This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (52) Citing Articles via Google Scholar Google Scholar Articles by Mason, P. J. Articles by Freedman, J. E. Search for Related Content PubMed PubMed Citation Articles by Mason, P. J. Articles by Freedman, J. E.

FOCUS ISSUE: ASPIRIN: STATE-OF-THE-ART PAPER

Aspirin Resistance and Atherothrombotic Disease

Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.

Manuscript received June 8, 2004; revised manuscript received August 10, 2004, accepted August 23, 2004.

^_* Reprint requests and correspondence: Dr. Peter J. Mason, Brigham and Women’s Hospital, Division of Cardiovascular Medicine, 75 Francis Street, Boston, Massachusetts 02115. (Email: pjmason{at}partners.org).

Acute coronary syndromes and other manifestations of atherothrombotic disease are primarily caused by atherosclerotic plaque rupture or fissuring and subsequent occlusive or subocclusive thrombus formation. Platelets play a critical role in the pathophysiology of atherothrombotic disease, and aspirin is the most commonly used antiplatelet agent. Clinical trials have demonstrated the efficacy of aspirin in both primary and secondary prevention of myocardial infarction, stroke, and cardiovascular death. Despite its proven benefit, the absolute risk of recurrent vascular events among patients taking aspirin remains relatively high, an estimated 8% to 18% after two years. Therapeutic resistance to aspirin might explain a portion of this risk. Although formal diagnostic criteria and a validated method of measurement are lacking, aspirin resistance may affect between 5% and 45% of the population. Given the prevalence of cardiovascular disease, the potential impact of aspirin resistance is large. Currently, however, there are many unanswered questions regarding the biological mechanism, diagnosis, population prevalence, clinical relevance, and optimal therapeutic intervention for aspirin resistance.

Abbreviations and Acronyms   ADP = adenosine diphosphate   CAD = coronary artery disease   COX = cyclooxygenase   CRP = C-reactive protein   MI = myocardial infarction   NSAIDs = non-steroidal anti-inflammatory drugs   PFA = platelet function analyzer   PG = prostaglandin   PGH2 = prostaglandin H2   PGI2 = endothelium-derived prostacyclin   PURSUIT = Platelet IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy trial   RPFA = rapid platelet function assay   TX = thromboxane

This article has been cited by other articles:

				J. Fauler Clinical pharmacology of antithrombotic drugs in coronary artery disease Therapeutic Advances in Cardiovascular Disease, December 1, 2009; 3(6): 465 - 478. [Abstract] [PDF]

				A R Muir, M F McMullin, C Patterson, and P P McKeown Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease Heart, August 1, 2009; 95(15): 1225 - 1229. [Abstract] [Full Text] [PDF]

				F. Van de Werf New antithrombotic agents: are they needed and what can they offer to patients with a non-ST-elevation acute coronary syndrome? Eur. Heart J., July 2, 2009; 30(14): 1695 - 1702. [Abstract] [Full Text] [PDF]

				J. E. Freedman and E. M. Hylek Clopidogrel, Genetics, and Drug Responsiveness N. Engl. J. Med., January 22, 2009; 360(4): 411 - 413. [Full Text] [PDF]

				G. De Luca Adjunctive antithrombotic therapy during primary percutaneous coronary intervention Eur. Heart J. Suppl., December 1, 2008; 10(suppl_J): J2 - J14. [Abstract] [Full Text] [PDF]

				J. E. Herrera-Galeano, D. M. Becker, A. F. Wilson, L. R. Yanek, P. Bray, D. Vaidya, N. Faraday, and L. C. Becker A Novel Variant in the Platelet Endothelial Aggregation Receptor-1 Gene Is Associated With Increased Platelet Aggregability Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1484 - 1490. [Abstract] [Full Text] [PDF]

				C. H. Hennekens and S. Borzak Cyclooxygenase-2 Inhibitors and Most Traditional Nonsteroidal Anti-inflammatory Drugs Cause Similar Moderately Increased Risks of Cardiovascular Disease Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2008; 13(1): 41 - 50. [Abstract] [PDF]

				J. E. Freedman Heritability, Platelet Function, and Aspirin: A Link Established but Cause Unknown Circulation, May 15, 2007; 115(19): 2468 - 2470. [Full Text] [PDF]

				M. P Dorsch, J. S. Lee, D. R Lynch, S. P Dunn, J. E Rodgers, T. Schwartz, E. Colby, D. Montague, and S. S Smyth Aspirin Resistance in Patients with Stable Coronary Artery Disease with and without a History of Myocardial Infarction Ann. Pharmacother., May 1, 2007; 41(5): 737 - 741. [Abstract] [Full Text] [PDF]

				A. Undas, K. E. Brummel-Ziedins, and K. G. Mann Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions Blood, March 15, 2007; 109(6): 2285 - 2292. [Abstract] [Full Text] [PDF]

				P. J. Mason, A. K. Jacobs, and J. E. Freedman Reply J. Am. Coll. Cardiol., August 15, 2006; 48(4): 847 - 847. [Full Text] [PDF]

				A. O. Maree, H. Jneid, and D. J. Fitzgerald Aspirin Resistance and Atherothrombotic Disease J. Am. Coll. Cardiol., August 15, 2006; 48(4): 846 - 847. [Full Text] [PDF]

				R. P. Giugliano and E. Braunwald The Year in Non-ST-Segment Elevation Acute Coronary Syndromes J. Am. Coll. Cardiol., July 18, 2006; 48(2): 386 - 395. [Full Text] [PDF]

				J. E. Freedman The Aspirin Resistance Controversy: Clinical Entity or Platelet Heterogeneity? Circulation, June 27, 2006; 113(25): 2865 - 2867. [Full Text] [PDF]

				R. S. Hillman Platelet Aspirin Resistance Detection and Validation J. Am. Coll. Cardiol., June 20, 2006; 47(12): 2565 - 2565. [Full Text] [PDF]

				K. Leineweber, D. Bose, M. Vogelsang, M. Haude, R. Erbel, and G. Heusch Intense Vasoconstriction in Response to Aspirate From Stented Saphenous Vein Aortocoronary Bypass Grafts J. Am. Coll. Cardiol., March 7, 2006; 47(5): 981 - 986. [Abstract] [Full Text] [PDF]

				D. J. Angiolillo, A. Fernandez-Ortiz, E. Bernardo, C. Ramirez, M. Sabate, P. Jimenez-Quevedo, R. Hernandez, R. Moreno, J. Escaned, F. Alfonso, et al. Clopidogrel Withdrawal Is Associated With Proinflammatory and Prothrombotic Effects in Patients With Diabetes and Coronary Artery Disease Diabetes, March 1, 2006; 55(3): 780 - 784. [Abstract] [Full Text] [PDF]