Catheter thrombosis and percutaneous coronary intervention: fundamental perspectives on blood, artificial surfaces and antithrombotic drugs

  • Mark Y. Chan
  • Jeffrey I. Weitz
  • Yahye Merhi
  • Robert A. Harrington
  • Richard C. Becker


Recent reports of catheter thrombosis among patients undergoing percutaneous coronary intervention (PCI) have had a significant impact on the development of new antithrombotic therapies. The overall incidence of this complication is unknown, mainly because of underreporting in contemporary clinical trials of coronary intervention. The etiology and pathophysiology of catheter thrombosis is also poorly understood. Introduction of a catheter or guidewire may not provoke the intense thrombotic response that follows angioplasty or stenting, but factors such as catheter materials and device size, equipment surface properties, flow conditions, procedural time and complexity, as well as the antiplatelet and anticoagulant drugs administered during the procedure influence the likelihood, rate and clinical impact of thrombosis. The crucial role of cellular interactions involving tissue-factor bearing cells and platelets in the process of thrombosis also needs to be critically explored when considering blood contact with an exogenous material. Focusing on the inherently prothrombotic environment of percutaneous coronary intervention, we review the physiologic underpinnings of catheter and guidewire thrombosis, and explore the effect of antithrombotic drugs at the interface between blood and material surfaces. We also propose a clinical classification for the diagnosis and investigation of catheter thrombosis in clinical trials of anticoagulant therapy and PCI.


Device Anticoagulant Thrombosis Angioplasty Stenting 



We would like to thank Leslie M. Eibest from the Duke Department of Biology for her assistance with the environmental SEM imaging. Dr. Mark Y. Chan receives salary support from the National Medical Research Council, Singapore, Singapore and the National University Heart Centre. Singapore, Singapore, and tuition fee and research support from the Montreal Heart Institute, Montreal, QC. This work was partially funded by a research grant from The Snyderman Foundation, Durham, NC.

Conflicts of interest statement

Mark Y. Chan––research support from Regado Biosciences, Inc, Eli-Lilly, Daichii-Sankyo and Sanofi-Aventis, Jeffrey I. Weitz––consultant for Daiichi-Sankyo, Sanofi-Aventis and The Medicines Company, Yahya Mehri––research support from Archemix Inc., Robert A. Harrington––Dr. Harrington’s conflicts of interest can be found at, Richard C. Becker––research support from Regado Biosciences, The Medicines Company, Bristol-Myers Squibb, AstraZeneca, and Bayer.


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Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  • Mark Y. Chan
    • 1
    • 2
  • Jeffrey I. Weitz
    • 3
  • Yahye Merhi
    • 4
  • Robert A. Harrington
    • 5
  • Richard C. Becker
    • 6
  1. 1.National University Heart CentreSingaporeSingapore
  2. 2.SingaporeSingapore
  3. 3.Henderson Research Center and McMaster UniversityHamiltonCanada
  4. 4.Thrombosis and Hemostasis Laboratory, Montreal Heart InstituteUniversity of MontrealMontrealCanada
  5. 5.Division of Cardiovascular Medicine, Duke Cardiovascular Thrombosis Center and Duke Clinical Research InstituteDuke University School of MedicineDurhamUSA
  6. 6.Divisions of Cardiovascular Medicine & Hematology, Duke Cardiovascular Thrombosis Center and Duke Clinical Research InstituteDuke University School of MedicineDurhamUSA

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