Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Review Article
  • Published:

Antiplatelet drug 'resistance'. Part 1: mechanisms and clinical measurements

Nature Reviews Cardiology volume 6, pages 273–282 (2009)Cite this article

Abstract

Antiplatelet drug therapy has become one of the cornerstones of treatment for patients with cardiovascular disease. Large clinical trials have shown that antiplatelet medications have important clinical benefits and prevent adverse outcomes in patients with coronary artery disease. Recurrent adverse cardiovascular events still occur in a substantial proportion of patients on standard dual antiplatelet therapy, however, which has been attributed to nonresponsiveness to this treatment. Both pharmacological and pharmacokinetc mechanisms are involved in variability in responsiveness to antiplatelet agents, and include drug bioavailability, medication noncompliance, drug–drug interactions, cytochrome P450 activity, and genetic polymorphisms. Numerous observational studies have consistently shown an association between antiplatelet drug nonresponsiveness and adverse clinical outcomes. However, these studies are limited by varying antiplatelet drug dosing regimens, heterogeneous laboratory assessments for ex vivo platelet function, and wide interindividual variation in platelet responses. Only within the last 2 years have randomized clinical trials indicated that increased dosing with antiplatelet drugs could reduce adverse clinical outcomes. Nonetheless, large clinical trials with standardized laboratory methods and well-defined protocols are needed that will definitively determine the association between antiplatelet drug nonresponsiveness and clinical events, and establish therapeutic strategies to overcome blunted antiplatelet effects.

Key Points

  • Antiplatelet drugs are an established therapy for patients with cardiovascular disease, particularly for the prevention of cardiovascular events in those undergoing percutaneous coronary intervention with stenting

  • Some patients consistently demonstrate a diminished platelet response to these agents when measured by multiple ex vivo methods

  • Medication noncompliance, antiplatelet drug bioavailability, drug–drug interactions, genetic polymorphisms, inconsistent dosing, and nonstandardized laboratory tests have challenged the concept that ex vivo assessment of antiplatelet responses can predict clinical outcomes

  • Evidence has emerged that patients with intact platelet responsiveness while on antiplatelet therapy are at risk for future cardiovascular events

  • A challenge for the future will be the prompt identification of patients with reduced platelet responsiveness, so that therapy can be initiated to overcome this effect and improve clinical outcomes

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Mechanism of aspirin inhibition of cyclo-oxygenase.
Figure 2: The prevalence of aspirin resistance as determined by various platelet assays.
Figure 3: Distribution of platelet aggregation in response to 5 µmol of adenosine 5′-diphosphate in 544 patients after receiving clopidogrel treatment.

Similar content being viewed by others

References

  1. Fuster, V. et al. Atherosclerotic plaque rupture and thrombosis. Evolving concepts. Circulation 82 (Suppl), II47–II59 (1990).

    CAS  PubMed  Google Scholar 

  2. Fuster, V. et al. The pathogenesis of coronary artery disease and the acute coronary syndromes (1). N. Engl. J. Med. 326, 242–250 (1992).

    CAS  PubMed  Google Scholar 

  3. Topol, E. J. Toward a new frontier in myocardial reperfusion therapy: emerging platelet preeminence. Circulation 97, 211–218 (1998).

    CAS  PubMed  Google Scholar 

  4. Samara, W. M. & Gurbel, P. A. The role of platelet receptors and adhesion molecules in coronary artery disease. Coronary Artery Dis. 14, 65–79 (2003).

    Google Scholar 

  5. Yusuf, S. et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N. Engl. J. Med. 345, 494–502 (2001).

    CAS  PubMed  Google Scholar 

  6. Mehta, S. R. et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study. Lancet 358, 527–533 (2001).

    CAS  PubMed  Google Scholar 

  7. Steinhubl, S. R. et al. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial. JAMA 288, 2411–2420 (2002).

    CAS  PubMed  Google Scholar 

  8. Gurbel, P. A. et al. Platelet reactivity in patients and recurrent events post-stenting: results of the PREPARE Post-Stenting Study. J. Am. Coll. Cardiol. 46, 1820–1826 (2005).

    CAS  PubMed  Google Scholar 

  9. Singh, M. et al. Geographical differences in the rates of angiographic restenosis and ischemia-driven target vessel revascularization after percutaneous coronary interventions: results from the Prevention of Restenosis With Tranilast and its Outcomes (PRESTO) Trial. J. Am. Coll. Cardiol. 47, 34–39 (2006).

    PubMed  Google Scholar 

  10. Maree, A. O. & Fitzgerald, D. J. Variable platelet response to aspirin and clopidogrel in atherothrombotic disease. Circulation 115, 2196–2207 (2007).

    PubMed  Google Scholar 

  11. Quick, A. J. Salicylates and bleeding: the aspirin tolerance test. Am. J. Med. Sci. 252, 265–269 (1966).

    CAS  PubMed  Google Scholar 

  12. Wiviott, S. D. et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N. Engl. J. Med. 357, 2001–2015 (2007).

    CAS  PubMed  Google Scholar 

  13. Bonello, L. et al. Adjusted clopidogrel loading doses according to vasodilator-stimulated phosphoprotein phosphorylation index decrease rate of major adverse cardiovascular events in patients with clopidogrel resistance: a multicenter randomized prospective study. J. Am. Coll. Cardiol. 51, 1404–1411 (2008).

    CAS  PubMed  Google Scholar 

  14. Jack, D. B. One hundred years of aspirin. Lancet 350, 437–439 (1997).

    CAS  PubMed  Google Scholar 

  15. [No authors listed] Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 324, 71–86 (2002).

    PubMed Central  Google Scholar 

  16. Berenbaum, F. COX-3: fact or fancy? Joint Bone Spine 71, 451–453 (2004).

    PubMed  Google Scholar 

  17. Fitzgerald, D. J. & Maree, A. Aspirin and clopidogrel resistance. In Hematol. Am. Soc. Hematol. Educ. Progr, 2007 114–120 (2007).

  18. Maree, A. O. & Fitzgerald, D. J. Aspirin and coronary artery disease. Thromb. Haemost. 92, 1175–1181 (2004).

    CAS  PubMed  Google Scholar 

  19. Cattaneo, M. Laboratory detection of 'aspirin resistance': what test should we use (if any)? Eur. Heart J. 28, 1673–1675 (2007).

    PubMed  Google Scholar 

  20. Gonzalez-Conejero, R. et al. Biological assessment of aspirin efficacy on healthy individuals: heterogeneous response or aspirin failure? Stroke 36, 276–280 (2005).

    CAS  PubMed  Google Scholar 

  21. Gurbel, P., Becker, R. C., Mann, K. G., Steinhubl, S. R. & Michelson, A. D. Platelet function monitoring in patients with coronary artery disease. J. Am. Coll. Cardiol. 50, 1822–1834 (2007).

    CAS  PubMed  Google Scholar 

  22. Lordkipanidze, M. et al. A comparison of six major platelet function tests to determine the prevalence of aspirin resistance in patients with stable coronary artery disease. Eur. Heart J. 28, 1702–1708 (2007).

    CAS  PubMed  Google Scholar 

  23. Hovens, M. M. et al. Prevalence of persistent platelet reactivity despite use of aspirin: a systematic review. Am. Heart J. 153, 175–181 (2007).

    CAS  PubMed  Google Scholar 

  24. Zimmermann, N. et al. Functional and biochemical evaluation of platelet aspirin resistance after coronary artery bypass surgery. Circulation 108, 542–547 (2003).

    CAS  PubMed  Google Scholar 

  25. Maree, A. O. et al. Growth arrest specific gene (GAS) 6 modulates platelet thrombus formation and vascular wall homeostasis and represents an attractive drug target. Curr. Pharm. Des. 13, 2656–2661 (2007).

    CAS  PubMed  Google Scholar 

  26. Weber, A. A. et al. Towards a definition of aspirin resistance: a typological approach. Platelets 13, 37–40 (2002).

    CAS  PubMed  Google Scholar 

  27. Winocour, P. D. Platelet turnover in advanced diabetes. Eur. J. Clin. Invest. 24 (Suppl. 1), 34–37 (1994).

    PubMed  Google Scholar 

  28. Davi, G. et al. Diabetes mellitus, hypercholesterolemia, and hypertension but not vascular disease per se are associated with persistent platelet activation in vivo. Evidence derived from the study of peripheral arterial disease. Circulation 96, 69–75 (1997).

    CAS  PubMed  Google Scholar 

  29. Vejar, M. et al. Dissociation of platelet activation and spontaneous myocardial ischemia in unstable angina. Thromb. Haemost. 63, 163–168 (1990).

    CAS  PubMed  Google Scholar 

  30. Cipollone, F. et al. Oxidant stress and aspirin-insensitive thromboxane biosynthesis in severe unstable angina. Circulation 102, 1007–1013 (2000).

    CAS  PubMed  Google Scholar 

  31. Feher, G., Feher, A., Pusch, G., Lupkovics, G., Szapary, L. & Papp, E. The genetics of antiplatelet drug resistance. Clin. Genet. 75, 1–18 (2009).

    CAS  PubMed  Google Scholar 

  32. Maree, A. O. et al. Cyclooxygenase-1 haplotype modulates platelet response to aspirin. J. Thromb. Haemost. 3, 2340–2345 (2005).

    CAS  PubMed  Google Scholar 

  33. Macchi, L. 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. 42, 1115–1119 (2003).

    CAS  PubMed  Google Scholar 

  34. Rao, G. H. et al. Ibuprofen protects platelet cyclooxygenase from irreversible inhibition by aspirin. Arteriosclerosis 3, 383–388 (1983).

    CAS  PubMed  Google Scholar 

  35. Catella-Lawson, F. et al. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N. Engl. J. Med. 345, 1809–1817 (2001).

    CAS  PubMed  Google Scholar 

  36. Cox, D. et al. Effect of enteric coating on antiplatelet activity of low-dose aspirin in healthy volunteers. Stroke 37, 2153–2158 (2006).

    CAS  PubMed  Google Scholar 

  37. Kulkarni, S. P. et al. Long-term adherence with cardiovascular drug regimens. Am. Heart J. 151, 185–191 (2006).

    PubMed  Google Scholar 

  38. Biondi-Zoccai, G. G. et al. A systematic review and meta-analysis on the hazards of discontinuing or not adhering to aspirin among 50,279 patients at risk for coronary artery disease. Eur. Heart J. 27, 2667–2674 (2006).

    PubMed  Google Scholar 

  39. Alberts, M. J. et al. Antiplatelet effect of aspirin in patients with cerebrovascular disease. Stroke 35, 175–178 (2004).

    CAS  PubMed  Google Scholar 

  40. Grotemeyer, K. H., Scharafinski, H. W. & Husstedt, I. W. Two-year follow-up of aspirin responder and aspirin nonresponder. A pilot study including 180 post-stroke patients. Thromb. Res. 71, 397–403 (1993).

    CAS  PubMed  Google Scholar 

  41. Snoep, J. D. et al. Association of laboratory-defined aspirin resistance with a higher risk of recurrent cardiovascular events: a systematic review and meta-analysis. Arch. Intern. Med. 167, 1593–1599 (2007).

    PubMed  Google Scholar 

  42. Gurbel, P. A. et al. Evaluation of dose-related effects of aspirin on platelet function: results from the Aspirin-Induced Platelet Effect (ASPECT) study. Circulation 115, 3156–3164 (2007).

    CAS  PubMed  Google Scholar 

  43. De Miguel, A., Ibanez, B. & Badimon, J. J. Clinical implications of clopidogrel resistance. Thromb. Haemost. 100, 196–203 (2008).

    CAS  PubMed  Google Scholar 

  44. Savi, P. et al. The antiaggregating activity of clopidogrel is due to a metabolic activation by the hepatic cytochrome P450–451A. Thromb. Haemost. 72, 313–317 (1994).

    CAS  PubMed  Google Scholar 

  45. Järemo, P., Lindahl, T. L., Fransson, S. G. & Richter, A. J. Individual variations of platelet inhibition after loading doses of clopidogrel. J. Intern. Med. 252, 233–238 (2002).

    PubMed  Google Scholar 

  46. Serebruany, V. et al. Variability in platelet responsiveness to clopidogrel among 544 individuals. J. Am. Coll. Cardiol. 45, 246–251 (2005).

    CAS  PubMed  Google Scholar 

  47. O'Donoghue, M. & Wiviott, S. D. Clopidogrel response variability and future therapies: clopidogrel: does one size fit all? Circulation 114, e600–e606 (2006).

    PubMed  Google Scholar 

  48. Michelson, A. D. Platelet function testing in cardiovascular diseases. Circulation 110, e489–e493 (2004).

    PubMed  Google Scholar 

  49. Farid, N. A. et al. Cytochrome P450 3A inhibition by ketoconazole affects prasugrel and clopidogrel pharmacokinetics and pharmacodynamics differently. Clin. Pharmacol. Ther. 81, 735–741 (2007).

    CAS  PubMed  Google Scholar 

  50. Lau, W. C. et al. Contribution of hepatic cytochrome P450 3A4 metabolic activity to the phenomenon of clopidogrel resistance. Circulation 109, 166–171 (2004).

    CAS  PubMed  Google Scholar 

  51. Lau, W. C. et al. Atorvastatin reduces the ability of clopidogrel to inhibit platelet aggregation: a new drug–drug interaction. Circulation 107, 32–37 (2003).

    CAS  PubMed  Google Scholar 

  52. Gilard, M. et al. Influence of omeprazole on the antiplatelet action of clopidogrel associated with aspirin: the randomized, double-blind OCLA (Omeprazole Clopidogrel Aspirin) study. J. Am. Coll. Cardiol. 51, 256–260 (2008).

    CAS  PubMed  Google Scholar 

  53. Angiolillo, D. J. et al. Contribution of gene sequence variations of the hepatic cytochrome P450 3A4 enzyme to variability in individual responsiveness to clopidogrel. Arterioscler. Thromb. Vasc. Biol. 26, 1895–1900 (2006).

    CAS  PubMed  Google Scholar 

  54. Beer, J. H., S. Pederiva & Pontiggia, L. Genetics of platelet receptor single-nucleotide polymorphisms: clinical implications in thrombosis. Ann. Med. 32 (Suppl. 1), 10–14 (2000).

    CAS  PubMed  Google Scholar 

  55. Collet J. P. et al. Cytochrome P450 2C19 polymorphism in young patients treated with clopidogrel after myocardial infarction: a cohort study. Lancet 373, 309–317 (2009).

    CAS  PubMed  Google Scholar 

  56. Mega, J. L. et al. Cytochrome P450 polymorphisms and response to clopidogrel. N. Engl. J. Med. 360, 354–362 (2009).

    CAS  PubMed  Google Scholar 

  57. Spertus, J. A. et al. Prevalence, predictors, and outcomes of premature discontinuation of thienopyridine therapy after drug-eluting stent placement: results from the PREMIER registry. Circulation 113, 2803–2809 (2006).

    CAS  PubMed  Google Scholar 

  58. Hamann, G. F. et al. Adherence to secondary stroke prevention strategies—results from the German Stroke Data Bank. Cerebrovasc. Dis. 15, 282–288 (2003).

    PubMed  Google Scholar 

  59. Gurbel, P. A. et al. Clopidogrel loading with eptifibatide to arrest the reactivity of platelets: results of the Clopidogrel Loading With Eptifibatide to Arrest the Reactivity of Platelets (CLEAR PLATELETS) study. Circulation 111, 1153–1159 (2005).

    CAS  PubMed  Google Scholar 

  60. Muller, I. et al. Effect of a high loading dose of clopidogrel on platelet function in patients undergoing coronary stent placement. Heart 85, 92–93 (2001).

    CAS  PubMed  PubMed Central  Google Scholar 

  61. Smith, S. C., Jr. et al. ACC/AHA/SCAI Guideline update for percutaneous coronary intervention—summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention). Circulation 113, 156–175 (2005).

    Google Scholar 

  62. Serebruany, V. L. The “clopidogrel resistance” trap. Am. J. Cardiol. 100, 1044–1046 (2007).

    CAS  PubMed  Google Scholar 

  63. Mani, H. et al. Determination of clopidogrel main metabolite in plasma: a useful tool for monitoring therapy? Ther. Drug. Monit. 30, 84–89 (2008).

    CAS  PubMed  Google Scholar 

  64. von Beckerath, N. et al. Absorption, metabolization, and antiplatelet effects of 300-, 600-, and 900-mg loading doses of clopidogrel: results of the ISAR-CHOICE (Intracoronary Stenting and Antithrombotic Regimen: Choose Between 3 High Oral Doses for Immediate Clopidogrel Effect) Trial. Circulation 112, 2946–2950 (2005).

    CAS  PubMed  Google Scholar 

  65. Gurbel, P. A. et al. Clopidogrel for coronary stenting: response variability, drug resistance, and the effect of pretreatment platelet reactivity. Circulation 107, 2908–2913 (2003).

    PubMed  Google Scholar 

  66. Steinhubl, S. R. et al. Point-of-care measured platelet inhibition correlates with a reduced risk of an adverse cardiac event after percutaneous coronary intervention: results of the GOLD (AU-Assessing Ultegra) multicenter study. Circulation 103, 2572–2578 (2001).

    CAS  PubMed  Google Scholar 

  67. Muller, I. et al. Prevalence of clopidogrel non-responders among patients with stable angina pectoris scheduled for elective coronary stent placement. Thromb. Haemost. 89, 783–787 (2003).

    CAS  PubMed  Google Scholar 

  68. Buonamici, P. et al. Impact of platelet reactivity after clopidogrel administration on drug-eluting stent thrombosis. J. Am. Coll. Cardiol. 49, 2312–2317 (2007).

    CAS  PubMed  Google Scholar 

  69. Horstrup, K. et al. Phosphorylation of focal adhesion vasodilator-stimulated phosphoprotein at Ser157 in intact human platelets correlates with fibrinogen receptor inhibition. Eur. J. Biochem. 225, 21–27 (1994).

    CAS  PubMed  Google Scholar 

  70. Gurbel, P. A. & Tantry, U. S. Clopidogrel resistance? Thromb. Res. 120, 311–321 (2007).

    CAS  PubMed  Google Scholar 

  71. Barragan, P. et al. Resistance to thienopyridines: clinical detection of coronary stent thrombosis by monitoring of vasodilator-stimulated phosphoprotein phosphorylation. Cathet. Cardiovasc. Interv. 59, 295–302 (2003).

    Google Scholar 

  72. Cattaneo, M. Aspirin and clopidogrel: efficacy, safety, and the issue of drug resistance. Arterioscler. Thromb. Vasc. Biol. 24, 1980–1987 (2004).

    CAS  PubMed  Google Scholar 

  73. Nguyen, T. A., Diodati J. G. & Pharand, C. Resistance to clopidogrel: a review of the evidence. J. Am. Coll. Cardiol. 45, 1157–1164 (2005).

    CAS  PubMed  Google Scholar 

  74. Gori, A. M. et al. Incidence and clinical impact of dual nonresponsiveness to aspirin and clopidogrel in patients with drug-eluting stents. J. Am. Coll. Cardiol. 52, 734–739 (2008).

    CAS  PubMed  Google Scholar 

  75. Eikelboom, J. W. 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 105, 1650–1655 (2002).

    CAS  PubMed  Google Scholar 

  76. Gum, 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. 41, 961–965 (2003).

    CAS  PubMed  Google Scholar 

  77. Cotter, G. et al. Lack of aspirin effect: aspirin resistance or resistance to taking aspirin? Am. Heart J. 147, 293–300 (2004).

    CAS  PubMed  Google Scholar 

  78. Pamukcu, B. 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 22, 103–110 (2006).

    CAS  PubMed  Google Scholar 

  79. Stejskal, D. et al. Aspirin resistance measured by cationic propyl gallate platelet aggregometry and recurrent cardiovascular events during 4 years of follow-up. Eur. J. Intern. Med. 17, 349–354 (2006).

    CAS  PubMed  Google Scholar 

  80. Matetzky, S. et al. Clopidogrel resistance is associated with increased risk of recurrent atherothrombotic events in patients with acute myocardial infarction. Circulation 109, 3171–3175 (2004).

    CAS  PubMed  Google Scholar 

  81. Lev, E. I. et al. Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance. J. Am. Coll. Cardiol. 47, 27–33 (2006).

    CAS  PubMed  Google Scholar 

  82. Bliden, K. P. et al. Increased risk in patients with high platelet aggregation receiving chronic clopidogrel therapy undergoing percutaneous coronary intervention: is the current antiplatelet therapy adequate? J. Am. Coll. Cardiol. 49, 657–666 (2007).

    CAS  PubMed  Google Scholar 

  83. Ajzenberg, N. et al. Enhanced shear-induced platelet aggregation in patients who experience subacute stent thrombosis: a case–control study. J. Am. Coll. Cardiol. 45, 1753–1756 (2005).

    PubMed  Google Scholar 

  84. Geisler, T. et al. Low response to clopidogrel is associated with cardiovascular outcome after coronary stent implantation. Eur. Heart J. 27, 2420–2425 (2006).

    CAS  PubMed  Google Scholar 

  85. Gurbel, P. A. et al. Clopidogrel effect on platelet reactivity in patients with stent thrombosis: results of the CREST Study. J. Am. Coll. Cardiol. 46, 1827–1832 (2005).

    CAS  PubMed  Google Scholar 

  86. Cuisset, T. et al. High post-treatment platelet reactivity identified low-responders to dual antiplatelet therapy at increased risk of recurrent cardiovascular events after stenting for acute coronary syndrome. J. Thromb. Haemost. 4, 542–549 (2006).

    CAS  PubMed  Google Scholar 

  87. Hochholzer, W. et al. Impact of the degree of peri-interventional platelet inhibition after loading with clopidogrel on early clinical outcome of elective coronary stent placement. J. Am. Coll. Cardiol. 48, 1742–1750 (2006).

    CAS  PubMed  Google Scholar 

  88. Patti, G. et al. Point-of-care measurement of clopidogrel responsiveness predicts clinical outcome in patients undergoing percutaneous coronary intervention results of the ARMYDA-PRO (Antiplatelet therapy for Reduction of Myocardial Damage during Angioplasty-Platelet Reactivity Predicts Outcome) study. J. Am. Coll. Cardiol. 52, 1128–1133 (2008).

    CAS  PubMed  Google Scholar 

  89. Marcucci, R. et al. Cardiovascular death and nonfatal myocardial infarction in acute coronary syndrome patients receiving coronary stenting are predicted by residual platelet reactivity to ADP detected by a point-of-care Assay: a 12-month follow-up. Circulation 119, 237–242 (2009).

    PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Mount sinai Medical Center, New York, NY, USA

    Joseph M. Sweeny

  2. Mount Sinai School of Medicine, New York, NY, USA

    Valentin Fuster

  3. National Heart and Lung Institute, Imperial College London, UK

    Diana A. Gorog

Authors
  1. Joseph M. Sweeny
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Diana A. Gorog
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Valentin Fuster
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Valentin Fuster.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Sweeny, J., Gorog, D. & Fuster, V. Antiplatelet drug 'resistance'. Part 1: mechanisms and clinical measurements. Nat Rev Cardiol 6, 273–282 (2009). https://doi.org/10.1038/nrcardio.2009.10

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1038/nrcardio.2009.10

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing