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

Andrew Blann University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UKThrombosis 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.