Lower versus standard intensity oral anticoagulant therapy (OAT) in elderly warfarin-experienced patients with non-valvular atrial fibrillation

2010 ◽  
Vol 103 (02) ◽  
pp. 442-449 ◽  
Author(s):  
Umberto Cucchini ◽  
Gentian Denas ◽  
Bruce Davidson ◽  
Filippo Marzot ◽  
Seena Padayattil Jose ◽  
...  

SummaryIt has been observed that elderly patients with nonvalvular atrial fibrillation (NVAF) benefit from standard [an international normalised ratio (INR) goal of 2.0–3.0] oral anticoagulant treatment (OAT). The hypothesis that lower-intensity anticoagulation therapy can offset the higher bleeding risk in this population has never been tested in an ‘ad hoc’ clinical trial. Patients over 75 years of age with NVAF were randomised to receive warfarin to maintain the INR at 1.8 (range 1.5–2.0) or at a standard target of 2.5 (range 2.0–3.0). There were 135 patients in the low-intensity and 132 in the standard-intensity groups. During a mean follow-up lasting 5.1 years, 59 primary outcome events (thromboembolism and major haemorrhage) were recorded, 24 (3.5 per 100 patient-years) in the low-intensity group and 35 (5.0 per 100 patient-years) in the standard-intensity group (HR=0.7, 95% CI 0.4–1.1, p=0.1). The reduction in the primary endpoint was mainly due to a diminution in major bleedings (1.9 vs. 3.0 per 100 patient-years; HR=0.6, 95% CI 0.3–1.2, p=0.1). The median achieved INR value was 1.86 in the low-intensity and 2.24 in the standard-intensity group (p<0.001). The frequency of INR testing was 26.1 ± 13.5 vs. 24.3 ± 11.6 days, p<0.0001). In this exploratory study we observed a low rate of stroke and major bleeding in elderly patients (>75) being managed in an anticoagulation clinic for primary stroke prevention with low-intensity anticoagulation (INR 1.5–2.0). However, further trials are needed to confirm the hypothesis generated by the present study.

2019 ◽  
Vol 25 ◽  
pp. 107602961987024 ◽  
Author(s):  
Christine L. Baker ◽  
Amol D. Dhamane ◽  
Jigar Rajpura ◽  
Jack Mardekian ◽  
Oluwaseyi Dina ◽  
...  

We compared the risks of switching to another oral anticoagulant (OAC) and discontinuation of direct oral anticoagulants (DOACs) among elderly patients with nonvalvular atrial fibrillation (NVAF) who were prescribed rivaroxaban or dabigatran versus apixaban. Patients (≥65 years of age) with NVAF prescribed DOACs (January 1, 2013 to September 30, 2017) were identified from the Humana research database and grouped into DOAC cohorts. Cox regression analyses were used to evaluate whether the risk for switching to another OAC or discontinuing index DOACs differed among cohorts. Of the study population (N = 38 250), 55.9% were prescribed apixaban (mean age: 78.6 years; 49.8% female), 37.3% rivaroxaban (mean age: 77.4 years; 46.7% female), and 6.8% dabigatran (mean age: 77.0 years; 44.0% female). Compared to patients prescribed apixaban, patients prescribed rivaroxaban (hazard ratio [HR]: 2.08; 95% confidence interval [CI], 1.92-2.25; P < .001) or dabigatran (HR: 3.74; 95% CI, 3.35-4.18, P < .001) had a significantly higher risk of switching to another OAC during the follow-up; compared to patients prescribed apixaban, the risks of discontinuation were also higher for patients treated with rivaroxaban (HR: 1.10; 95% CI, 1.07-1.13, P < .001) or dabigatran (HR: 1.29; 95% CI, 1.23-1.35, P < .001).


2017 ◽  
Vol 158 (39) ◽  
pp. 1545-1549
Author(s):  
János Tomcsányi ◽  
Balázs Salfer ◽  
Bence Nagy

Abstract: Introduction: Despite a progress in the management of patients with atrial fibrillation this arrhythmia is one of the major causes of stroke, heart failure, sudden death and cardiovascular morbidity. Oral anticoagulation with vitamin K antagonist or non-vitamin K antagonist markedly reduces stroke and mortality in atrial fibrillation patients. Aim: To estimate the real-life vitamin K antagonist and non-vitamin K antagonist oral anticoagulant treatment in past years in Hungary. Method: Analysis of the National Health Insurance Administation database for atrial fibrillation (BNO: I48) between 2010–2015. We assumed that AF patient would turn to health care provides at least once either as inpatients or outpatients in a 5-year period. The patient was accepted as adherent after 6 months therapy and at least 80% oral anticoagulant prescription. Results: The prevalence of AF in Hungary is 3%. The mortality rate of AF 7%–10% per year. The adherence of the old oral anticoagulant treatment was 55%, but it was 69% among patient treated by “new” oral anticoagulant treatment. However, one third of the patients are not treated by effective old or new oral anticoagulant treatment. Conclusions: We need more effort to improve the effective and high adherence oral anticoagulant therapy in our country. Orv Hetil. 2017; 158(39): 1545–1549.


Author(s):  
J Harenberg ◽  
R Haas ◽  
R Zimmermann

Duration and discontinuation of oral anticoagulant therapy in the prophylaxis of recurrent thrombembolic diseases is often discussed. After stopping of the therapy an elevated incidence of rethromboses are observed. Therefore we determined fibrinopeptide A (FPA) as the most sensitive parameter of thrombin activity in vivo in patients treated with phenprocoumon in order to get information on the effectivity of the oral anticoagulant therapy and on the rebound phenomenon after discontinuation of the treatment.In 136 outpatients a significant relation between FPA and the effectivity of the anticoagulant therapy was observed: 2.7 ng/ml plasma (mean, thrombotest values < 5%), 3.5 ng/ml (5%-15%) and 4.1 ng/ml (>15%, p < 0.01). Normal FPA were 1.4ng/ml. In 11 patients with low FPA the oral anticoagulants were discontinued. FPA was determined in weekly intervalls. Within four weeks a continous increase of FPA from 1.6 ng/ml (median) to 3.8 ng/ml was observed. After eight weeks FPA was 8.2 ng/ ml (p < 0.05). The in vitro release of FPA after 10 min incubation of blood increased from 3.4ng/ml to 72 ng/ml after eight weeks (p < 0.05, normal release up to 5 ng/ml).The data indicate the clinical relevance and the different therapeutic implications of the determination of FPA in patients treated with phenprocoumon. They further give the first criterion, which outlines the effectivity of an oral anticoagulation therapy by reducing the thrombin activity in vivo. They give some evidence for a rebound like phenomenon after discontinuation of the oral anticoagulant treatment.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Svennberg ◽  
L Friberg

Abstract Background and objectives Previous studies have suggested that atrial fibrillation is a risk factor for pulmonary embolism. Oral anticoagulant therapy is the mainstay of treatment for atrial fibrillation and pulmonary embolism. We wanted to investigate if atrial fibrillation remained associated with the development of pulmonary embolism if oral anticoagulant treatment was accounted for. Method In this retrospective registry study a random sample of 20% of the adult Swedish population comprising approximately 1.5 million individuals were included during 2010–2017 in a cohort analysis. The endpoint was acute pulmonary embolism. In the cohort study, patients were analysed according to oral anticoagulant treatment and presence of atrial fibrillation at baseline. Results The group with atrial fibrillation was &gt;25 years older than the group without and had almost three times higher incidence of pulmonary embolism (2.91 vs 1.09 /1000 year at risk, p&lt;0.001). Individuals with atrial fibrillation on oral anticoagulant therapy had a lower risk of pulmonary embolism in multi-variable analysis (HR 0.59, CI 0.45–0.77). In the unadjusted analysis participants with atrial fibrillation without oral anticoagulant therapy showed an increased risk of pulmonary embolism (HR 3.33, CI 3.05–3.63). However, after multi-variable adjustment this association disappeared (HR 0.98, CI 0.89–1.07). In the entire atrial fibrillation cohort, no association was seen with the development of pulmonary embolism after multi-variable adjustment (HR 0.92, CI 0.84–1.01). The higher rate of pulmonary embolism among patients with atrial fibrillation can be fully explained by differences in age and co-morbidity. Conclusion Atrial fibrillation does not appear to be a clinically relevant risk factor for pulmonary embolism. Oral anticoagulant therapy protects against the development of pulmonary embolism in patients with atrial fibrillation. Associations with pulmonary embolism Funding Acknowledgement Type of funding source: Other. Main funding source(s): The main author has received funding from Stockholm County Council (Clinical postdoctorial appointment)


TH Open ◽  
2020 ◽  
Vol 04 (01) ◽  
pp. e20-e32 ◽  
Author(s):  
Paulus Kirchhof ◽  
Michael D. Ezekowitz ◽  
Yanish Purmah ◽  
Sonja Schiffer ◽  
Isabelle L. Meng ◽  
...  

Abstract Introduction This X-VeRT (eXplore the efficacy and safety of once-daily oral riVaroxaban for the prevention of caRdiovascular events in patients with nonvalvular aTrial fibrillation scheduled for cardioversion) substudy evaluated the effects of treatment with rivaroxaban or a vitamin-K antagonist (VKA) on levels of biomarkers of coagulation (D-dimer, thrombin–antithrombin III complex [TAT] and prothrombin fragment [F1.2]) and inflammation (high sensitivity C-reactive protein [hs-CRP] and high-sensitivity interleukin-6 [hs-IL-6]) in patients with atrial fibrillation (AF) who were scheduled for cardioversion and had not received adequate anticoagulation at baseline (defined as, in the 21 days before randomization: no oral anticoagulant; international normalized ratio <2.0 with VKA treatment; or <80% compliance with non-VKA oral anticoagulant treatment). Methods Samples for biomarker analysis were taken at baseline (n = 958) and treatment completion (42 days after cardioversion; n = 918). The influence of clinical characteristics on baseline biomarker levels and the effect of treatment on changes in biomarker levels were evaluated using linear and logistic models. Results Baseline levels of some biomarkers were significantly associated with type of AF (D-dimer and hs-IL-6) and with history of congestive heart failure (hs-CRP, D-dimer, and hs-IL-6). Rivaroxaban and VKA treatments were associated with reductions from baseline in levels of D-dimer (−32.3 and −37.6%, respectively), TAT (−28.0 and −23.1%, respectively), hs-CRP (−12.5 and −17.9%, respectively), and hs-IL-6 (−9.2 and −9.8%, respectively). F1.2 levels were reduced from baseline in patients receiving a VKA (−53.0%) but not in those receiving rivaroxaban (2.7%). Conclusion Anticoagulation with rivaroxaban reduced levels of key inflammation and coagulation biomarkers to a similar extent as VKAs, with the exception of F1.2. Further investigation to confirm the value of these biomarkers in patients with AF is merited.


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