Antiplatelet therapy in prevention of cardio- and venous thromboembolic events

Steven R. Steinhubl, John W. Eikelboom, Elaine M. Hylek, Harold L. Dauerman, Susan S. Smyth, Richard C. Becker

Research output: Contribution to journalReview articlepeer-review

12 Scopus citations


The contribution of platelets in the pathophysiology of low-shear thrombosis - specifically, in atrial fibrillation (AF) and venous thromboembolic events (VTE) - remains less clear than for arterial thrombosis. AF itself appears to lead to platelet activation, offering a potential target for aspirin and other antiplatelet agents. Randomized trial results suggest a small benefit of aspirin over placebo, and of dual antiplatelet therapy (aspirin plus clopidogrel) over aspirin alone, for prevention of cardioembolic events in AF. Antiplatelet therapy thus can represent an option for patients with AF who are unsuitable for therapy with warfarin or novel oral anticoagulant agents. For VTE, the rationale for antiplatelet therapy reflects the venous response to disrupted blood flow - interactions among monocytes, neutrophil extracellular traps, and platelets. Early randomized trials generally showed poorer performance of aspirin relative to heparins and danaparoid sodium in prevention of VTE. However, results from large placebo- and dalteparin-controlled randomized trials have spurred changes in the most recent practice guidelines - aspirin is now recommended after major orthopedic surgery for patients who cannot receive other antithrombotic therapies.

Original languageEnglish
Pages (from-to)362-371
Number of pages10
JournalJournal of Thrombosis and Thrombolysis
Issue number3
StatePublished - Apr 2014

Bibliographical note

Funding Information:
Conflict of interest SRS has received honoraria from AstraZeneca. JWE has received grant support from BMS/sanofi-aventis, Boehringer Ingelheim, and Daiichi/Eli Lilly; has received honoraria from AstraZeneca, BMS/sanofi-aventis, Boehringer Ingelheim, and Daii-chi/Eli Lilly; and has consulted for AstraZeneca, BMS/sanofi-aventis, Boehringer Ingelheim, and Daiichi/Eli Lilly. EMH has received honoraria from Boehringer Ingelheim and Bristol-Myers Squibb and has consulted for Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, Janssen, and Pfizer. HLD has received grant support from Abbott Vascular and St. Jude Medical and has consulted for The Medicines Company. SSS has received grant support from AstraZeneca. RCB has received grant support from AstraZeneca and has consulted for Eli Lilly/Daiichi and Merck.

Funding Information:
Acknowledgments The authors thank Patricia A. French of Left Lane Communications for assistance in drafting and editing the manuscript. The 2013 Platelet Colloquium was supported by unrestricted grants from AstraZeneca Pharmaceuticals; Merck & Co., Inc.; Regado Biosciences, Inc.; St. Jude Medical, Inc.; and The Medicines Company.


  • Fibrillation
  • Platelets
  • Thrombosis

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine


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