1,723,060 research outputs found
Atrial Fibrillation and Stroke: Making Sense of Recent Observations on Anticoagulation
No full textAtrial fibrillation (AF) is the most prevalent heart rhythm disorder. AF accounts for a great proportion of deaths because it independently increases all-cause mortality and cardiovascular mortality risks. Ischemic stroke is the most common cardiovascular adverse event in AF patients. Oral anticoagulation (OAC) therapy with vitamin K antagonists (VKA) has been central for stroke prevention. Several drugs with a direct inhibitory effects on thrombin and factor Xa have been developed. These non-vitamin K antagonist oral anticoagulants (NOACs) are as effective and safer than warfarin. This review provides an overview of current guidelines and summarizes current evidence for the prevention of stroke in AF patients according to most relevant patients' subgroups and clinical features
Major Outcomes in Atrial Fibrillation Patients with One Risk Factor: Impact of Time in Therapeutic Range
Full text linkBACKGROUND:
The benefits and harms of oral anticoagulation (OAC) therapy in patients with only one stroke risk factor (i.e. CHA2DS2-VASc= 1 in males, or 2 in females) has been subject of debate.
METHODS:
We analysed all patients with only one stroke risk factor from the merged datasets of SPORTIF III and V trials. Anticoagulation control was defined according to time in therapeutic range (TTR).
RESULTS:
Of the original trial cohort, 1,097 patients had only one stroke risk factor. Stroke/systemic thromboembolic event had an incidence of 0.9 per 100 patient-years, with an incidence of 1.6 per 100 patient-years for all-cause death and 2.3%/patient-years for the composite outcome of stroke/systemic thromboembolic event/all-cause death. There were no significant differences in the risk for stroke/systemic thromboembolic event between sexes, nor between the different stroke risk factors amongst these atrial fibrillation patients with only one stroke risk factor. Cox regression analysis in patients treated with warfarin only found TTR to be inversely associated with stroke/systemic thromboembolic event (p=0.034) and all-cause death (p=0.015). Chronic heart failure was significantly associated with the outcome of all-cause death (p=0.0019) and the composite outcome of stroke/systemic thromboembolic event/all-cause death (p=0.021). There was a significant inverse linear association between TTR and the cumulative risk for both stroke/systemic thromboembolic event and all-cause death (both p<0.001).
CONCLUSIONS:
In atrial fibrillation patients with only one additional stroke risk factor (i.e. CHA2DS2-VASc= 1 in males or 2 in females), rates of major adverse events (stroke/systemic thromboembolic event, mortality) were high, despite anticoagulation. TTR in warfarin-treated patients was inversely associated with the occurrence of both stroke/systemic thromboembolic event and all-cause death
Later Is Not Always Better: Timing of Oral Anticoagulant Resumption After Endoscopic Procedures, Between New Data and Residual Uncertainties
No full textImpact of quality of anticoagulation control on outcomes in patients with atrial fibrillation taking aspirin: An analysis from the SPORTIF trials
No full textBACKGROUND: Concomitant aspirin (ASA) is often prescribed in anticoagulated patients with atrial fibrillation (AF). We aimed to investigate the relationship between ASA use and quality of anticoagulation control determining major adverse outcomes.METHODS: An ancillary analysis of patients in the warfarin arm of the SPORTIF III and V trials was performed. Quality of anticoagulation control was defined using time in therapeutic range (TTR).RESULTS: 3624 AF patients on warfarin were available for analysis: 1712 (47.2%) were ASA non-users with good anticoagulation control (TTR≥65%) [Group I], 380 (10.5%) were ASA users with TTR≥65% [Group II], 1192 (32.9%) were ASA non-users with TTR<65% [Group III] and 340 (9.4%) were ASA users with TTR<65% [Group IV]. CHA2DS2-VASc was similar across the groups (p=0.350), conversely HAS-BLED was progressively higher (p<0.001). At follow-up, stroke/systemic embolism rates were similar across the groups (p=0.162). Conversely, a progressively higher rate for major bleeding was found (p=0.034), as well as higher rates for all-cause death in Group III and IV (p<0.001). Kaplan-Meier analyses found a progressively higher risk for major bleeding across the groups (p=0.005) and a higher all-cause death risk in Group III and IV (p<0.001). Cox regression analysis confirmed that Group III and IV were at higher risk for major bleeding (p=0.005) and all-cause death (p=0.010).CONCLUSIONS: Poor anticoagulation control is associated with higher bleeding risk, which is even greater with concomitant ASA use, with no difference in stroke/SE risk. Poor anticoagulation control is associated with a higher risk for all-cause death, independent of concomitant ASA use.</p
Modelling projections for the uptake of edoxaban in an European population to 2050:effects on stroke, thromboembolism, and health economics perspectives
No full textAIMS: In the coming decades, the number of Europeans with atrial fibrillation (AF) is set to rise as the population ages, and so with it will the number of strokes. The risk of thromboembolism (principally stroke and systemic embolism) and death can be reduced by the use of the vitamin K antagonists (VKA, e.g. warfarin) and more so by non-VKA oral anticoagulants (NOACs) such as edoxaban.METHODS AND RESULTS: We modelled the effect of the increasing use of edoxaban in preference to warfarin in a European AF population from both clinical and economic perspectives. We estimate that the introduction of NOACs in 2010 eliminated over 88 000 thromboembolisms and deaths annually, of which over 17 000 were ischaemic strokes. At a 1-year cost of €30k per ischaemic stroke, this strategy saved €510 million annually. Should the use of edoxaban increase from 11% in 2013 to 75% by 2030, we expect that rate of thromboembolism and death will fall from 5.67 to 5.42 total events per million patients per year, which will further eliminate over 12 000 of these events annually. At an inflation-adjusted 1-year cost of approximately €35k per ischaemic stroke, this will save €44.5 million each year. At a conservative rate of increase in the AF population of 2.2-fold from 2005, in 2050 there will be around 180 000 AF-related ischaemic strokes that, at an inflation-adjusted cost of around €62k per stroke, sums to €11 116 million. Should the rate of AF rise 2.6-fold from 2005, then in 2050 there will be 214 500 ischaemic strokes that will cost around €13 300 million.CONCLUSION: Our data point to a substantial increase in the human and economic cost burden of AF and so emphasize the need to reduce this burden. This may be achieved by the increased use of oral anticoagulants, particularly with the NOACs such as edoxaban.</p
Dabigatran in clinical practice: Contemporary overview of the evidence
Full text linkOral anticoagulation is the cornerstone of stroke prevention in non-valvular atrial fibrillation (AF) and management of venous thromboembolism (VTE), resulting in a reduction in thrombotic complications and mortality. Benefit of vitamin K antagonists (VKAs) in such patients has been unambiguously confirmed, but VKA use is complicated by need for regular monitoring of the international normalized ratio and multiple drug and food interactions. Dabigatran is an oral direct thrombin inhibitor that can be used with fixed doses, without the need for routine anticoagulation laboratory monitoring and the advantage of few drug or diet interactions. Dabigatran is effective for stroke and systemic thromboembolism in AF and for the prophylaxis and treatment of VTE. The drug has a good safety profile and consistently shows a reduction in intracranial hemorrhage risk compared to warfarin. A specific reversal agent for dabigatran has been approved by FDA and EU. This review provides a summary of publications assessing clinical utility of dabigatran for different indications
Simple decision-making between a vitamin K antagonist and a non-vitamin K antagonist oral anticoagulant: using the SAMe-TT2R2score
Full text linkStroke prevention with oral anticoagulation (OAC) is central to the modern management of atrial fibrillation (AF) patients.1 For many years, vitamin K antagonists (VKAs, e.g. warfarin) have been the default class of OAC, but we now recognize that it is not simply prescribing VKA but very close attention to quality of anticoagulation control is necessary, as reflected by the individual time in therapeutic range (TTR).2 An average individual TTR of >70% is recommended to maximize efficacy and safety of the VKAs.2,3
Nonetheless, the VKAs have significant inter- and intra-patient variability, partly from diet and drug interactions, thus necessitating regular international normalised ratio (INR) monitoring.2 More recently, we have had the non-VKA oral anticoagulants (NOACs, previously referred to as new or novel OACs4) available, which offer efficacy, safety, and relative convenience compared with the VKAs, for stroke prevention in AF
Quantifying time in atrial fibrillation and the need for anticoagulation
Full text linkAtrial fibrillation (AF) is one of the major cardiovascular diseases, and the number of patients with AF is predicted to increase markedly in the coming years. Despite recent advance in management of patients with AF, AF remains one of the main causes of stroke or systemic embolism. Application of simple stroke risk-stratification schemes, such as the CHA2DS2-VASc score has been introduced to identify patients who mostly benefit from oral anticoagulants (OACs) for stroke prevention. Current medical devices allow the detection of short and asymptomatic episodes of AF, termed atrial high rate episodes (AHREs), which are also associated with an increased risk of thromboembolism. Early diagnosis of AF has clinical importance for a timely initiation of OAC, while strokes often occur without AHRE detected within 30days before the event. Consequently, it is unclear whether any AHRE imply the same therapeutic requirements as clinical AF. The exact estimation of AF burden and correct risk stratification in patients with asymptomatic AF and AHRE remains a challenge in clinical practice
Difficult decision making in the management of patients with atrial fibrillation and acute coronary syndrome or invasive cardiovascular interventions: new recommendations for daily practice
Full text linkThis editorial refers to 'Management of antithrombotic therapy in atrial fibrillation patients presenting with acute coronary syndrome and/or undergoing percutaneous coronary or valve interventions: a joint consensus document of the European Society of Cardiology Working Group on Thrombosis, European Heart Rhythm Association (EHRA), European Association of Percutaneous Cardiovascular Interventions (EAPCI) and European Association of Acute Cardiac Care (ACCA) endorsed by the Heart Rhythm Society (HRS) and Asia-Pacific Heart Rhythm Society (APHRS).' by Lip et al., on page 3155-3179
Interaction between dietary Vitamin K intake and anticoagulation by Vitamin K antagonists: is it really true?: A systematic review
No full textEducational advice is often given to patients starting treatment with vitamin K Antagonists (VKAs). A great emphasis is made on nutritional information. Common belief is that dietary vitamin K intake could counteract the anticoagulant effect by VKAs and for many years, patients have been discouraged to consume vitamin-K-rich foods, such as green leafy vegetables.The objective of this study is to summarize the current evidence supporting the putative interaction between dietary vitamin K intake and changes in INR with the VKAs.Data sources are MEDLINE via PubMed and Cochrane database.All clinical studies investigating the relationship between dietary vitamin K and measures of anticoagulation were included. We excluded all studies of supplementation of vitamin K alone.We performed a systematic review of the literature up to October 2015, searching for a combination of "food," "diet," "vitamin K," "phylloquinone," "warfarin," "INR," "coagulation," and "anticoagulant."Two dietary interventional trials and 9 observational studies were included. We found conflicting evidence on the effect of dietary intake of vitamin K on coagulation response. Some studies found a negative correlation between vitamin K intake and INR changes, while others suggested that a minimum amount of vitamin K is required to maintain an adequate anticoagulation. Median dietary intake of vitamin K1 ranged from 76 to 217 μg/day among studies, and an effect on coagulation may be detected only for high amount of vitamin intake (>150 μg/day).Most studies included patients with various indications for VKAs therapy, such as atrial fibrillation, prosthetic heart valves, and venous thromboembolism. Thus, INR target was dishomogeneous and no subanalyses for specific populations or different anticoagulants were conducted. Measures used to evaluate anticoagulation stability were variable.The available evidence does not support current advice to modify dietary habits when starting therapy with VKAs. Restriction of dietary vitamin K intake does not seem to be a valid strategy to improve anticoagulation quality with VKAs. It would be, perhaps, more relevant to maintain stable dietary habit, avoiding wide changes in the intake of vitamin K
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