ST elevation myocardial infarction anticoagulant and antithrombotic therapy: Difference between revisions
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Unfractionated heparin inhibits Factor IIa more than Factor Xa | Unfractionated heparin inhibits Factor IIa more than Factor Xa | ||
===Unfractionated Heparin in the Management of the STEMI Patient=== | |||
By itself, [[unfractionated heparin]] ([[UFH]]) actually exerts little or no effect on [[thrombin]], and for this reason UFH is not classified as a direct thrombin inhibitor. The enzymatic activity is actually achieved by [[antithrombin III]] ([[AT III]]). When UFH combines with ATIII, the activity of ATIII is tremendously increased, and for this reason, UFH is classified as an indirect thrombin inhibitor. | |||
==References== | ==References== | ||
Revision as of 00:50, 22 April 2009
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] As an active clinical researcher, Dr. Gibson has received research and grant support from the majority of manufacturers of antithrombin and antiplatelet agents. You can view his complete disclosure statement here.
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Overview
Management of the patient with ST elevation myocardial infarction requires inhibition of both the the generation of thrombin (i.e inhibition of the coagulation cascade via antithrombins) as well as the platelet (via antiplatelet agents). Selection of the appropriate antithrombin depends upon a variety of factors including the choice of revascularization strategy. This chapter reviews data supporting the optimal selection of both parenteral antithrombotic and oral antithrombotic (anticoagulant) agents for a given patient.
Sites of Action of Antithrombins
The majority of established and investigational antithrombins target two factors in the coagulation cascade: Factor Xa and Factor II. [1] factor Xa lies higher in the coagulation cascade at the intersection of the intrisic and extrinsic pathway. Inhibition of Factor Xa limits the initial thrombin generation irrespective of whether the coagulation cascade was initiated by the intrinsic or extrinsic pathway. Factor II (thrombin) lies lower in the coagulation cascade and is involved in the conversion of fibrinogen to fibrin.
Parenteral Drugs Targeting Factor Xa
Indirect Inhibitors Requiring Antithrombin
Idraparinux
Direct Inhibitors Not Requiring Antithrombin
DX-9065a
Otamixaban
Oral Drugs Targeting Factor Xa
Rivaroxaban
Apixaban
LY517717
YM150
DU-176b
PRT-054021
Parenteral Drugs Targeting Factor IIa
Oral Drugs Targeting Factor IIa
Dabigatran
Ximelogatran (removed from market)
Parenteral Drugs Targeting Both Factor IIa and Factor Xa
Enoxaparin inhibits Factor Xa more than Factor IIa
Unfractionated heparin inhibits Factor IIa more than Factor Xa
Unfractionated Heparin in the Management of the STEMI Patient
By itself, unfractionated heparin (UFH) actually exerts little or no effect on thrombin, and for this reason UFH is not classified as a direct thrombin inhibitor. The enzymatic activity is actually achieved by antithrombin III (AT III). When UFH combines with ATIII, the activity of ATIII is tremendously increased, and for this reason, UFH is classified as an indirect thrombin inhibitor.
References
- ↑ Weitz JI (2006). "Emerging anticoagulants for the treatment of venous thromboembolism". Thromb. Haemost. 96 (3): 274–84. doi:10.1160/TH06-05-0234. PMID 16953267. Unknown parameter
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