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

Coagulation abnormalities and cardiovascular disease.

T G DeLoughery1

  • 1Department of Medicine, Oregon Health Sciences University, Portland 97201-3098, USA. delought@ohsu.edu

Current Opinion in Lipidology
|November 11, 1999
PubMed
Summary

Genetic defects causing excessive venous thrombosis are common. However, links between common genetic variations in key clotting factors and heart disease risk remain unclear, despite their role in thrombosis.

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

Reversal of warfarin era thinking.

Journal of internal medicine·2017
Same author

Unexpected pharmacokinetics of recombinant porcine factor VIII in a patient with acquired factor VIII deficiency and spontaneous epidural haematoma.

Haemophilia : the official journal of the World Federation of Hemophilia·2017
Same author

Ibrutinib-associated bleeding: pathogenesis, management and risk reduction strategies.

Journal of thrombosis and haemostasis : JTH·2017
Same author

Between Scylla and Charybdis: antithrombotic therapy in hematopoietic progenitor cell transplant patients.

Bone marrow transplantation·2011
Same author

Therapeutic efficacy of aortic administration of N-acetylcysteine as a chemoprotectant against bone marrow toxicity after intracarotid administration of alkylators, with or without glutathione depletion in a rat model.

Cancer research·2001
Same author

Recurrent thromboembolic disease following splenectomy for pyruvate kinase deficiency.

American journal of hematology·2001

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Genetics

Background:

  • Excessive venous thrombosis is linked to genetic defects in 60-80% of patients.
  • Increased plasma levels of fibrinogen and PAI-1 correlate with myocardial infarction risk.
  • Common polymorphisms in coagulation factors (Factor VIII, PAI-1, fibrinogen) have an ambiguous association with ischemic cardiac disease.

Purpose of the Study:

  • To clarify the association between common genetic polymorphisms of coagulation proteins and ischemic heart disease.
  • To investigate the role of venous hypercoagulable states in coronary ischemic syndrome.
  • To explore pathogenic polymorphisms in platelet receptors and lipoprotein mediation in coagulation.

Main Methods:

  • Review of existing literature on genetic defects and thrombosis.
  • Analysis of studies investigating polymorphisms in Factor VIII, PAI-1, and fibrinogen.
  • Examination of research on platelet receptors and lipoproteins in coagulation processes.

Main Results:

  • While genetic defects are prevalent in thrombosis, their link to ischemic heart disease is not definitively established.
  • Two common venous hypercoagulable states lack convincing evidence implicating them in ischemic heart disease.
  • Lipoproteins are identified as potential mediators in coagulation processes.

Conclusions:

  • The relationship between common coagulation protein polymorphisms and ischemic heart disease requires further investigation.
  • Current evidence does not strongly support the role of common venous hypercoagulable states in ischemic heart disease.
  • Further research into platelet receptor polymorphisms and lipoprotein involvement is warranted.

Related Experiment Videos