Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Heparin-induced thrombocytopenia

D B Brieger1, K H Mak, K Kottke-Marchant

  • 1Department of Cardiology, Joseph J. Jacobs Center for Vascular Biology, The Cleveland Clinic Foundation, Ohio 44195, USA.

Journal of the American College of Cardiology
|June 17, 1998
PubMed
Summary

Heparin-induced thrombocytopenia (HIT) is a serious immune complication of heparin therapy. Promptly stopping heparin and exploring alternative anticoagulants like direct thrombin inhibitors are crucial for managing HIT.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clinical effectiveness in everyday practice: improving outcomes for all patients through a national acute coronary syndrome data collaborative.

Internal medicine journal·2012
Same author

Acute coronary syndrome and stable coronary artery disease: are they so different? Long-term outcomes in a contemporary PCI cohort.

International journal of cardiology·2012
Same author

Unperceived treatment gaps in acute coronary syndromes.

International journal of clinical practice·2009
Same author

Impact of acute and chronic risk factors on use of evidence-based treatments in patients in Australia with acute coronary syndromes.

Heart (British Cardiac Society)·2009
Same author

Polymorphonuclear leukocyte phagocytic function increases in plasminogen knockout mice.

Thrombosis research·2008
Same author

Hypertriglyceridaemia is associated with early non-patency of coronary bypass grafts.

Heart (British Cardiac Society)·2006

Area of Science:

  • Cardiology
  • Immunology
  • Pharmacology

Background:

  • Heparin-induced thrombocytopenia (HIT) is an increasingly recognized complication of heparin anticoagulation, particularly in cardiovascular disease patients.
  • The pathophysiology involves an immune response to the heparin-platelet factor 4 complex, leading to platelet activation and thrombocytopenia.
  • Advances in laboratory diagnostics for pathogenic antibodies offer potential for earlier HIT detection.

Purpose of the Study:

  • To review the current understanding of HIT pathophysiology.
  • To discuss diagnostic approaches and management strategies for HIT.
  • To highlight the challenges in anticoagulation management for HIT patients and explore alternative therapies.

Main Methods:

  • Literature review of recent studies on HIT pathophysiology, diagnosis, and management.

Related Experiment Videos

  • Analysis of the role of heparin-platelet factor 4 antibodies in HIT.
  • Evaluation of current and emerging anticoagulant alternatives for HIT patients.
  • Main Results:

    • Heparin-platelet factor 4 complex is identified as the primary antigen in most HIT cases.
    • New diagnostic assays are available but require defined optimal application.
    • Immediate cessation of heparin is mandatory upon HIT diagnosis.

    Conclusions:

    • Effective management of HIT requires prompt heparin withdrawal and careful consideration of alternative anticoagulation.
    • Direct thrombin inhibitors represent a promising alternative for anticoagulation in HIT patients, pending further clinical trial results.
    • Further research is needed to establish optimal diagnostic criteria and therapeutic strategies for HIT, especially in acute coronary syndromes.