It is well established that older individuals with atrial fibrillation (AF) are less likely to receive oral anticoagulant (OAC) therapy compared with their younger counterparts, 1, 2 and when treated with vitamin K
Vitamin K
Vitamin K is a group of structurally similar, fat-soluble vitamins found in foods and in dietary supplements. The human body requires vitamin K for complete synthesis of certain proteins that are needed for blood coagulation or for controlling binding of calcium in bones and other tissues. T…
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Is there a role for anticoagulation in the treatment of atrial fibrillation (AFIB)?
This article presents the current status of the use of anticoagulation for the treatment of AF, particularly with the use of non-vitamin K-dependent anticoagulants. Comparisons between these agents and warfarin are made and methods for assessment of anticoagulant activity and reversal are discussed.
Does antithrombotic therapy prevent stroke in patients with nonvalvular atrial fibrillation?
Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation. Ann Intern Med. 2007; 146 :857–67.
Which medications are used to treat atrial fibrillation (AFIB) on hemodialysis?
Chan KE, Edelman ER, Wenger JB et al. Dabigatran and rivaroxaban use in atrial fibrillation patients on hemodialysis. Circulation , 2015; 131 :972–9.. [ PMC free article] [ PubMed] [ Google Scholar] [ Ref list] 31. Heidbuchel H, Verhamme P, Alings M et al. European Heart Rhythm Association.
Which medications should be avoided in patients with atrial fibrillation (AFIB)?
Nonsteroidal anti-inflammatory drugs increase the risk of both serious bleeding and thromboembolism in anticoagulated patients with AF. 18 Antiplatelet therapy with aspirin plus clopidogrel, or – less effectively – aspirin only, should be considered in patients who refuse any OAC, or cannot tolerate anticoagulants for reasons unrelated to bleeding.
What is the bleed rate for dabigatran?
What are the risk factors for CHA2DS2 VASC?
How long does it take for a syringe to reach therapeutic levels?
What does TIA mean in risk factor?
How many people will have AF by 2050?
Is rivaroxaban a factor XA inhibitor?
Is AF a prothrombotic disease?
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What is the best anticoagulant to take for AFib?
Type of anticoagulation – For most patients with atrial fibrillation (AF) with an indication for anticoagulation, we recommend a direct oral anticoagulant (DOAC) rather than a vitamin K antagonist (VKA; eg, warfarin) (Grade 1A).
Why does the patient with atrial fibrillation require anticoagulation therapy?
Atrial fibrillation (A-fib) increases your risk of blood clots forming in the heart, which can lead to stroke (see 'Risk of stroke' above). Because of this, you will likely need treatment to reduce the risk of developing blood clots.
Do anticoagulants treat atrial fibrillation?
The results of these trials, combined with previous studies, suggest that anticoagulation is the treatment of choice for patients with atrial fibrillation associated with rheumatic valvular disease, prosthetic valve disease, and now NVAF.
Which drug is used for long term anticoagulation in atrial fibrillation?
If successful, rhythm control can eliminate or delay the need for long-term anticoagulation with warfarin in some patients. Several antiarrhythmic drugs are commonly used to prevent atrial fibrillation recurrence, such as quinidine, flecainide, propafenone, sotalol, and dofetilide.
What is the most effective treatment for atrial fibrillation?
Heart rate medicines: The most common way to treat atrial fibrillation is with drugs that control your heartbeat. These slow your rapid heart rate so your heart can pump better. You may need other drugs. Some are called beta-blockers.
Why multiple drugs are given when a patient has atrial fibrillation?
Anti-arrhythmic medications. These drugs are used to maintain a normal heart rhythm, not just to control the heart rate. Because they tend to have more side effects than drugs that control the heart rate, anti-arrhythmics tend to be used more sparingly.
Do all AFib patients need blood thinners?
Research suggests that about 10 percent of AFib patients don't need blood thinners because their risk of having a stroke is so low. National data also suggests that an additional 20 percent of AFib patients are not taking a blood thinner when they should be.
What are the benefits of anticoagulant?
Anticoagulants are medicines that help prevent blood clots. They're given to people at a high risk of getting clots, to reduce their chances of developing serious conditions such as strokes and heart attacks. A blood clot is a seal created by the blood to stop bleeding from wounds.
Why does atrial fibrillation cause clots?
AFib interferes with the flow of blood through your heart. This can cause blood to pool in your heart's upper chambers, which can cause blood clots to form.
What is the first drug of choice for atrial fibrillation?
Amiodarone as a first-choice drug for restoring sinus rhythm in patients with atrial fibrillation: a randomized, controlled study. Chest.
Which is better for AFib Eliquis or Xarelto?
There is strong evidence that the medication apixaban (Eliquis) is preferable to rivaroxaban (Xarelto) for stroke prevention in patients with atrial fibrillation (AF), with both reduced rates of severe bleeding complications as well as strokes, according to study published Dec. 21 in JAMA.
2020 ESC Guidelines for Atrial Fibrillation: Key Points
Authors: Hindricks G, Potpara T, Dagres N, et. al. Citation: 2020 ESC Guidelines for the Diagnosis and Management of Atrial Fibrillation Developed in Collaboration With the European Association of Cardio-Thoracic Surgery (EACTS): The Task Force for the Diagnosis and Management of Atrial Fibrillation of the European Society of Cardiology (ESC) Developed With the Special Contribution of the ...
2020 ACC Expert Consensus Pathway for Anticoagulant and Antiplatelet ...
Authors: Kumbhani DJ, Cannon CP, Beavers CJ, et al. Citation: 2020 ACC Expert Consensus Decision Pathway for Anticoagulant and Antiplatelet Therapy in Patients With Atrial Fibrillation or Venous Thromboembolism Undergoing Percutaneous Coronary Intervention or With Atherosclerotic Cardiovascular Disease: A Report of the American College of Cardiology Solution Set Oversight Committee.
Anticoagulation in Atrial Fibrillation – Current Concepts - PMC
Anticoagulation. Adjusted-dose warfarin and antiplatelet agents reduce the risk of stroke by approximately 60 % and 20 %, respectively, in patients with AF.12 In general, oral anticoagulation is preferred in patients with CHA 2 DS 2-VASc score ≥2, and no anticoagulation in patients with a score of 0 (see Figure 1 and Table 1).In patients with CHA 2 DS 2-VASc score of 1, anticoagulation ...
Management of Atrial Fibrillation in 2021: An Updated Comparison of the ...
Given its complexity, the management of atrial fibrillation (AF) has relied increasingly on expert guideline recommendations; however, discrepancies between these professional societies can lead to confusion among practicing clinicians. This article compares the recommendations in the 2019 American …
What is the bleed rate for dabigatran?
Major bleeding occurred less frequently with dabigatran 110 mg, and rates of major bleeding were similar with dabigatran 150 mg and warfarin: major bleeding occurred at a rate of 3.36 % per year in patients taking warfarin, 3.11 % per year in patients taking high-dose dabigatran (RR 0.93, 95 % CI 0.81–1.07, p=0.031 versus warfarin) and 2.71 % in patients taking low-dose dabigatran (RR 0.8, 95 % CI 0.69–0.93, p=0.003 versus warfarin). Both doses of dabigatran were associated with a significantly reduced risk of haemorrhagic stroke and intracranial haemorrhage when compared with warfarin.
How many metabolites are cleared by the liver?
One-third cleared renally, two-thirds metabol ised by the liver
How long does it take for a syringe to reach therapeutic levels?
Slow onset and offset of action, requiring 3–6 days to reach therapeutic levels
What does TIA mean in risk factor?
The name of the score is derived from the first letter of each risk factor. TIA = transient ischaemic attack.
How many people will have AF by 2050?
AF is a growing clinical problem owing to the ageing population, and the advances in treatment and improved survival of patients with cardiac disorders such as ischaemic heart disease and heart failure, which predispose to AF.4It is estimated that, by 2050, up to 16 million people in the US will suffer from AF,5which is already the commonest arrhythmia encountered in clinical practice.6The healthcare costs are substantial and AF accounts for 1 % of the National Health Service expenditure in the UK.7
What are the risk factors for CHA2DS2 VASC?
Table 1outlines the risk factors that make up the CHA2DS2-VASc score. Congestive heart failure is defined as left ventricular ejection fraction ≤40 %. Hypertension is defined as blood pressure consistently above 140/90 mmHg or treated hypertension on medication. Vascular disease is defined as previous myocardial infarction, peripheral arterial disease or aortic plaque.
Is Apixaban a direct factor XA inhibitor?
Apixaban is an oral, selective and reversible direct factor Xa inhibitor. 45The ARISTOTLE (Apixaban for the prevention of stroke in subjects with atrial fibrillation) study was a randomised, Phase III, double-blind trial comparing apixaban 5 mg twice daily with warfarin titrated to an INR between 2 and 3 in over 18,000 patients.46The primary outcome was stroke (either ischaemic or haemorrhagic) or systemic embolism, which occurred at a rate of 1.27 % per year in the apixaban group versus 1.60 % per year in the warfarin group (HR 0.79, 95 % CI 0.66–0.95, p<0.001 for non-inferiority, p=0.01 for superiority). This was primarily driven by a reduction in haemorrhagic stroke, which occurred at a rate of 0.24 % per year in the apixaban group versus 0.47 % per year in the warfarin group (HR 0.51, 95 % CI 0.35–0.75, p<0.001), as the rates of ischaemic stroke were similar (0.97 % per year in the apixaban group versus 1.05 % per year in the warfarin group [HR 0.92, 95 % CI 0.74–1.13, p=0.42]).
What is the glomerular filtration rate for AF?
For patients with AF and severe kidney disease (stage G4 or G5; estimated glomerular filtration rate <30 mL/min/1.73 m 2 ), on dialysis, or with acute renal injury, DOAC is generally avoided and VKA is generally the preferred long-term anticoagulant. Patients with stage 4 and 5 CKD are at higher risk of having unpredictable sudden deterioration in renal function than patients with normal renal function, and such deterioration could cause an abrupt reduction in clearance of a DOAC that depends on renal metabolism. In such a setting, use of an agent such as warfarin that allows for therapeutic drug monitoring may be preferred. A time in the therapeutic range of >70 percent is desirable. (See "Direct oral anticoagulants (DOACs) and parenteral direct-acting anticoagulants: Dosing and adverse effects", section on 'Chronic kidney disease' and "Warfarin and other VKAs: Dosing and adverse effects", section on 'Monitoring (PT/INR)' .)
Why do older people take DOACs?
Older adults — For most older patients, including those over the age of 75 years, we prefer DOACs (also referred to as non-vitamin K oral anticoagulants [NOACs]) to warfarin because of the reduced risk of intracranial hemorrhage versus warfarin. Since there are no head to head randomized trials comparing DOACs in this patient group, we do not have a preference for a specific DOAC.
What is the recommended INR for VKA?
Vitamin K antagonist — For patients with AF treated with VKA (eg, warfarin ), an INR between 2.0 and 3.0 is recommended with an average TTR >70 percent [ 18,19 ]. This is based upon the increased risk of stroke observed with INR values significantly below 2 (four- to sixfold at an INR of 1.3 compared with an INR of 2 or above) and the increased risk of bleeding associated with INR above 3.0 ( figure 1) [ 20-24 ]. Dosing of warfarin is discussed in detail separately. (See "Warfarin and other VKAs: Dosing and adverse effects", section on 'Warfarin administration' .)
What is the INR for a stroke?
However, we recommend an INR between 2.0 and 3.0 for these patients as well [ 24 ].
Can you bridge DOAC with heparin?
DOAC — For patients with AF starting DOAC, effective anticoagulation is achieved within a few hours. We do not bridge patients starting DOAC with heparin. For patients prescribed one of the DOACs, we suggest that clinicians review dosing recommendations from regulatory agencies and available in drug information compendia such as Lexicomp. (See 'Dosing' below.)
Is there a randomized controlled trial comparing DOACs?
Regarding the relative efficacy and safety of the DOAC agents, no randomized controlled trials (RCTs) directly comparing the DOACs have been published. Published observational studies have many limitations and are no substitute for head to head RCTs [ 10-14 ].
Can you continue VKA with AF?
However, it is reasonable to continue VKA in these patients.
What are the inhibitors of factor XA?
Factor Xa inhibitors act indirectly or directly. Heparin and low-molecular-weight heparins indirectly inhibit FXa among other targets, including thrombin, potentiating the anticoagulant action of antithrombin (antithrombin III). However, their action is completely non-selective in the case of unfractionated heparin, and only partially selective for low-molecular- weight heparins. New indirect inhibitors, fondaparinux and idraparinux, are synthetic analogues of the unique pentasaccharide sequence that mediates the interaction of heparins with antithrombin. 28 Once the pentasaccharide/antithrombin complex binds FXa, the pentasaccharide dissociates from the antithrombin/Xa complex and can be re-utilised to catalyse other similar types of reactions.
Does vitamin K antagonist cause stroke?
Although to date warfarin and other vitamin K antagonists have clearly had the greatest efficacy among commonly available treatments in preventing stroke in atrial fibrillation, their use is associated with a substantial risk of major bleeding and is impractical because of their narrow therapeutic window, their interaction with drugs and foods and the need for frequent coagulation monitoring. Several new anticoagulants are undergoing phase III clinical trials in atrial fibrillation with the aim of demonstrating non-inferiority compared with vitamin K antagonists or superiority compared with aspirin in patients in whom vitamin K antagonists are contraindicated or not tolerated. In the recently released Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) trial, the first such drug, dabigatran etexilate, was proved substantially equivalent to 2–3 international normalised ratio (INR)-adjusted warfarin at the dosage of 110mg twice a day (BID), with superior efficacy at a dosage of 150mg BID. With these new drugs, cardiologists and internists are witnessing a real revolution in the thromboprophylaxis in atrial fibrillation.
Does warfarin affect coagulation?
Warfarin and related coumarinic VKAs exert their anticoagulant effect by interfering with the cyclic interconversion of vitamin K and its 2,3 epoxide (vitamin K epoxide), modulating the gamma-carboxylation of glutamate residues (Gla) on the N-terminal regions of vitamin K-dependent proteins, including the coagulation factors FII (prothrombin), FVII, FIX and FX, as well as of the anticoagulant proteins C and S. The gamma-carboxylation of these proteins is required for their activity. Treatment with coumarins results in the hepatic production of partially carboxylated and decarboxylated proteins with reduced coagulant activity. 27
Does Warfarin cause stroke?
Warfarin and similar coumarin derivatives (vitamin K antagonists [VKAs]) clearly have the greatest efficacy among the currently available treatments (mostly aspirin) in preventing stroke in atrial fibrillation (AF). 1 However, they carry a substantial risk of major bleeding (approximately 1.2% per year) and have a narrow therapeutic window, which necessitates frequent coagulation monitoring to ensure appropriate dosing. 2 The marked variability in the dose–response relationship of VKAs often makes it difficult for the patient to remain within the ideal international normalised ratio (INR) range. While absorption of the various coumarin derivatives from the gastrointestinal tract is generally quite good, their pharmacokinetics are influenced by many other factors, including numerous drug interactions, the dietary intake of vitamin K, hepatic dysfunction, changes in the gut flora, patient compliance and alcohol intake. These factors frequently occur, so that even within the controlled setting of a clinical trial it has not been possible for patients to remain within the therapeutic window more than 50% of the time. 3 Thus, in addition to careful patient selection required for any anticoagulant to screen out patients who may be at increased risk of haemorrhage, 4–7 every patient treated with VKAs needs frequent, assiduous and unpleasant monitoring of the INR to reduce the risk of undertreatment or overtreatment. In addition to the common contraindications to any anticoagulants, such as dementia, elevated creatinine, anaemia with haemoglobin <10g/l, blood pressure >180/100mmHg despite treatment, severe chronic alcoholism, previous intracranial haemorrhage, severe bleeding despite a therapeutic control, predisposition to head trauma and requirements for non-steroidal anti-inflammatory drugs, 8–11 used in most trials as criteria to exclude patients from enrolment, there are specific reasons why VKAs are poorly tolerated and actually impractical for many patients with AF. These include the clear deterioration in the patient’s quality of life: 12 the patient is tied to the medical system for lifelong anticoagulation monitoring, with restriction of travelling, anxiety, cost and loss of freedom, as well as caution in the use of other drugs and in dietary patterns because of potential interactions of VKAs with drugs and foods. 13 Finally, the high inter-patient variability of VKA requirements has recently been linked to genetic factors. Polymorphisms of vitamin K epoxide reductase complex subunit 1 (VKORC1), a major enzyme of the vitamin K cycle responsible for vitamin K reduction, can affect sensitivity to warfarin therapy and be involved in warfarin resistance. 14 Genetic variants in cytochrome P450 2C9 (CYP2C9), largely responsible for the metabolism of warfarin, also contribute to such variability. 15
Is Fondaparinux a direct inhibitor of FXA?
After the results with the parenteral fondaparinux, proving the concept of the antithrombotic effect due to FXa inhibition, a number of oral FXa inhibitors have entered clinical development. These agents, having a molecular weight of approximately 500Da, are direct inhibitors of FXa, as they do not require a plasma co-factor for their action, and are selective for FXa, as their Ki is at least 5,000 times lower than that for any other serine protease. The direct inhibitors of FXa are inhibitors of the catalytic site of this important coagulation factor. It has been shown that the direct inhibitors of FXa can inhibit FXa both in the fluid phase and in the context of the prothrombinase complex. The clinical relevance of this biochemical feature is unclear.
What is the bleed rate for dabigatran?
Major bleeding occurred less frequently with dabigatran 110 mg, and rates of major bleeding were similar with dabigatran 150 mg and warfarin: major bleeding occurred at a rate of 3.36 % per year in patients taking warfarin, 3.11 % per year in patients taking high-dose dabigatran (RR 0.93, 95 % CI 0.81–1.07, p=0.031 versus warfarin) and 2.71 % in patients taking low-dose dabigatran (RR 0.8, 95 % CI 0.69–0.93, p=0.003 versus warfarin). Both doses of dabigatran were associated with a significantly reduced risk of haemorrhagic stroke and intracranial haemorrhage when compared with warfarin.
What are the risk factors for CHA2DS2 VASC?
Table 1outlines the risk factors that make up the CHA2DS2-VASc score. Congestive heart failure is defined as left ventricular ejection fraction ≤40 %. Hypertension is defined as blood pressure consistently above 140/90 mmHg or treated hypertension on medication. Vascular disease is defined as previous myocardial infarction, peripheral arterial disease or aortic plaque.
How long does it take for a syringe to reach therapeutic levels?
Slow onset and offset of action, requiring 3–6 days to reach therapeutic levels
What does TIA mean in risk factor?
The name of the score is derived from the first letter of each risk factor. TIA = transient ischaemic attack.
How many people will have AF by 2050?
AF is a growing clinical problem owing to the ageing population, and the advances in treatment and improved survival of patients with cardiac disorders such as ischaemic heart disease and heart failure, which predispose to AF.4It is estimated that, by 2050, up to 16 million people in the US will suffer from AF,5which is already the commonest arrhythmia encountered in clinical practice.6The healthcare costs are substantial and AF accounts for 1 % of the National Health Service expenditure in the UK.7
Is rivaroxaban a factor XA inhibitor?
Rivaroxaban is an oral, reversible, direct factor Xa inhibitor. 43Although its half-life is 7–12 hours, factor Xa is inhibited for up to 24 hours. This permits once-daily dosing, which is in contrast with the other novel oral anticoagulants. ROCKET-AF (An efficacy and safety study of rivaroxaban with warfarin for the prevention of stroke and non-central nervous system systemic embolism in patients with non-valvular atrial fibrillation) was a Phase III, randomised, double-blind, non-inferiority trial comparing rivaroxaban (20 mg once daily or 15 mg once daily in patients with moderate renal impairment) with warfarin (INR 2.5) in over 14,000 patients with non-valvular AF and a history of stroke, transient ischaemic attack (TIA) or non-central nervous system embolism or at least two independent risk factors for future stroke.44Rivaroxaban was similar to warfarin for the primary endpoint of stroke or systemic embolism (event rate 1.71 % per 100 patient years with rivaroxaban versus 2.16 % with warfarin; hazard ratio [HR] 0.79, 95 % CI 0.66–0.96, p<0.001 for non-inferiority).
Is AF a prothrombotic disease?
Atrial fibrillation (AF) leads to a prothrombotic state1and places patients at risk of thromboembolic disease. The most common and serious complication of thromboembolism is stroke, and AF is held responsible for 25 % of all strokes.2Strokes in the context of AF are associated with a higher mortality, longer hospital stay and lower levels of independence at discharge.3These factors combine to make antithrombotic therapy the most important management consideration for AF patients.