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Nonvitamin K antagonist oral anticoagulants (NOACs): the tide continues to come in

Authors Blann A

Received 2 June 2015

Accepted for publication 30 June 2015

Published 20 August 2015 Volume 2015:11 Pages 489—492

DOI https://doi.org/10.2147/VHRM.S89736

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Jaya Mallela

Peer reviewer comments 2

Editor who approved publication: Professor Daniel Duprez


Andrew Blann

University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK

Thrombosis is the major common endpoint in most human diseases. In the coronary circulation, occlusive thrombi and/or the rupture of atherosclerotic plaque causes myocardial infarction, and in the cerebral circulation thrombosis, causes ischemic stroke. In the venous circulation, venous thromboembolism (VTE), manifesting clinically as pulmonary embolus and deep vein thrombosis (DVT), is a frequent complication among inpatients, and contributes to longer hospital stays with increased morbidity and mortality. Until perhaps 5 years ago, heparinoids (unfractionated heparin, low molecular weight heparin [LMWH], and fondaparinux) and vitamin K antagonists (VKAs: warfarin, acenocoumarol, phenocoumarol) were the only options for the prevention of thrombotic stroke in atrial fibrillation, and of VTE in general. Although effective, these traditional drugs have several practical, management, and clinical disadvantages, a fact that our colleagues in industry have not been slow to recognize and address by developing improved drugs, now collectively known as nonvitamin K antagonist oral anti coagulants (NOACs). These agents are steadily replacing the heparinoids and VKAs in both inpatient and outpatient prevention and treatment of thrombosis.

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