et al.: Dimorphism in the P2Y1 ADP receptor gene is associated with increased platelet activation response to ADP. Arterioscler. Thromb. Vasc. Biol. 2005, 25: 252-257.
20. Schwartz K.A., Schwartz D.E., Ghosheh K. et al.: Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarction. Am. J. Cardiol. 2005, 95: 973-975.
21. Harisson P., Platelet function analysis. Blood Reviews 2005, 19: 111-123.
22. Hart R.G., Leonard A.D., Talbert R.L. et al.: Aspirin dosage and thromboxane synthesis in patients with vascular disease. Pharmacotherapy 2003, 23: 579-84.
23. Grotemeyer K.H., Scharafinski H.W., Husstedt I.W.: Two-year follow-up of aspirin responder and aspirin non responder. A pilotstudy including 180 post-stroke patients. Thromb. Res. 1993, 71: 397-403.
24. Grundmann K., Jaschonek K., Kleine B. et al.: Aspirin non-responder status in patients with recurrent cerebral ischemic attacks. J. Neurol. 2003, 250: 63-66.
25. Mueller M.R., Salat A., Stangl P. et al.: Variable platelet response to low-dose ASA and the risk of limb deterioration in patients submitted to peripheral arterial angioplasty. Thromb. Haemost. 1997, 78: 1003-1007.
26. Gum P.A., Kottke-Marchant K., Poggio E.D. et al.: Profile and prevalence of aspirin resistance in patients with cardiovascular disease. Am. J. Cardiol. 2001, 88: 230-235.
27. Gum P.A., Kottke-Marchant K., Welsh P.A. et al.: A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease. J. Am. Coll. Cardiol. 2003, 41: 961-965.
28. Pamukcu B., Oflaz H., Onur I. et al.: Clinical relevance of aspirin resistance in patients with stable coronary artery disease: a prospective follow-up study (PROSPECTAR). Blood Coagul. Fibrinolysis 2007, 18: 187-192.
29.Chen W.H., Cheng X., Lee P.Y. et al.: Aspirin resistance and adverse clinical events in patients with coronary artery disease. Am. J. Med. 2007, 120: 631-635.
30. Pamukcu B., Oflaz H., Oncul A. et al.: The role of aspirin resistance on outcome in patients with acute coronary syndrome and the effect of clopidogrel therapy in the prevention of major cardiovascular events. J. Thromb. Thrombolysis. 2006, 22: 103-110.
31.Eikelboom J.W., Hirsh J., Weitz J.I. et al.: Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation 2002, 105: 1650-1655.
32. Gianetti J., Parri M.S., Sbrana S. et al.: Platelet activation predicts recurrent ischemic events after percutaneous coronary angioplasty: a 6 months prospective study. Thromb. Res. 2006, 118: 487-493.
33. Fuchs I., Frossard M., Spiel A. et al.: Platelet function in patients with acute coronary syndrome (ACS) predicts recurrent ACS. J. Thromb. Haemost. 2006, 4: 2547-2552.
34. Frossard M., Fuchs I., Leitner J.M. et al.: Platelet function predicts myocardial damage in patients with acute myocardial infarction. Circulation 2004, 110: 1392-1397.
35. Chen W.H., Lee P.Y., Ng W. et al.: Aspirin resistance is associated with a high incidence of myonecrosis after non-urgent percutaneous coronary intervention despite clopidogrel pretreatment. J. Am. Coll. Cardiol. 2004; 43: 1122-1126.
36. Chen W.H., Lee P.Y., Ng W. et al.: Relation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary intervention. Am. J. Cardiol. 2005, 96: 760-763.