Clinician update: Direct thrombin inhibitors and low molecular weight heparins in acute coronary syndrome

Joanna J. Wykrzykowska, Sekar Kathiresan, Ik-Kyung Jang

Research output: Chapter in Book/Report/Conference proceedingChapterAcademicpeer-review

Abstract

Thrombin plays a central role in the pathogenesis of acute coronary syndromes (ACS) including both unstable angina (UA) and acute myocardial infarction (AMI) (1). It promotes platelet aggregation, its own autocatalysis, and catalysis of fibrinogen to fibrin (2,3). Antithrombin and antiplatelet therapies have become the cornerstones of the treatment of cardiovascular disease. The usual medical regimen for non-ST segment elevation MI includes intravenous unfractionated heparin (UFH), aspirin, thienopyridine, and glycoprotein IIb/IIIa inhibitors, and for ST-elevation MI, aspirin, UFH, and thrombolytic agents.
Original languageEnglish
Title of host publicationClinical, Interventional and Investigational Thrombocardiology
PublisherCRC Press
Pages495-524
ISBN (Electronic)9780849344954
ISBN (Print)0824754190
Publication statusPublished - 1 Jan 2005
Externally publishedYes

Publication series

NameClinical, Interventional and Investigational Thrombocardiology

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