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Coagulation cascade with targets for current and novel anticoagulant agents. LMWH, low-molecular-weight heparin; UFH, unfractionated heparin
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Atrial fibrillation (AF) is the most common form of cardiac arrhythmia and associated with significant mortality and morbidity. It is a powerful predictor of future embolic stroke, such that anticoagulation is recommended in the majority of patients. For many years this has predominantly been in the form of vitamin K antagonists. However, there are...
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The Atrial Fibrillation Better Care (ABC) pathway was proposed for a more integrated atrial fibrillation (AF) care. We investigated if adherence to the ABC pathway was associated to the quality of anticoagulation control in a cohort of AF outpatients starting vitamin K antagonists (VKAs) between July 2016 and June 2018. Patients were considered adh...
Bleeding risk represents a major concern in anticoagulated patients with atrial fibrillation (AF). Several bleeding prediction scores have been described: HAS-BLED, ATRIA, HEMORR 2 HAGES and ORBIT. Of these, only HAS-BLED considers quality of anticoagulation control amongst Vitamin K antagonist (VKA) users. We hypothesised that predictive value of...
Citations
... Pharmacological approaches to anticoagulation have for decades relied on vitamin K antagonists (VKAs) such as warfarin (used in the UK, Italy and Belgium), fluindione (France), phenprocoumon (Germany) However, there are still a number of issues raised in the literature regarding the use of anticoagulants and NOACs in particular. One concern is the fact that there is no established antidote for NOACs (Dweck et al. 2012, Sardar et al. 2014, Zarraga & Kron 2013. VKAs can be reversed with vitamin K (although this may take 24 hours or more), but no such direct antidote exists for NOACs -although a number are being investigated. ...
... Moreover, NOACs have shorter half-lives than VKAs, which means that missed doses of NOACs are more likely to result in clinical consequences than in the case of VKAs (Sardar et al. 2014, Zarraga & Kron 2013. On the other hand, shorter half-lives may have advantages in relation to elective surgery because they allow patients to stop treatment closer to the date of an operation (Dweck et al. 2012). ...
... It found that apixaban was better than warfarin in terms of preventing stroke or systemic embolism, and it caused less bleeding (Granger et al. 2011). Total mortality was also reduced relative to warfarin, although there was no significant reduction in the incidence of ischaemic stroke (Dweck et al. 2012). The RE-LY (Randomized Evaluation of Long-term anticoagulation therapy) trial tested two twice-daily doses of dabigatran (150mg and 110mg) against warfarin, and the 150mg twice-daily dose was associated with a significant reduction in stroke or systemic embolism with no difference in major bleeding compared with warfarin (Connolly et al. 2009). ...
Atrial fibrillation (AF) is a condition that confers increased thromboembolic risk. Oral anticoagulant (OAC) therapy can attenuate this risk. However, use of OAC therapy is determined largely by the presence of additional clinical factors (encapsulated by the CHA2DS2VASc score) that incrementally elevate stroke risk. Currently, there is no specific recommendation regarding urgency of initiation of OAC therapy in the presence of new onset AF, except where cardioversion is being considered. Recently, it has become increasingly apparent that there is a period immediately following the onset of AF of particularly accentuated thromboembolic risk (with respect to chronic AF): the physiological bases for this risk are as yet incompletely understood. However, given that both inflammation and impaired nitric oxide (NO) signalling are pivotally involved in the pathogenesis of AF, these factors may also mediate thrombotic risk in the context of new onset AF. Advances in OAC therapy have recently been achieved, with development of agents that are comparable to or superior than warfarin for mitigation of stroke risk, but with a safety profile similar to aspirin therapy. Thus, the incremental increase in thromboembolic risk experienced by new onset AF patients constitutes a previously widely neglected case in favour of the rapid application of OAC therapy to such individuals. This review seeks to summarise the thromboembolic risk observed in new onset AF and the emerging understanding of the physiological bases for this risk.
