CLINICAL SIGNIFICANCE OF ASPIRIN RESISTANCE IN PATIENTS WITH CARDIO-VASCULAR DISEASES
https://doi.org/10.20996/1819-6446-2006-2-3-46-50
Abstract
Atherothrombosis is a complication of ischemic heart disease, and it leads to development of acute coronary syndrome. Atherothrombosis is characterized by sudden destruction of atherosclerotic plaque, which results into platelets activation and thrombus formation. Aspirin - one of the most widely used antiaggregate drugs, prevents development of the recurring myocardium infarction, stroke, sudden coronary death. But in number of patients aspirin is not efficient. Development of repeated thrombotic complications with aspirin therapy or resistance to aspirin is independent predictor of high coronary risk. There are controversial data about aspirin resistance incidence, which varies from 5 to 48%. Possible reasons for this are discussed: low compliance with treatment, peculiarities of functional condition of platelets, genetically given variability of platelet receptors etc. Different methods, based on estimation of platelets activity are proposed to assess the possibility of repeated thrombotic complications, caused by resistance to aspirin. Further researches including valid number of patients are needed to assess incidence of aspirin resistance and to reveal mechanisms of its development.
About the Authors
P. J. Dovgalevsky
Saratov Research Center of Cardiology, Roszdrav
Russian Federation
Russian Federation
N. V. Furman
Saratov Research Center of Cardiology, Roszdrav
Russian Federation
Russian Federation
N. F. Puchinian
Saratov Research Center of Cardiology, Roszdrav
Russian Federation
Russian Federation
References
1. Концепция атеротромбоза. НАЦИОНАЛЬНОЕ ОБЩЕСТВО ПО АТЕРОТРОМБОЗУ WWW.NOAT.RU.
2. Панченко Е.П., Добровольский А.Б. Тромбозы в кардиологии. Механизмы развития и возможности терапии. М.: Спорт и культура 1999: 464.
3. Mason PJ, Jacobs AK, Freedman JE. Aspirin Resistance and Atherothrombotic Disease. J Am Coll Cardiol 2005; 46:986 –93
4. Bhatt DL, Topol EJ. Antiplatelet and anticoagulant therapy in the secondary prevention of ischemic heart disease. Med Clin North Am 2000; 84(1): 163-179.
5. 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
6. Awtry EH, Loscalzo J: Aspirin. Circulation 2000, 101:1206-18
7. ESC Expert Consensus Document on the Use of Antiplatelet Agents. The Task Force on the Use of Antiplatelet Agents in Patients with Atherosclerotic Cardiovascular Disease of the European Society of Cardiology. Eropean Heart Journal 2004; 25: 166-181.
8. Taylor DW, Barnett HJM, Ferguson GG et al. Low-dose and high?dose acetylsalicylic acid for patients undergoing carotid endarterectomy: a randomised controlled trial. Lancet 1999; 353: 2179-84.
9. Gum PA, Kottke-Marchant K, Poggio ED et al. Profile and prevalence of aspirin resistance in patients with cardiovascular disease. Am J Cardiol 2001; 88:230-5.
10. Gum PA, Kottke-Marchant K, Welsh PA 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: 961-5.
11. Eikelboom JW, Hirsh J, Weitz JI et al. Aspirinresistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation 2002; 105: 1650-5.
12. Grundmann K, Jaschonek K, Kleine B et al. Aspirin non-responder status in patients with recurrent cerebral ischemic attacks. J Neurol 2003; 250: 63-6.
13. 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; 43:1122-6.
14. Patrono C, Coller B, FitzGerald GA et al. Platelet-active drugs: the relationships among dose, e.ectiveness, and side e.ects. Chest 2004; 126: 234S-64.
15. Mueller MR, 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; 78:1003-7.
16. Cotter G, Shemesh E, Zehavi M et al. Lack of aspirin effect: aspirin resistance or resistance to taking aspirin? Am Heart J 2004; 147: 293-300.
17. Catella-Lawson F, Reilly MP, Kapoor SC et al. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med 2001; 345:1809-17.
18. Kurth T, Glynn RJ, Walker AM et al. Inhibition of clinical benefits of aspirin on first myocardial infarction by nonsteroidal anti-inflammatory drugs. Circulation 2003; 108:1191-5.
19. Pulcinelli FM, 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.
20. 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.
21. Kawasaki T, Ozeki Y, Igawa T et al. Increased platelet sensitivity to collagen in individuals resistant to low-dose aspirin. Stroke 2000; 31: 591–5.
22. Erlinge D, Borna C, Lazarowski E et al. Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels. Thrombosis Journal 2005; 3: 10.
23. Syrbe G, Redlich H, Weidlich B et al.: Individual dosing of ASA pro-phylaxis by controlling platelet aggregation. Clin Appl Thromb Hemost 2001; 7: 209-13.
24. Valles J, Santos MT, 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.
25. Freedman JE. CD40-CD40L and platelet function: beyond hemostasis. Circ Res 2003; 92: 944-6.
26. Cipollone F, Rocca B, Patrono C. Cyclooxygenase-2 expression and inhibition in atherothrombosis. Arterioscler Thromb Vasc Biol 2004; 24:246-55.
27. Undas A, Brummel K, Musial J et al. Pl(A2) polymorphism of beta(3) integrins is associated with enhanced thrombin generation and impaired antithrombotic action of aspirin at the site of microvascular injury. Circulation 2001; 104: 2666-72.
28. Michelson AD, Furman MI, Goldschmidt-Clermont P et al. Platelet GP IIIa Pl(A) polymorphisms display different sensitivities to agonists. Circulation 2000;101:1013-8.
29. Bhatt DL, Topol EJ. Scientific and therapeutic advances in antiplatelet therapy. Nature Rev 2003; 2:15-28.
30. Kundu SK, Heilmann EJ, Sio R et al. Description of an in vitro platelet function analyzer – PFA-100. Semin Thromb Hemost 1995; 21(Suppl 2):106-12.
31. Homoncik M, Jilma B, Hergovich N et al. Monitoring of aspirin (ASA) pharmacodynamics with the platelet function analyzer PFA-100. Thromb Haemost 2000; 82: 316-21.
32. Michelson AD, Cattaneo M, Eikelboom JW et al. Aspirin Resistance: position paper of the Working Group on Aspirin Resistance. J Thromb Haemost 2005; 3: 1309-11.
Review
For citations:
Dovgalevsky P.J., Furman N.V., Puchinian N.F. CLINICAL SIGNIFICANCE OF ASPIRIN RESISTANCE IN PATIENTS WITH CARDIO-VASCULAR DISEASES. Rational Pharmacotherapy in Cardiology. 2006;2(3):46-50. (In Russ.) https://doi.org/10.20996/1819-6446-2006-2-3-46-50
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