Atrial fibrillation anticoagulation

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anahita Deylamsalehi, M.D.[2]Cafer Zorkun, M.D., Ph.D. [3] George Leef, MD; Arzu Kalayci, M.D. [4], Syed Hassan A. Kazmi BSc, MD [5]; Sabawoon Mirwais, M.B.B.S, M.D.[6]

Overview

Oral anticoagulation is used to prevent stroke and systemic embolization and is considered a mainstay of atrial fibrillation management. Anticoagulation is recommended for atrial fibrillation (AF) patients who are at high risk for stroke based on CHADS2-VASc score who do not have an unacceptable risk of bleeding (HAS-BLED score). Treatment with anticoagulation can be done with warfarin, or one of the novel oral anticoagulants (NOACs). Four novel oral anticoagulants (NOACs) have been approved for use in nonvalvular atrial fibrillation (AF) as alternatives to warfarin. Anti-platelet therapy is not recommended for stroke reduction in atrial fibrillation (AF).

Atrial fibrillation anticoagulation

Anticoagulation therapy is a critical part of treatment in patients with atrial fibrillation who have considerable stroke risk. The treatment is focused on decreasing the risk of thrombosis formation without increasing the risk of bleeding. To measure both risks there are two scores, explained below; CHADS2-VASc and ORBIT. Without proper anticoagulation treatment, rate of death due to stroke will be high among atrial fibrillation patients.[1][2]

CHADS2-VASc score

For more information regards CHA2DS2-VASc Score click here
For more information regards CHA2DS2-VASc Score click here


 
 
 
 
 
 
 
 
Calculate the CHA2DS2-VASc score
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
CHA2DS2-VASc score > 2
 
 
 
 
CHA2DS2-VASc score of 1 in males
 
 
 
 
CHA2DS2-VASc score of 1 in females OR CHA2DS2-VASc score of zero
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Offer oral anticoagulant
 
 
 
 
Consider direct oral anticoagulant
In the presence of any contraindications or when direct oral anticoagulant is not tolerated vitamin K antagonist should be considered
 
 
 
 
Treatment with an anticoagulant is not required.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Follow up these patients again (at age 65 and 75 or when diabetes, stroke or other vascular diseases develop)
 
 
 

ORBIT Bleeding Risk Score


Factores Scores
Male patients with hemoglobin lower than <13 mg/dL or hematocrit <40% Yes: +2
No: 0
Female patients with hemoglobin lower than <12 mg/dL or hematocrit <36% Yes: +2
No: 0
Age Younger than 74 : 0
Older than 74 : +1
History of previous bleeding (such as hemorrhagic stroke, gastrointestinal bleeding and intracranial hemorrhage) Yes: +2
No: 0
GFR <60 mL/min/1.73 m2 Yes: +1
No: 0
Antiplatelet treatment Yes: +1
No: 0


The ORBIT Score Interpretation
Score Interpretation
Lower than 2 Low risk
3 Medium risk
Higher than 4 High risk


Anticoagulation Treatment Summary for Acute Atrial Fibrillation - NICE Guideline

  • The following algorithm is a summary of acute atrial fibrillation management, based on NICE guideline 2021:[4]
 
 
 
 
 
 
 
 
 
Acute Atrial Fibrillation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
New-onset atrial fibrillation
 
Previously diagnosed AF with shorter than 48 hours onset
 
 
New-onset atrial fibrillation with unknown time of onset
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Offer heparin in the absence of contraindications
 
Offer oral anticoagulation if:
There is high chance of AF recurrence (such as previous history of unsuccessful cardioversion, structural heart disease and long-lasting AF (>12 months))
Unsuccessful sinus rhythm restoration within 48 hours of AF onset
Access stroke and bleeding risk to evaluate risks and benefits
 
 
Offer oral anticoagulation after assessing the risk and benefits of anticoagulation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Heparin must be continued until proper risk assessment for bleeding and stroke, then it should be replaced with a proper antithrombotic therapy
 
 
 
 
 
 
 

Anticoagulation Options

Warfarin

Novel Oral Anticoagulants

Antiplatelet Therapy for Atrial Fibrillation (not recommended)

Aspirin Monotherapy

Dual Antiplatelet Therapy

Anticoagulation in end stage renal disease

Anticoagulation Reassessment

Based on NICE guideline updated in 2021 the following are indications for reassessing the anticoagulation treatment in the patients who are under treatment:[4]

  • If there are 2 INR measures higher than 5 or only one INR measure higher than 8 within the last 6 months
  • If there are 2 INR measures lower than 1.5 within the last 6 months
  • Time in therapeutic range (TTR) lower than 65%

In order to have a safe anticoagulation treatment, NICE guideline recommends to evaluate the following factors when anticoagulation reassessment is considered:[4]

Interruption of Anticoagulation

2019 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline


Class of Recommendation Recommendation Comment/Rationale
I
IIa
IIb
III

2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease (VHD)

Recommendation for Anticoagulation for Atrial Fibrillation (AF) in Patients with VHD

COR LOE RECOMMENDATION COMMENT/RATIONALE
I B-NR Anticoagulation with a vitamin K antagonist (VKA) is indicated for patients with rheumatic mitral stenosis (MS) and AF. MODIFIED: VKA as opposed to the direct oral anticoagulants (DOACs) are indicated in patients with AF and rheumatic MS to prevent thromboembolic events. The RCTs of DOACs versus VKA have not included patients with MS. The specific recommendation for anticoagulation of patients with MS is contained in a subsection of the topic on anticoagulation.
I C-LD Anticoagulation is indicated in patients with AF and a CHA2DS2-VASc score of 2 or greater with native aortic valve disease, tricuspid valve disease, or mitral regurgitation. NEW: Post hoc subgroup analyses of large RCTs comparing DOAC versus warfarin in patients with AF have analyzed patients with native valve disease other than MS and patients who have undergone cardiac surgery. These analyses consistently demonstrated that the risk of stroke is similar to or higher than that of patients without VHD. Thus, the indication for anticoagulation in these patients should follow Guideline Determined Medical Therapy (GDMT) according to the CHA2DS2-VASc score.
IIa C-LD It is reasonable to use a DOAC as an alternative to a VKA in patients with AF and native aortic valve disease, tricuspid valve disease, or MR and a CHA2DS2-VASc score of 2 or greater. NEW: Several thousand patients with native VHD (exclusive of more than mild rheumatic MS) have been evaluated in RCTs comparing DOACs versus warfarin. Subgroup analyses have demonstrated that DOACs, when compared with warfarin, appear as effective and safe in patients with VHD as in those without VHD.

2017 ESC/EACTS Guidelines for the Management of Atrial Fibrillation in Patients With Valvular Heart Disease (VHD)

Recommendations Class of

Recommendation

Level of

Evidence

Anticoagulation
NOACs should be considered as an alternative to VKAs in patients with aortic stenosis, aortic regurgitation and mitral regurgitation presenting with atrial fibrillation[28] IIa B
NOACs should be considered as an alternative to VKAs after the third month of implantation in patients who have atrial fibrillation associated with a surgical or transcatheter aortic valve bioprosthesis IIa C
The use of NOACs is not recommended in patients with atrial fibrillation and moderate to severe mitral stenosis III C
NOACS are contraindicated in patients with a mechanical valve[29] III B
Surgical Interventions
Surgical ablation of atrial fibrillation should be considered in patients with symptomatic atrial fibrillation who undergo valve surgery[30] IIa A
Surgical ablation of atrial fibrillation may be considered in patients with asymptomatic atrial fibrillation who undergo valve surgery, if feasible, with minimal risk IIb C
Surgical excision or external clipping of the LA appendage may be considered in patients undergoing valve surgery[31] IIb B
  • LA = left atrial
  • NOAC = non-vitamin K antagonist oral anticoagulant
  • VHD = valvular heart disease
  • VKA = vitamin K antagonist

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation (DO NOT EDIT)[3]

Prevention of Thromboembolism

Risk-Based Antithrombotic Therapy

Template:Seealso

Class I
"1. In patients with AF, antithrombotic therapy should be individualized based on shared decision-making after discussion of the absolute and RRs of stroke and bleeding, and the patient’s values and preferences. (Level of Evidence: C) "
"2. Selection of antithrombotic therapy should be based on the risk of thromboembolism irrespective of whether the AF pattern is paroxysmal, persistent, or permanent. (Level of Evidence: B) "
"3. In patients with nonvalvular AF, the CHA2DS2-VASc score is recommended for assessment of stroke risk. (Level of Evidence: B) "
"4. For patients with AF who have mechanical heart valves, warfarin is recommended and the target international normalized ratio (INR) intensity (2.0 to 3.0 or 2.5 to 3.5) should be based on the type and location of the prosthesis. (Level of Evidence: B) "
"5. For patients with nonvalvular AF with prior stroke, transient ischemic attack (TIA), or a CHA2DS2-VASc score of 2 or greater, oral anticoagulants are recommended. Options include: warfarin (INR 2.0 to 3.0) (Level of Evidence: A), dabigatran (Level of Evidence: B), rivaroxaban (Level of Evidence: B), or apixaban (Level of Evidence: B)."
"6. Among patients treated with warfarin, the INR should be determined at least weekly during initiation of antithrombotic therapy and at least monthly when anticoagulation (INR in range) is stable. (Level of Evidence: A) "
"7. For patients with nonvalvular AF unable to maintain a therapeutic INR level with warfarin, use of a direct thrombin or factor Xa inhibitor (dabigatran, rivaroxaban, or apixaban) is recommended. (Level of Evidence: C) "
"8. Re-evaluation of the need for and choice of antithrombotic therapy at periodic intervals is recommended to reassess stroke and bleeding risks. (Level of Evidence: C) "
"9. Bridging therapy with unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) is recommended for patients with AF and a mechanical heart valve undergoing procedures that require interruption of warfarin. Decisions regarding bridging therapy should balance the risks of stroke and bleeding. (Level of Evidence: C) "
"10. For patients with AF without mechanical heart valves who require interruption of warfarin or newer anticoagulants for procedures, decisions about bridging therapy (LMWH or UFH) should balance the risks of stroke and bleeding and the duration of time a patient will not be anticoagulated. (Level of Evidence: C) "
"11. Renal function should be evaluated prior to initiation of direct thrombin or factor Xa inhibitors and should be re-evaluated when clinically indicated and at least annually. (Level of Evidence: B) "
"12. For patients with atrial flutter, antithrombotic therapy is recommended according to the same risk profile used for AF. (Level of Evidence: C) "
Class III: No Benefit
"1. The direct thrombin inhibitor, dabigatran, and the factor Xa inhibitor, rivaroxaban, are not recommended in patients with AF and end-stage CKD or on hemodialysis because of the lack of evidence from clinical trials regarding the balance of risks and benefits. (Level of Evidence: C) "
Class III: Harm
"1. The direct thrombin inhibitor, dabigatran, should not be used in patients with AF and a mechanical heart valve. (Level of Evidence: B) "
Class IIa
"1. For patients with nonvalvular AF and a CHA2DS2-VASc score of 0, it is reasonable to omit antithrombotic therapy. (Level of Evidence: B) "
"2. For patients with nonvalvular AF with a CHA2DS2-VASc score of 2 or greater and who have end-stage CKD (creatinine clearance [CrCl] <15 mL/min) or are on hemodialysis, it is reasonable to prescribe warfarin (INR 2.0 to 3.0) for oral anticoagulation. (Level of Evidence: B) "
Class IIb
"1. For patients with nonvalvular AF and a CHA2DS2-VASc score of 1, no antithrombotic therapy or treatment with an oral anticoagulant or aspirin may be considered. (Level of Evidence: C) "
"2. For patients with nonvalvular AF and moderate-to-severe CKD with CHA2DS2-VASc scores of 2 or greater, treatment with reduced doses of direct thrombin or factor Xa inhibitors may be considered (e.g., dabigatran, rivaroxaban, or apixaban), but safety and efficacy have not been established. (Level of Evidence: C) "
"3. In patients with AF undergoing percutaneous coronary intervention, bare-metal stents may be considered to minimize the required duration of dual antiplatelet therapy. Anticoagulation may be interrupted at the time of the procedure to reduce the risk of bleeding at the site of peripheral arterial puncture. (Level of Evidence: C) "
"4. Following coronary revascularization (percutaneous or surgical) in patients with AF and a CHA2DS2-VASc score of 2 or greater, it may be reasonable to use clopidogrel (75 mg once daily) concurrently with oral anticoagulants but without aspirin. (Level of Evidence: B) "

2011 ACCF/AHA/HRS Focused Update on the Management of Patients With Atrial Fibrillation (Updating the 2006 Guideline) (DO NOT EDIT)[32]

Combining Anticoagulant with Antiplatelet Therapy

Class IIb
"1. The addition of clopidogrel to aspirin (ASA) to reduce the risk of major vascular events, including stroke, might be considered in patients with AF in whom oral anticoagulation with warfarin is considered unsuitable due to patient preference or the physician’s assessment of the patient’s ability to safely sustain anticoagulation. (Level of Evidence: B) "

2010 ACCF/ACG/AHA Expert Consensus Document on the Concomitant Use of Proton Pump Inhibitors and Thienopyridines - Summary of Findings and Consensus Recommendations[33] (DO NOT EDIT)

  1. Clopidogrel reduces major CV events compared with placebo or aspirin.
  2. Dual antiplatelet therapy with clopidogrel and aspirin, compared with aspirin alone, reduces major CV events in patients with established ischemic heart disease, and it reduces coronary stent thrombosis but is not routinely recommended for patients with prior ischemic stroke because of the risk of bleeding.
  3. Clopidogrel alone, aspirin alone, and their combination are all associated with increased risk of GI bleeding.
  4. Patients with prior GI bleeding are at highest risk for recurrent bleeding on antiplatelet therapy. Other clinical characteristics that increase the risk of GI bleeding include advanced age; concurrent use of anticoagulants, steroids, or nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin; and Helicobacter pylori infection. The risk of GI bleeding increases as the number of risk factors increases.
  5. Use of a PPI or histamine H2 receptor antagonist (H2RA) reduces the risk of upper GI bleeding compared with no therapy. PPIs reduce upper GI bleeding to a greater degree than do H2RAs.
  6. PPIs are recommended to reduce GI bleeding among patients with a history of upper GI bleeding. PPIs are appropriate in patients with multiple risk factors for GI bleeding who require antiplatelet therapy.
  7. Routine use of either a PPI or an H2RA is not recommended for patients at lower risk of upper GI bleeding, who have much less potential to benefit from prophylactic therapy.
  8. Clinical decisions regarding concomitant use of PPIs and thienopyridines must balance overall risks and benefits, considering both CV and GI complications.
  9. Pharmacokinetic and pharmacodynamic studies, using platelet assays as surrogate endpoints, suggest that concomitant use of clopidogrel and a PPI reduces the antiplatelet effects of clopidogrel. The strongest evidence for an interaction is between omeprazole and clopidogrel. It is not established that changes in these surrogate endpoints translate into clinically meaningful differences.
  10. Observational studies and a single randomized clinical trial (RCT) have shown inconsistent effects on CV outcomes of concomitant use of thienopyridines and PPIs. A clinically important interaction cannot be excluded, particularly in certain subgroups, such as poor metabolizers of clopidogrel.
  11. The role of either pharmacogenomic testing or platelet function testing in managing therapy with thienopyridines and PPIs has not yet been established.

Sources

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