This Article Full Text Full Text (PDF) Correction (v113,pe856) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hennekens, C. H. Articles by FitzGerald, G. A. Search for Related Content PubMed PubMed Citation Articles by Hennekens, C. H. Articles by FitzGerald, G. A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB ACETYLSALICYLIC ACID Related Collections Primary prevention Secondary prevention Arterial thrombosis Platelet function inhibitors AHA Statements and Guidelines Epidemiology Platelets

(Circulation. 2004;110:1706-1708.)
© 2004 American Heart Association, Inc.

Special Report

Terms and Conditions

Semantic Complexity and Aspirin Resistance

Charles H. Hennekens, MD, DrPH; Karsten Schror, MD; Steven Weisman, PhD; Garret A. FitzGerald, MD

From the Department of Medicine and Epidemiology and Public Health, University of Miami School of Medicine, Miami, and Agatston Research Institute (ARI), Miami Beach, Fla (C.H.H.); UniversitätsKlinikum, Heinrich-Heine-Universität, Düsseldorf (K.S.); Innovative Science Solutions, Morristown, NJ (S.W.); and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia (G.A.F.).

Correspondence to Charles H. Hennekens, MD, 2800 S Ocean Blvd, PHA, Boca Raton, FL 33432. E-mail profchhmd@prodigy.net

Received November 7, 2003; de novo received March 30, 2004; revision received June 1, 2004; accepted June 3, 2004.

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
The term aspirin resistance has been used to describe the occurrence of cardiovascular events despite regular aspirin intake at recommended doses.¹ In this context, such treatment failures resemble those with any drugs, including statins, ß-blockers, and ACE inhibitors.^2,3 In secondary prevention, the clinical effectiveness of aspirin has been clearly demonstrated and is comparable to that of these other agents in that they all reduce nonfatal cardiovascular disease events by 25% to 30% and fatal events by 15% to 20% in randomized trials.³ These results represent a small to moderate but clinically worthwhile reduction in risk. Conversely, they suggest that 70% to 75% of nonfatal and 80% to 85% of fatal events are not prevented by these drugs.

Mechanistic approaches to investigating aspirin resistance have relied heavily on ex vivo evaluations of platelet function. Although thrombosis is the proximate cause of virtually all occlusive vascular events,⁴ other factors, such as vascular function,⁵ and perhaps interactions with other blood cells, such as monocytes,⁶ are also probably relevant. It is unknown precisely how the impact of aspirin on the ex vivo response to selected concentrations of single aggregating agonists might model its efficacy in preventing clinical events in vivo. Multiple factors may confound platelet aggregometry, including posture, time of day, smoking, exercise, and blood cholesterol.^7–9 Indeed, platelet aggregability may recover despite sustained inhibition of thromboxane during chronic dosing with aspirin.¹⁰ The term aspirin resistance is insufficiently precise to offer a credible basis for clinical decision making. More usefully, the multiple potential causes of . . . [Full Text of this Article]

This article has been cited by other articles:

				C. Patrono, C. Baigent, J. Hirsh, and G. Roth Antiplatelet Drugs: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition) Chest, June 1, 2008; 133(6_suppl): 199S - 233S. [Abstract] [Full Text] [PDF]

				A. Y. Gasparyan, T. Watson, and G. Y.H. Lip The Role of Aspirin in Cardiovascular Prevention: Implications of Aspirin Resistance J. Am. Coll. Cardiol., May 13, 2008; 51(19): 1829 - 1843. [Abstract] [Full Text] [PDF]

				G. Krasopoulos, S. J Brister, W S. Beattie, and M. R Buchanan Aspirin "resistance" and risk of cardiovascular morbidity: systematic review and meta-analysis BMJ, January 26, 2008; 336(7637): 195 - 198. [Abstract] [Full Text] [PDF]

				C. H. Hennekens, O. Sechenova, D. Hollar, and V. L. Serebruany Dose of Aspirin in the Treatment and Prevention of Cardiovascular Disease: Current and Future Directions. Journal of Cardiovascular Pharmacology and Therapeutics, September 1, 2006; 11(3): 170 - 176. [Abstract] [PDF]

				E. D. Michos, R. Ardehali, R. S. Blumenthal, R. A. Lange, and H. Ardehali Aspirin and Clopidogrel Resistance Mayo Clin. Proc., April 1, 2006; 81(4): 518 - 526. [Abstract] [Full Text] [PDF]

				P. C. Williams, M. J. Coffey, B. Coles, S. Sanchez, J. D. Morrow, J. R. Cockcroft, M. J. Lewis, and V. B. O'Donnell In vivo aspirin supplementation inhibits nitric oxide consumption by human platelets Blood, October 15, 2005; 106(8): 2737 - 2743. [Abstract] [Full Text] [PDF]

				E. R. Bates and W. C. Lau Controversies in Antiplatelet Therapy for Patients With Cardiovascular Disease Circulation, May 3, 2005; 111(17): e267 - e271. [Full Text] [PDF]