Current evidence and clinical implications of aspirin resistance
2009; Elsevier BV; Volume: 50; Issue: 6 Linguagem: Inglês
10.1016/j.jvs.2009.06.023
ISSN1097-6809
AutoresGeorge Kasotakis, Iraklis I. Pipinos, Thomas G. Lynch,
Tópico(s)Venous Thromboembolism Diagnosis and Management
ResumoAtherothrombosis, characterized by atherosclerotic plaque rupture and subsequent occlusive or subocclusive thrombus formation is the primary cause of acute ischemic syndromes involving all vascular beds and accounts for more than one-third of all deaths in the developed world. Platelet activation and aggregation constitute the most critical component in the pathophysiology of atherothrombotic disease. Aspirin is currently the most commonly used antiplatelet agent and one of the most frequently prescribed drugs, with as many as 30 million Americans on chronic aspirin regimens. Multiple well-designed prospective randomized clinical trials have demonstrated aspirin's efficacy in both primary and secondary prevention of a wide variety of entities that the atherothrombotic disease spectrum encompasses, such as cerebrovascular, coronary artery, and peripheral vascular disease. Despite its proven benefit, however, a growing body of evidence suggests that up to 70% of aspirin-takers may still be at risk for atherothrombotic complications due to resistance. Patients with laboratory-confirmed aspirin resistance seem to have an almost fourfold increase in their risk for acute thrombotic episodes, which underlines the magnitude of the problem for the vascular specialist. In this article, we review the physiology of platelet activation and the role of aspirin as an antiplatelet agent; the various laboratory assays used in assessing aspirin effectiveness; and current data on aspirin resistance and its clinical implications in patients with cardiovascular disease. We also review the studies that explore this phenomenon in patients with peripheral arterial disease and discuss the optimal management options in aspirin-resistant individuals. Suggestions are advanced for the direction of future trials evaluating aspirin resistance in patients with vascular disease. Atherothrombosis, characterized by atherosclerotic plaque rupture and subsequent occlusive or subocclusive thrombus formation is the primary cause of acute ischemic syndromes involving all vascular beds and accounts for more than one-third of all deaths in the developed world. Platelet activation and aggregation constitute the most critical component in the pathophysiology of atherothrombotic disease. Aspirin is currently the most commonly used antiplatelet agent and one of the most frequently prescribed drugs, with as many as 30 million Americans on chronic aspirin regimens. Multiple well-designed prospective randomized clinical trials have demonstrated aspirin's efficacy in both primary and secondary prevention of a wide variety of entities that the atherothrombotic disease spectrum encompasses, such as cerebrovascular, coronary artery, and peripheral vascular disease. Despite its proven benefit, however, a growing body of evidence suggests that up to 70% of aspirin-takers may still be at risk for atherothrombotic complications due to resistance. Patients with laboratory-confirmed aspirin resistance seem to have an almost fourfold increase in their risk for acute thrombotic episodes, which underlines the magnitude of the problem for the vascular specialist. In this article, we review the physiology of platelet activation and the role of aspirin as an antiplatelet agent; the various laboratory assays used in assessing aspirin effectiveness; and current data on aspirin resistance and its clinical implications in patients with cardiovascular disease. We also review the studies that explore this phenomenon in patients with peripheral arterial disease and discuss the optimal management options in aspirin-resistant individuals. Suggestions are advanced for the direction of future trials evaluating aspirin resistance in patients with vascular disease. Atherothrombosis, characterized by atherosclerotic lesion disruption with associated thrombotic complications, is the primary cause of acute ischemic syndromes involving all vascular beds and accounts for up to 35% of all deaths in the developed world.1Rosamond W. Flegal K. Furie K. et al.Heart disease and stroke statistics–2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.Circulation. 2008; 117: e25-e146PubMed Google Scholar In a meta-analysis of 287 randomized trials involving more than 200,000 patients, the Antithrombotic Trialists' Collaboration has demonstrated a 22% reduction in morbidity and mortality from serious ischemic cardiovascular episodes with aspirin therapy compared to placebo.2Antithrombotic Trialists CollaborationCollaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients.BMJ. 2002; 324: 71-86Crossref PubMed Google Scholar As a result, aspirin (acetylsalicylic acid [ASA]) has become the most cost-effective and widely used agent in the primary and secondary prevention of atherosclerotic disease, with an estimated 30 million Americans on a chronic aspirin regimen. However, despite its wide acceptance and utilization, aspirin's antiplatelet effect is not uniform and persistent platelet reactivity has been demonstrated in up to 70% of patients on aspirin therapy3Grundmann K. Jaschonek K. Kleine B. Dichgans J. Topka H. Aspirin non-responder status in patients with recurrent cerebral ischemic attacks.J Neurol. 2003; 250: 63-66Crossref PubMed Scopus (248) Google Scholar, 4Alberts M.J. Bergman D.L. Molner E. Jovanovic B.D. Ushiwata I. Teruya J. Antiplatelet effect of aspirin in patients with cerebrovascular disease.Stroke. 2004; 35: 175-178Crossref PubMed Scopus (184) Google Scholar, 5McCabe D.J. Harrison P. Mackie I.J. et al.Assessment of the antiplatelet effects of low to medium dose aspirin in the early and late phases after ischaemic stroke and TIA.Platelets. 2005; 16: 269-280Crossref PubMed Scopus (69) Google Scholar, 6Berrouschot J. Schwetlick B. von Twickel G. et al.Aspirin resistance in secondary stroke prevention.Acta Neurologica Scandinavica. 2006; 113: 31-35Crossref PubMed Scopus (55) Google Scholar, 7Helgason C.M. Bolin K.M. Hoff J.A. Winkler S.R. Mangat A. Tortorice K.L. Brace L.D. Development of aspirin resistance in persons with previous ischemic stroke.Stroke. 1994; 25: 2331-2336Crossref PubMed Scopus (415) Google Scholar, 8Grotemeyer K.H. Scharafinski H.W. Husstedt I.W. Two-year follow-up of aspirin responder and aspirin non responder A pilot-study including 180 post-stroke patients.Thromb Res. 1993; 71: 397-403Abstract Full Text PDF PubMed Scopus (420) Google Scholar, 9Grotemeyer K.H. Effects of acetylsalicylic acid in stroke patients Evidence of nonresponders in a subpopulation of treated patients.Thromb Res. 1991; 63: 587-593Abstract Full Text PDF PubMed Scopus (139) Google Scholar, 10Zimmermann N. Wenk A. Kim U. et al.Functional and biochemical evaluation of platelet aspirin resistance after coronary artery bypass surgery.Circulation. 2003; 108: 542-547Crossref PubMed Scopus (270) Google Scholar, 11Yilmaz M.B. Balbay Y. Caldir V. Ayaz S. Guray Y. Guray U. Korkmaz S. Late saphenous vein graft occlusion in patients with coronary bypass: possible role of aspirin resistance.Thromb Res. 2005; 115: 25-29Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar, 12Buchanan M.R. Biological basis and clinical implications of acetylsalicylic acid resistance.Can J Cardiol. 2006; 22: 149-151Abstract Full Text PDF PubMed Scopus (13) Google Scholar, 13Buchanan M.R. Acetylsalicylic acid resistance and clinical outcome–the Hobikoglu study is worth noting.Can J Cardiol. 2007; 23: 207-208Abstract Full Text PDF PubMed Scopus (4) Google Scholar, 14Poston R.S. Gu J. Brown J.M. et al.Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass grafting.J Thorac Cardiovasc Surg. 2006; 131: 122-130Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar, 15Chen 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: 760-763Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar, 16Zhang Y. Liang J. Zhou Y.J. Yuan H. Zhang Y.Z. Dong L. Study on the relationship between aspirin resistance and incidence of myonecrosis after non-emergent percutaneous coronary intervention.[Article in Chinese] Zhonghua Xin Xue Guan Bing Za Zhi (Chinese J Cardiovasc Dis). 2005; 33: 695-699PubMed Google Scholar, 17Lev E.I. Patel R.T. Maresh K.J. et al.Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance.J Am Coll Cardiol. 2006; 47: 27-33Abstract Full Text Full Text PDF PubMed Scopus (439) Google Scholar, 18Gurbel P.A. Bliden K.P. Hiatt B.L. O'Connor C.M. Clopidogrel for coronary stenting: response variability, drug resistance, and the effect of pretreatment platelet reactivity.Circulation. 2003; 107: 2908-2913Crossref PubMed Scopus (1410) Google Scholar, 19Macchi L. Christiaens L. Brabant S. et al.Resistance in vitro to low-dose aspirin is associated with platelet PlA1 (GP IIIa) polymorphism but not with C807T(GP Ia/IIa) and C-5T Kozak (GP Ibalpha) polymorphisms.J Am Coll Cardiol. 2003; 42: 1115-1119Abstract Full Text Full Text PDF PubMed Scopus (165) Google Scholar, 20Christiaens L. Macchi L. Herpin D. et al.Resistance to aspirin in vitro at rest and during exercise in patients with angiographically proven coronary artery disease.Thromb Res. 2002; 108: 115-119Abstract Full Text Full Text PDF PubMed Scopus (76) Google Scholar, 21Pamukcu B. Oflaz H. Nisanci Y. The role of platelet glycoprotein IIIa polymorphism in the high prevalence of in vitro aspirin resistance in patients with intracoronary stent restenosis.Am Heart J. 2005; 149: 675-680Abstract Full Text Full Text PDF PubMed Scopus (70) Google Scholar, 22Macchi L. Christiaens L. Brabant S. Sorel N. Allal J. Mauco G. Brizard A. Resistance to aspirin in vitro is associated with increased platelet sensitivity to adenosine diphosphate.Thromb Res. 2002; 107: 45-49Abstract Full Text Full Text PDF PubMed Scopus (187) Google Scholar, 23Gum P.A. Kottke-Marchant K. Welsh P.A. White J. Topol E.J. A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease.J Am Coll Cardiol. 2003; 41: 961-965Abstract Full Text Full Text PDF PubMed Scopus (946) Google Scholar, 24Friend M. Vucenik I. Miller M. Research pointers: platelet responsiveness to aspirin in patients with hyperlipidaemia.BMJ. 2003; 326: 82-83Crossref PubMed Google Scholar, 25Tantry U.S. Bliden K.P. Gurbel P.A. Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation.J Am Coll Cardiol. 2005; 46: 1705-1709Abstract Full Text Full Text PDF PubMed Scopus (292) Google Scholar, 26Lee P.Y. Chen W.H. Ng W. Cheng X. Kwok J.Y. Tse H.F. Lau C.P. Low-dose aspirin increases aspirin resistance in patients with coronary artery disease.Am J Med. 2005; 118: 723-727Abstract Full Text Full Text PDF PubMed Scopus (174) Google Scholar, 27Borna C. Lazarowski E. van Heusden C. Ohlin H. Erlinge D. Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels.Thromb J. 2005; 3: 10Crossref PubMed Scopus (86) Google Scholar, 28Andersen K. Hurlen M. Arnesen H. Seljeflot I. Aspirin non-responsiveness as measured by PFA-100 in patients with coronary artery disease.Thromb Res. 2002; 108: 37-42Abstract Full Text Full Text PDF PubMed Scopus (225) Google Scholar, 29Hobikoglu G.F. Norgaz T. Aksu H. Ozer O. Erturk M. Nurkalem Z. Narin A. High frequency of aspirin resistance in patients with acute coronary syndrome.Tohoku J Exp Med. 2005; 207: 59-64Crossref PubMed Scopus (41) Google Scholar, 30Stejskal D. Prosková J. Lacnák B. et al.[Use of assessment of aggregation of thrombocytes induced by cationic propyl gallate to estimate recurrence of cardiovascular complications].[Article in Czech] Vnitr Lek. 2004; 50: 591-599PubMed Google Scholar, 31Faraday N. Braunstein J.B. Heldman A.W. Bolton E.D. Chiles K.A. Gerstenblith G. Schulman S.P. Prospective evaluation of the relationship between platelet-leukocyte conjugate formation and recurrent myocardial ischemia in patients with acute coronary syndromes.Platelets. 2004; 15: 9-14Crossref PubMed Scopus (21) Google Scholar, 32Schwartz K.A. Schwartz D.E. Ghosheh K. Reeves M.J. Barber K. DeFranco A. Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarction.Am J Cardiol. 2005; 95: 973-975Abstract Full Text Full Text PDF PubMed Scopus (204) Google Scholar, 33Cotter G. Shemesh E. Zehavi M. et al.Lack of aspirin effect: aspirin resistance or resistance to taking aspirin?.Am Heart J. 2004; 147: 293-300Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar, 34Sane D.C. McKee S.A. Malinin A.I. Serebruany V.L. Frequency of aspirin resistance in patients with congestive heart failure treated with antecedent aspirin.Am J Cardiol. 2002; 90: 893-895Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar, 35Payne D.A. Jones C.I. Hayes P.D. Webster S.E. Ross Naylor A. Goodall A.H. Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?.Thromb Haemost. 2004; 92: 89-96PubMed Google Scholar, 36Assadian A. Lax J. Meixner-Loicht U. Hagmüller G.W. Bayer P.M. Hübl W. Aspirin resistance among long-term aspirin users after carotid endarterectomy and controls: flow cytometric measurement of aspirin-induced platelet inhibition.J Vasc Surg. 2007; 45 (discussion 1147): 1142-1147Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar, 37Ziegler S. Maca T. Alt E. Speiser W. Schneider B. Minar E. Monitoring of antiplatelet therapy with the PFA-100 in peripheral angioplasty patients.Platelets. 2002; 13: 493-497Crossref PubMed Scopus (61) Google Scholar, 38Mueller 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: 1003-1007PubMed Google Scholar, 39Malinin A. Spergling M. Muhlestein B. Steinhubl S. Serebruany V. Assessing aspirin responsiveness in subjects with multiple risk factors for vascular disease with a rapid platelet function analyzer.Blood Coagul Fibrinolysis. 2004; 15: 295-301Crossref PubMed Scopus (65) Google Scholar, 40Wang J.C. Aucoin-Barry D. Manuelian D. et al.Incidence of aspirin nonresponsiveness using the Ultegra Rapid Platelet Function Assay-ASA.Am J Cardiol. 2003; 92: 1492-1494Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar, 41Marshall P.W. Williams A.J. Dixon R.M. Growcott J.W. Warburton S. Armstrong J. Moores J. A comparison of the effects of aspirin on bleeding time measured using the Simplate method and closure time measured using the PFA-100, in healthy volunteers.Br J Clin Pharmacol. 1997; 44: 151-155Crossref PubMed Scopus (109) Google Scholar, 42Hillarp A. Lethagen S. Mattiasson I. Aspirin resistance is not a common biochemical phenotype explained by unblocked cyclooxygenase-1 activity.J Thromb Haemost. 2003; 1: 196-197Crossref PubMed Scopus (12) Google Scholar (Table I), suggesting that up to 21 million Americans on aspirin regimens may not enjoy its beneficial cardiovascular effects. In this article, we review the currently available data on aspirin resistance; its prevalence and etiology; the laboratory assays used to assess aspirin effect; and the implications of aspirin resistance in the practice of vascular surgery.Table IPrevalence of aspirin resistance as diagnosed by laboratory assays in various clinical settingsClinical settingInvestigatorn =Platelet assayASA dose (mg)PrevalenceCVDGrundmann et al3Grundmann K. Jaschonek K. Kleine B. Dichgans J. Topka H. Aspirin non-responder status in patients with recurrent cerebral ischemic attacks.J Neurol. 2003; 250: 63-66Crossref PubMed Scopus (248) Google Scholar53PFA-10010022.6%CVDAlberts et al4Alberts M.J. Bergman D.L. Molner E. Jovanovic B.D. Ushiwata I. Teruya J. Antiplatelet effect of aspirin in patients with cerebrovascular disease.Stroke. 2004; 35: 175-178Crossref PubMed Scopus (184) Google Scholar39PFA-1008156.0%CVDAlberts et al4Alberts M.J. Bergman D.L. Molner E. Jovanovic B.D. Ushiwata I. Teruya J. Antiplatelet effect of aspirin in patients with cerebrovascular disease.Stroke. 2004; 35: 175-178Crossref PubMed Scopus (184) Google Scholar87PFA-10032528.0%CVDMcCabe et al5McCabe D.J. Harrison P. Mackie I.J. et al.Assessment of the antiplatelet effects of low to medium dose aspirin in the early and late phases after ischaemic stroke and TIA.Platelets. 2005; 16: 269-280Crossref PubMed Scopus (69) Google Scholar47PFA-10075-30046.8%CVDBerrouschot et al6Berrouschot J. Schwetlick B. von Twickel G. et al.Aspirin resistance in secondary stroke prevention.Acta Neurologica Scandinavica. 2006; 113: 31-35Crossref PubMed Scopus (55) Google Scholar240LTA30012.5%CVDHelgason et al7Helgason C.M. Bolin K.M. Hoff J.A. Winkler S.R. Mangat A. Tortorice K.L. Brace L.D. Development of aspirin resistance in persons with previous ischemic stroke.Stroke. 1994; 25: 2331-2336Crossref PubMed Scopus (415) Google Scholar306LTA325-130025.5%CVDGrotemeyer et al8Grotemeyer K.H. Scharafinski H.W. Husstedt I.W. Two-year follow-up of aspirin responder and aspirin non responder A pilot-study including 180 post-stroke patients.Thromb Res. 1993; 71: 397-403Abstract Full Text PDF PubMed Scopus (420) Google Scholar306LTA32525.0%CVDGrotemeyer9Grotemeyer K.H. Effects of acetylsalicylic acid in stroke patients Evidence of nonresponders in a subpopulation of treated patients.Thromb Res. 1991; 63: 587-593Abstract Full Text PDF PubMed Scopus (139) Google Scholar180PR150033.0%CABGZimmermann et al10Zimmermann N. Wenk A. Kim U. et al.Functional and biochemical evaluation of platelet aspirin resistance after coronary artery bypass surgery.Circulation. 2003; 108: 542-547Crossref PubMed Scopus (270) Google Scholar20LTA10015.0%CABGYilmaz et al11Yilmaz M.B. Balbay Y. Caldir V. Ayaz S. Guray Y. Guray U. Korkmaz S. Late saphenous vein graft occlusion in patients with coronary bypass: possible role of aspirin resistance.Thromb Res. 2005; 115: 25-29Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar14PFA-10080-3257.1%CABGBuchanan12Buchanan M.R. Biological basis and clinical implications of acetylsalicylic acid resistance.Can J Cardiol. 2006; 22: 149-151Abstract Full Text PDF PubMed Scopus (13) Google Scholar40BT32542.0%CABGBuchanan13Buchanan M.R. Acetylsalicylic acid resistance and clinical outcome–the Hobikoglu study is worth noting.Can J Cardiol. 2007; 23: 207-208Abstract Full Text PDF PubMed Scopus (4) Google Scholar289BT32554.0%CABGPoston et al14Poston R.S. Gu J. Brown J.M. et al.Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass grafting.J Thorac Cardiovasc Surg. 2006; 131: 122-130Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar225IA, TXB2 levels, TEG, CD62p32521.8%PCIChen et al15Chen 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: 760-763Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar151RPFA81-32519.2%PCIZhang et al16Zhang Y. Liang J. Zhou Y.J. Yuan H. Zhang Y.Z. Dong L. Study on the relationship between aspirin resistance and incidence of myonecrosis after non-emergent percutaneous coronary intervention.[Article in Chinese] Zhonghua Xin Xue Guan Bing Za Zhi (Chinese J Cardiovasc Dis). 2005; 33: 695-699PubMed Google Scholar256LTA10026.2%PCILev et al17Lev E.I. Patel R.T. Maresh K.J. et al.Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance.J Am Coll Cardiol. 2006; 47: 27-33Abstract Full Text Full Text PDF PubMed Scopus (439) Google Scholar150LTA81-32512.7%PCIGurbel et al18Gurbel P.A. Bliden K.P. Hiatt B.L. O'Connor C.M. Clopidogrel for coronary stenting: response variability, drug resistance, and the effect of pretreatment platelet reactivity.Circulation. 2003; 107: 2908-2913Crossref PubMed Scopus (1410) Google Scholar191TEG81-32523.6%Stable CADMacchi et al19Macchi L. Christiaens L. Brabant S. et al.Resistance in vitro to low-dose aspirin is associated with platelet PlA1 (GP IIIa) polymorphism but not with C807T(GP Ia/IIa) and C-5T Kozak (GP Ibalpha) polymorphisms.J Am Coll Cardiol. 2003; 42: 1115-1119Abstract Full Text Full Text PDF PubMed Scopus (165) Google Scholar160PFA-1009829.0%Stable CADChristiaens et al20Christiaens L. Macchi L. Herpin D. et al.Resistance to aspirin in vitro at rest and during exercise in patients with angiographically proven coronary artery disease.Thromb Res. 2002; 108: 115-119Abstract Full Text Full Text PDF PubMed Scopus (76) Google Scholar50PFA-10075-30020.0%Stable CADPamukcu et al21Pamukcu B. Oflaz H. Nisanci Y. The role of platelet glycoprotein IIIa polymorphism in the high prevalence of in vitro aspirin resistance in patients with intracoronary stent restenosis.Am Heart J. 2005; 149: 675-680Abstract Full Text Full Text PDF PubMed Scopus (70) Google Scholar62PFA-10030012.9%Stable CADMacchi et al22Macchi L. Christiaens L. Brabant S. Sorel N. Allal J. Mauco G. Brizard A. Resistance to aspirin in vitro is associated with increased platelet sensitivity to adenosine diphosphate.Thromb Res. 2002; 107: 45-49Abstract Full Text Full Text PDF PubMed Scopus (187) Google Scholar72PFA-10016029.2%Stable CADGum et al23Gum P.A. Kottke-Marchant K. Welsh P.A. White J. Topol E.J. A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease.J Am Coll Cardiol. 2003; 41: 961-965Abstract Full Text Full Text PDF PubMed Scopus (946) Google Scholar325PFA-1003259.5%Stable CADGum et al23Gum P.A. Kottke-Marchant K. Welsh P.A. White J. Topol E.J. A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease.J Am Coll Cardiol. 2003; 41: 961-965Abstract Full Text Full Text PDF PubMed Scopus (946) Google Scholar325LTA3255.5%Stable CADFriend et al24Friend M. Vucenik I. Miller M. Research pointers: platelet responsiveness to aspirin in patients with hyperlipidaemia.BMJ. 2003; 326: 82-83Crossref PubMed Google Scholar325LTA5625.0%Stable CADTantry et al25Tantry U.S. Bliden K.P. Gurbel P.A. Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation.J Am Coll Cardiol. 2005; 46: 1705-1709Abstract Full Text Full Text PDF PubMed Scopus (292) Google Scholar223LTA3250.4%Stable CADLee et al26Lee P.Y. Chen W.H. Ng W. Cheng X. Kwok J.Y. Tse H.F. Lau C.P. Low-dose aspirin increases aspirin resistance in patients with coronary artery disease.Am J Med. 2005; 118: 723-727Abstract Full Text Full Text PDF PubMed Scopus (174) Google Scholar468RPFA81-32527.0%MIBorna et al27Borna C. Lazarowski E. van Heusden C. Ohlin H. Erlinge D. Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels.Thromb J. 2005; 3: 10Crossref PubMed Scopus (86) Google Scholar64PFA-10075-32531.3%MIAndersen et al28Andersen K. Hurlen M. Arnesen H. Seljeflot I. Aspirin non-responsiveness as measured by PFA-100 in patients with coronary artery disease.Thromb Res. 2002; 108: 37-42Abstract Full Text Full Text PDF PubMed Scopus (225) Google Scholar58PFA-1007540.0%MIAndersen et al28Andersen K. Hurlen M. Arnesen H. Seljeflot I. Aspirin non-responsiveness as measured by PFA-100 in patients with coronary artery disease.Thromb Res. 2002; 108: 37-42Abstract Full Text Full Text PDF PubMed Scopus (225) Google Scholar71PFA-10016035.0%MIHobikoglu et al29Hobikoglu G.F. Norgaz T. Aksu H. Ozer O. Erturk M. Nurkalem Z. Narin A. High frequency of aspirin resistance in patients with acute coronary syndrome.Tohoku J Exp Med. 2005; 207: 59-64Crossref PubMed Scopus (41) Google Scholar204PFA-100100-30033.8%MIStejskal et al30Stejskal D. Prosková J. Lacnák B. et al.[Use of assessment of aggregation of thrombocytes induced by cationic propyl gallate to estimate recurrence of cardiovascular complications].[Article in Czech] Vnitr Lek. 2004; 50: 591-599PubMed Google Scholar103LTA10070.1%MIFaraday et al31Faraday N. Braunstein J.B. Heldman A.W. Bolton E.D. Chiles K.A. Gerstenblith G. Schulman S.P. Prospective evaluation of the relationship between platelet-leukocyte conjugate formation and recurrent myocardial ischemia in patients with acute coronary syndromes.Platelets. 2004; 15: 9-14Crossref PubMed Scopus (21) Google Scholar30LTA3256.7%MISchwartz et al32Schwartz K.A. Schwartz D.E. Ghosheh K. Reeves M.J. Barber K. DeFranco A. Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarction.Am J Cardiol. 2005; 95: 973-975Abstract Full Text Full Text PDF PubMed Scopus (204) Google Scholar190LTA81-3250.5%MICotter et al33Cotter G. Shemesh E. Zehavi M. et al.Lack of aspirin effect: aspirin resistance or resistance to taking aspirin?.Am Heart J. 2004; 147: 293-300Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar61TXB2 levels10014.7%CHFSane et al34Sane D.C. McKee S.A. Malinin A.I. Serebruany V.L. Frequency of aspirin resistance in patients with congestive heart failure treated with antecedent aspirin.Am J Cardiol. 2002; 90: 893-895Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar88PFA-10032555.0%CEAPayne et al35Payne D.A. Jones C.I. Hayes P.D. Webster S.E. Ross Naylor A. Goodall A.H. Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?.Thromb Haemost. 2004; 92: 89-96PubMed Google Scholar50LTA15056.0%Post-CEAAssadian et al36Assadian A. Lax J. Meixner-Loicht U. Hagmüller G.W. Bayer P.M. Hübl W. Aspirin resistance among long-term aspirin users after carotid endarterectomy and controls: flow cytometric measurement of aspirin-induced platelet inhibition.J Vasc Surg. 2007; 45 (discussion 1147): 1142-1147Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar86PFA-10010016.0%PVDZiegler et al37Ziegler S. Maca T. Alt E. Speiser W. Schneider B. Minar E. Monitoring of antiplatelet therapy with the PFA-100 in peripheral angioplasty patients.Platelets. 2002; 13: 493-497Crossref PubMed Scopus (61) Google Scholar52PFA-1001009.6%PVDMueller et al38Mueller 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: 1003-1007PubMed Google Scholar100LTA32560.0%Risk factorsMalinin et al39Malinin A. Spergling M. Muhlestein B. Steinhubl S. Serebruany V. Assessing aspirin responsiveness in subjects with multiple risk factors for vascular disease with a rapid platelet function analyzer.Blood Coagul Fibrinolysis. 2004; 15: 295-301Crossref PubMed Scopus (65) Google Scholar141LTA3250.7%Risk factorsMalinin et al39Malinin A. Spergling M. Muhlestein B. Steinhubl S. Serebruany V. Assessing aspirin responsiveness in subjects with multiple risk factors for vascular disease with a rapid platelet function analyzer.Blood Coagul Fibrinolysis. 2004; 15: 295-301Crossref PubMed Scopus (65) Google Scholar141RPFA3257.0%Risk factorsWang et al40Wang J.C. Aucoin-Barry D. Manuelian D. et al.Incidence of aspirin nonresponsiveness using the Ultegra Rapid Platelet Function Assay-ASA.Am J Cardiol. 2003; 92: 1492-1494Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar422RPFA81-32523.4%Healthy adultsMarshall et al41Marshall P.W. Williams A.J. Dixon R.M. Growcott J.W. Warburton S. Armstrong J. Moores J. A comparison of the effects of aspirin on bleeding time measured using the Simplate method and closure time measured using the PFA-100, in healthy volunteers.Br J Clin Pharmacol. 1997; 44: 151-155Crossref PubMed Scopus (109) Google Scholar12PFA-100, BT22508.3%Various patientsHillarp et al42Hillarp A. Lethagen S. Mattiasson I. Aspirin resistance is not a common biochemical phenotype explained by unblocked cyclooxygenase-1 activity.J Thromb Haemost. 2003; 1: 196-197Crossref PubMed Scopus (12) Google Scholar122IA75-1600.8%CVD, Cerebrovascular disease; CABG, coronary artery bypass grafting; PCI, percutaneous coronary intervention; CAD, coronary artery disease; MI, myocardial infarction; CHF, congestive heart failure; CEA, carotid endarterectomy; PVD, peripheral vascular disease; PFA-100, platelet function analysis; LTA, light transmission aggregometry; PR, platelet reactivity; BT, bleeding time; IA, impedance aggregometry; TEG, thromboelastography; RPFA, rapid platelet function assay; TXB, thromboxane B; CD62p, CD62p flow cytometry.The aspirin dose, the platelet assay utilized, and the number of individuals participating in each study are shown. As few as 0.4% or as many as 70% of chronic aspirin takers may be resistant to the medication. Open table in a new tab CVD, Cerebrovascular disease; CABG, coronary artery bypass grafting; PCI, percutaneous coronary intervention; CAD, coronary artery disease; MI, myocardial infarction; CHF, congestive heart failure; CEA, carotid endarterectomy; PVD, peripheral vascular disease; PFA-100, platelet function analysis; LTA, light transmission aggregometry; PR, platelet reactivity; BT, bleeding time; IA, impedance aggregometry; TEG, thromboelastography; RPFA, rapid p
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