in cost-utility analysis reflected more or less in keeping with published data (Table 5).[38]

However, this study made an assumption that the treatment was beneficial. In our opinion, this lifetime risk estimation in conjunction with CHADS2 index may be a useful tool in informed decision-making process for anticoagulation therapy. Warfarin has a notoriously narrow therapeutic window and carries significant risk if not closely monitored. There is increasing selleck inhibitor appreciation that kidney impairment could also decrease non-renal clearance and alter the bioavailability and response to drugs predominantly metabolized by the liver.[39, 40] Moderate and severe kidney impairment was associated with a reduction in warfarin dose requirements.[41] Initiation and maintenance of warfarin therapy is challenging because of the multitude of factors that influence click here its pharmacokinetics and pharmacodynamics. The risk of haemorrhage is especially increased during the first 30–90 days after initiation of oral anticoagulation because initial therapy often results in INR value >3.0.[20, 42] Reinecke et al. proposed that checking INR three times a week during the first month and checking at least every fortnight

for long term.[25] The prevalence of warfarin use among HD patients was reported to be 8–25%, with up to 70%.[21, 43] Despite common use of warfarin, the exact bleeding risk due to warfarin in HD patients with AF is largely unknown. Elliott et al. systemically reviewed the rates of bleeding episodes in HD patients treated with warfarin for any indication (mainly for venous access thrombosis) and concluded that warfarin use doubled the risk for major bleeding.[44] This systematic review concluded that both low- and full-intensity anticoagulation use in HD patients was associated with a significant bleeding

risk. The other comorbidities contributing to the increased bleeding risks of the patients may not be taken into account in these studies and this was the major limiting factor. A full-intensity anticoagulation L-NAME HCl therapy study in the same systematic review showed that 20 times higher bleeding rates in HD patients exposed to warfarin.[45] In Holden et al. study, warfarin was found to increase significantly the risk for bleeding up to three times and aspirin by four times.[46] In Chan et al. study, a significant higher bleeding rate was associated with warfarin or clopidogrel use (vs non-use) whereas the rates of bleeding between patients on aspirin and no mediation were statistically and clinically no different.[21] The results of both Holden et al. and Chan et al. studies indicated that the combination of warfarin and aspirin resulted in the highest incidence of major bleeding episodes.[21, 46] Olesen et al. concluded in his a large observational study that compared with non-user, warfarin mono-therapy (HR 1.27; 95% CI 0.91–1.77; P = 0.15), aspirin mono-therapy (HR 1.63; 95% CI 1.18–2.26; P = 0.