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Learning objectives
Understand the importance of venous thrombosis in cardiovascular medicine.
Appreciate the mode of action of different oral anticoagulants.
Recall the uses, risks and benefits of each non-vitamin K antagonist oral anticoagulants.
Introduction
Thrombosis is the common pathophysiology responsible for ischaemic heart disease, ischaemic stroke and venous thromboembolism (VTE), and a major contributor to the global disease burden.1 This effect is markedly more pronounced by considering the view that cancer is also a thrombotic disease.2 ,3 Cardiovascular disease (CVD, manifesting as acute coronary syndromes, myocardial infarction and stroke) is almost entirely related to thrombosis within arteries. However, many of the risk factors for arterial thrombosis are also risk factors for VTE, and in addition VTEs have additional risk factors such as obesity and cancer.4 ,5 Indeed, VTE is a risk factor for subsequent arterial thrombosis.6 Some risk factors (such as orthopaedic surgery, certain types of valve disease and cardioversion for atrial fibrillation (AF)) are so strong, that anticoagulation is mandatory.7
VTE, manifesting principally as deep vein thrombosis (DVT) and pulmonary embolism (PE) is a frequent complication among hospital inpatients and contributes to longer hospital stays, morbidity and mortality. For example, without antithrombotic prophylaxis, DVT has been documented in over a third of all major orthopaedic operations. Although traditionally considered separate diseases, it is now accepted that DVT and PE are a single clinical entity: 50–80% of those presenting with DVT have evidence of PE while over 80% of those presenting with a PE have asymptomatic DVT. Clinical practice of the prevention and treatment of VTE is compounded by the fact that some risk factors (such as active malignancy) are more likely than others (such as diabetes) to evoke a VTE.5 ,8
Anticoagulation is considered in numerous diverse clinical situations. However, the variable medical …
Footnotes
Correction notice Since this paper was first published online two errors have been identified. In the sixth row of table 2 ‘Dosing recommendation…) the third column entitled ‘Rivaroxaban’ reads ‘CrCl 15−29 mL/min: reduce dose for example, from 20 mg to 10 mg four times per day.’ This is incorrect and the recommendation should read ‘CrCl 15−29 mL/min: reduce dose for example, from 20 mg to 15 mg once a day’. In the third row of table 4 (Frequency of VTE...) the third column ‘Rivaroxaban’ reads '2.1−3.0% (p<0.01 for superiority) this is incorrect. The statement should read '2.1–3.0% (p<0.001 for non-inferiority).
Contributors ADB wrote the first draft, GYHL edited and enhanced the text.
Competing interests ADB has taken hospitality, speaker fees and research funds from Daiichi-Sankyo, Pfizer, Bayer and Boehringer Ingleheim. GYHL has served as a consultant for Bayer, Merck, Sanofi, BMS/Pfizer, Daiichi-Sankyo, Biotronik, Medtronic, Portola and Boehringer Ingelheim and has been on the speaker's bureau for Bayer, BMS/Pfizer, Boehringer Ingelheim, Daiichi-Sankyo, Roche, Medtronic and Microlife.
Provenance and peer review Commissioned; externally peer reviewed.