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

Evaluation of thrombolytic agents

W R Bell1

  • 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Drugs
|January 1, 1997
PubMed
Summary

Thrombolytic agents convert plasminogen to plasmin to break down clots. Despite improved specificity, newer agents show similar bleeding risks to older ones in clinical trials.

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

Oxidative damage in age-related macular degeneration.

Histology and histopathology·2007
Same author

H-Ras oncogene counteracts the growth-inhibitory effect of genistein in T24 bladder carcinoma cells.

British journal of cancer·2004
Same author

Potential clozapine target sites on peripheral hematopoietic cells and stromal cells of the bone marrow.

The pharmacogenomics journal·2003
Same author

Role of splenectomy in immune (idiopathic) thrombocytopenic purpura.

Blood reviews·2002
Same author

Thrombotic thrombocytopenic purpura associated with clopidogrel.

The New England journal of medicine·2000
Same author

Megakaryocyte-targeted synthesis of the integrin beta(3)-subunit results in the phenotypic correction of Glanzmann thrombasthenia.

Blood·2000

Area of Science:

  • Pharmacology
  • Cardiology
  • Hematology

Background:

  • Thrombolytic agents activate plasminogen to plasmin, a key enzyme in fibrinolysis.
  • First-generation agents (streptokinase, urokinase) have limited fibrin specificity, potentially causing systemic fibrinolysis and bleeding.
  • Second-generation agents (e.g., alteplase) were designed for enhanced fibrin specificity to minimize systemic effects.

Purpose of the Study:

  • To review the mechanism of action and clinical efficacy of thrombolytic agents.
  • To compare the bleeding complications associated with first- and second-generation thrombolytics.
  • To discuss the current and future applications of thrombolytic therapy.

Main Methods:

  • Review of existing literature on thrombolytic agents.
  • Analysis of clinical trial data comparing different generations of thrombolytics.
  • Discussion of therapeutic outcomes in acute myocardial infarction and other ischemic conditions.

Main Results:

  • Thrombolytic agents effectively reduce morbidity and mortality in acute myocardial infarction.
  • Clinical trials have not consistently demonstrated significant differences in bleeding incidence between first- and second-generation agents.
  • Despite enhanced specificity, second-generation agents do not appear to offer a significant reduction in bleeding complications.

Conclusions:

  • Thrombolytic therapy is crucial for managing acute myocardial infarction, significantly improving patient outcomes.
  • Current research is exploring thrombolytics for other ischemic conditions like stroke.
  • Future directions include optimizing drug administration and evaluating combination therapies with agents like aspirin and heparin.

Related Experiment Videos