Atrial fibrillation anticoagulation: Difference between revisions

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(/* Preventing Thromboembolism (DO NOT EDIT){{cite journal| author=Wann LS, Curtis AB, Ellenbogen KA, Estes NA, Ezekowitz MD, Jackman WM et al.| title=2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update o...)
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| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
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| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' Antithrombotic therapy to prevent [[thromboembolism]] is recommended for all patients with [[AF]], except those with lone AF or contraindications. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' Antithrombotic therapy to prevent [[thromboembolism]] is recommended for all patients with [[AF]], except those with lone AF or contraindications. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki>
|-
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| bgcolor="LightGreen"|<nowiki>"</nowiki>'''2.''' The selection of the antithrombotic agent should be based upon the absolute risks of stroke and bleeding and the relative risk and benefit for a given patient. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''2.''' The selection of the antithrombotic agent should be based upon the absolute risks of stroke and bleeding and the relative risk and benefit for a given patient. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki>
|-
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''3.''' For patients without mechanical heart valves at high risk of stroke, chronic oral anticoagulant therapy with a vitamin K antagonist is recommended in a dose adjusted to achieve the target intensity INR of 2.0 to 3.0, unless contraindicated. Factors associated with highest risk for stroke in patients with AF are prior thromboembolism (stroke, TIA, or systemic embolism) and rheumatic mitral stenosis. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''3.''' For patients without mechanical heart valves at high risk of stroke, chronic oral anticoagulant therapy with a vitamin K antagonist is recommended in a dose adjusted to achieve the target intensity INR of 2.0 to 3.0, unless contraindicated. Factors associated with highest risk for stroke in patients with AF are prior thromboembolism (stroke, TIA, or systemic embolism) and rheumatic mitral stenosis. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki>


|-
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| bgcolor="LightGreen"|<nowiki>"</nowiki>'''4.''' Anticoagulation with a vitamin K antagonist is recommended for patients with more than 1 moderate risk factor. Such factors include age 75 y or greater, hypertension, HF, impaired LV systolic function (ejection fraction 35% or less or fractional shortening less than 25%), and diabetes mellitus. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''4.''' Anticoagulation with a vitamin K antagonist is recommended for patients with more than 1 moderate risk factor. Such factors include age 75 y or greater, hypertension, HF, impaired LV systolic function (ejection fraction 35% or less or fractional shortening less than 25%), and diabetes mellitus. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki>


|-
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| bgcolor="LightGreen"|<nowiki>"</nowiki>'''5.''' INR should be determined at least weekly during initiation of therapy and monthly when stable.  ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''5.''' INR should be determined at least weekly during initiation of therapy and monthly when stable.  ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki>


|-
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| bgcolor="LightGreen"|<nowiki>"</nowiki>'''6.''' [[Aspirin]], 81–325 mg daily, is recommended in low-risk patients or in those with contraindications to oral anticoagulation. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''6.''' [[Aspirin]], 81–325 mg daily, is recommended in low-risk patients or in those with contraindications to oral anticoagulation. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki>


|-
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''7.''' For patients with [[AF]] who have mechanical heart valves, the target intensity of anticoagulation should be based on the type of prosthesis, maintaining an INR of at least 2.5. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''7.''' For patients with [[AF]] who have mechanical heart valves, the target intensity of anticoagulation should be based on the type of prosthesis, maintaining an INR of at least 2.5. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki>


|-
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''8.''' Antithrombotic therapy is recommended for patients with [[atrial flutter]] as for those with AF. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''8.''' Antithrombotic therapy is recommended for patients with [[atrial flutter]] as for those with AF. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>


|-
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| bgcolor="LightGreen"|<nowiki>"</nowiki>'''9.''' [[Dabigatran]] is useful as an alternative to [[warfarin]] for the prevention of stroke and [[systemic thromboembolism]] in patients with paroxysmal to permanent [[AF]] and risk factors for [[stroke]] or systemic [[embolization]] who do not have a [[prosthetic heart valve]] or hemodynamically significant valve disease, severe [[renal failure]] (creatinine clearance <15 mL/ min) or advanced liver disease (impaired baseline clotting function). ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]]) <nowiki>"</nowiki>
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''9.''' [[Dabigatran]] is useful as an alternative to [[warfarin]] for the prevention of stroke and [[systemic thromboembolism]] in patients with paroxysmal to permanent [[AF]] and risk factors for [[stroke]] or systemic [[embolization]] who do not have a [[prosthetic heart valve]] or hemodynamically significant valve disease, severe [[renal failure]] (creatinine clearance <15 mL/ min) or advanced liver disease (impaired baseline clotting function). ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki>
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|colspan="1" style="text-align:center; background:LightCoral"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class III]]
|colspan="1" style="text-align:center; background:LightCoral"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class III]]
|-
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|bgcolor="LightCoral"|<nowiki>"</nowiki>'''1.''' Long-term anticoagulation is not recommended for primary stroke prevention in patients below age 60 years without heart disease (lone AF).([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>
|bgcolor="LightCoral"|<nowiki>"</nowiki>'''1.''' Long-term anticoagulation is not recommended for primary stroke prevention in patients below age 60 years without heart disease (lone AF). ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>
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|-
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|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' For primary prevention of thromboembolism in patients with nonvalvular AF who have just 1 of the following validated risk factors, antithrombotic therapy with either aspirin or a vitamin K antagonist is reasonable, based upon an assessment of the risk of bleeding complications, ability to safely sustain adjusted chronic anticoagulation, and patient preferences: age greater than or equal to 75 y (especially in female patients), hypertension, HF, impaired LV function, or diabetes mellitus. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' For primary prevention of thromboembolism in patients with nonvalvular AF who have just 1 of the following validated risk factors, antithrombotic therapy with either aspirin or a vitamin K antagonist is reasonable, based upon an assessment of the risk of bleeding complications, ability to safely sustain adjusted chronic anticoagulation, and patient preferences: age greater than or equal to 75 y (especially in female patients), hypertension, HF, impaired LV function, or diabetes mellitus. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki>


|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''2.''' For patients with nonvalvular AF who have 1 or more of the following less well-validated risk factors, antithrombotic therapy with either aspirin or a vitamin K antagonist is reasonable for prevention of thromboembolism: age 65 to 74 y, female gender, or CAD. The choice of agent should be based upon the risk of bleeding complications, ability to safely sustain adjusted chronic anticoagulation, and patient preferences. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''2.''' For patients with nonvalvular AF who have 1 or more of the following less well-validated risk factors, antithrombotic therapy with either aspirin or a vitamin K antagonist is reasonable for prevention of thromboembolism: age 65 to 74 y, female gender, or CAD. The choice of agent should be based upon the risk of bleeding complications, ability to safely sustain adjusted chronic anticoagulation, and patient preferences. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki>


|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''3.''' It is reasonable to select antithrombotic therapy using the same criteria irrespective of the pattern (paroxysmal, persistent, or permanent) of AF. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''3.''' It is reasonable to select antithrombotic therapy using the same criteria irrespective of the pattern (paroxysmal, persistent, or permanent) of AF. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki>


|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''4.''' In patients with AF without a mechanical heart valve, it is reasonable to interrupt anticoagulation for up to 1 wk for procedures that carry a risk of bleeding. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''4.''' In patients with AF without a mechanical heart valve, it is reasonable to interrupt anticoagulation for up to 1 wk for procedures that carry a risk of bleeding. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>


|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''5.''' It is reasonable to re-evaluate the need for anticoagulation at regular intervals. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''5.''' It is reasonable to re-evaluate the need for anticoagulation at regular intervals. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>
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|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' In patients 75 years of age and older at risk of bleeding but without contraindications to anticoagulant therapy, and in patients who are unable to safely tolerate standard anticoagulation (INR 2.0 to 3.0), a lower INR target (2.0;
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' In patients 75 years of age and older at risk of bleeding but without contraindications to anticoagulant therapy, and in patients who are unable to safely tolerate standard anticoagulation (INR 2.0 to 3.0), a lower INR target (2.0;
range 1.6 to 2.5) may be considered for primary prevention of stroke and systemic embolism. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
range 1.6 to 2.5) may be considered for primary prevention of stroke and systemic embolism. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>


|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''2.''' When surgical procedures require interruption of oral anticoagulant therapy for longer than 1 wk in high-risk patients, unfractionated heparin may be administered or low-molecular-weight heparin given by subcutaneous injection, although the efficacy of these alternatives in this situation is uncertain. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''2.''' When surgical procedures require interruption of oral anticoagulant therapy for longer than 1 wk in high-risk patients, unfractionated heparin may be administered or low-molecular-weight heparin given by subcutaneous injection, although the efficacy of these alternatives in this situation is uncertain. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>


|-
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|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''3.''' Following percutaneous coronary intervention or revascularization surgery in patients with AF, low-dose aspirin (less than 100 mg per d) and/or clopidogrel (75 mg per d) may be given concurrently with anticoagulation to prevent myocardial ischemic events, but these strategies have not been thoroughly evaluated and are associated with an increased risk of bleeding. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''3.''' Following percutaneous coronary intervention or revascularization surgery in patients with AF, low-dose aspirin (less than 100 mg per d) and/or clopidogrel (75 mg per d) may be given concurrently with anticoagulation to prevent myocardial ischemic events, but these strategies have not been thoroughly evaluated and are associated with an increased risk of bleeding. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>


|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''4.''' In patients undergoing percutaneous coronary intervention, anticoagulation may be interrupted to prevent bleeding at the site of peripheral arterial puncture, but the vitamin K antagonist should be resumed as soon as possible after the procedure and the dose adjusted to achieve an INR in the therapeutic range. Aspirin may be given temporarily during the hiatus, but the maintenance regimen should then consist of the combination of clopidogrel, 75 mg daily, plus warfarin (INR 2.0 to 3.0). Clopidogrel should be given for a minimum of 1 mo after implantation of a bare metal stent, at least 3 mo for a sirolimus-eluting stent, at least 6 mo for a paclitaxel-eluting stent, and 12 mo or longer in selected patients, following which warfarin may be continued as monotherapy in the absence of a subsequent coronary event. When warfarin is given in combination with clopidogrel or low-dose aspirin, the dose intensity must be carefully regulated. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''4.''' In patients undergoing percutaneous coronary intervention, anticoagulation may be interrupted to prevent bleeding at the site of peripheral arterial puncture, but the vitamin K antagonist should be resumed as soon as possible after the procedure and the dose adjusted to achieve an INR in the therapeutic range. Aspirin may be given temporarily during the hiatus, but the maintenance regimen should then consist of the combination of clopidogrel, 75 mg daily, plus warfarin (INR 2.0 to 3.0). Clopidogrel should be given for a minimum of 1 mo after implantation of a bare metal stent, at least 3 mo for a sirolimus-eluting stent, at least 6 mo for a paclitaxel-eluting stent, and 12 mo or longer in selected patients, following which warfarin may be continued as monotherapy in the absence of a subsequent coronary event. When warfarin is given in combination with clopidogrel or low-dose aspirin, the dose intensity must be carefully regulated. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>


|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''5.''' In patients with AF younger than 60 y without heart disease or risk factors for thromboembolism (lone AF), the risk of thromboembolism is low without treatment and the effectiveness of aspirin for primary prevention of stroke relative to the risk of bleeding has not been established. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''5.''' In patients with AF younger than 60 y without heart disease or risk factors for thromboembolism (lone AF), the risk of thromboembolism is low without treatment and the effectiveness of aspirin for primary prevention of stroke relative to the risk of bleeding has not been established. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki>
|-
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''6.''' In patients with AF who sustain ischemic stroke or systemic embolism during treatment with low-intensity anticoagulation (INR 2.0 to 3.0), rather than add an antiplatelet agent, it may be reasonable to raise the intensity of anticoagulation to a maximum target INR of 3.0 to 3.5. ([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]]) <nowiki>"</nowiki>
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''6.''' In patients with AF who sustain ischemic stroke or systemic embolism during treatment with low-intensity anticoagulation (INR 2.0 to 3.0), rather than add an antiplatelet agent, it may be reasonable to raise the intensity of anticoagulation to a maximum target INR of 3.0 to 3.5. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki>
|}
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Revision as of 18:04, 2 November 2012

Conduction
Sinus rhythm
Atrial fibrillation
'
ICD-10 I48
ICD-9 427.31
DiseasesDB 1065
MedlinePlus 000184

Atrial Fibrillation Microchapters

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Atrial fibrillation anticoagulation On the Web

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Risk calculators and risk factors for Atrial fibrillation anticoagulation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Synonyms and keywords: AF; Afib; fib

Overview

Oral anticoagulation is a mainstay of atrial fibrillation management. For both primary and secondary prevention of stroke, there is a 61% relative risks reduction in the incidence of all cause stroke (both ischemic and hemorrhagic) associated with adjusted-dose oral anticoagulation.[1]

Increasing patient age (which is associated with smaller body weight, female gender and a progressive decline in renal function) and higher INRs or greater intensity of anticoagulation are both associated with a higher risk of major bleeding. This is critical in so far as bleeding is in turn associated with non-compliance with pharmacotherapy. [1][2][3] [1][4] Given that many patients with atrial fibrillation are elderly, there is often a narrow therapeutic window in achieving the optimal INR. The optimal INR should obviously maximize efficacy in reducing the risk of stroke and simultaneously minimize the risk of bleeding. In the setting of atrial fibrillation, an INR of 2 to 3 appears to be optimal. INRs lower than this, such as those in the range of 1.6 to 2.5, are associated with efficacy that is only 80% of that in the target range.[5][6] [7][8]

Based upon the RE-LY study, dabigatran was recently approved for the treatment of non-valvular atrial fibrillation.

Interruption of anticoagulation with coumadin

No mechanical valve, high risk of bleeding with procedure: Coumadin can be discontinued for one week without heparin bridging.

Presence of mechanical valve, patients with AF who are at high risk of stroke, or patients in whom Coumadin must be interrupted for over a week: These patients should be administered either unfractionated heparin or low molecular weight heparin.

Investigational antithrombin agents

Warfarin inhibits multiple factors in the anticoagulation cascade, and dabigatran is a direct thrombin (Factor 2) inhibitor. Newer agents that inhibit factor Xa are under investigation for the anticoagulation of patients with non-valvular atrial fibrillation. These agents include apixaban which is being evaluated in the Aristotle trial, edoxaban which is being evaluated in the Engage trial and rivaroxaban which was evaluated in the Rocket AF program. Slides from the Rocket-AF program can be downloaded here. A comparison of the RE-LY and Rocket AF trials can be found here.

Antiplatelet therapy for atrial fibrillation

Aspirin Monotherapy

Aspirin monotherapy is associated with only a modest and inconsistent reduction in the risk of stroke associated with atrial fibrillation. [8]

[9] Studies suggest that the efficacy of aspirin may be greater in patients with hypertension or diabetes. Aspirin may also be more efficacious in reducing the risk of non cardioembolic stroke as opposed to the more disabling cardioembolic form of stroke. [10][11]

Dual Antiplatelet therapy

Among patients who are not deemed candidates for Coumadin therapy (estimated to be approximately 40-50% of patients), dual antiplatelet therapy with both aspirin and clopidogrel (at a maintenance dose of 75 mg/day) was superior to aspirin monotherapy in the ACTIVE A trial. The primary endpoint of the trial was the composite of stroke, myocardial infarction, non–central nervous system systemic embolism, or death from vascular causes. After a median of 3.6 years of follow-up in 7,554 randomized patients, the addition of clopidogrel to aspirin alone yielded a reduction in events from 7.6% to 6.8% (relative risk reduction with clopidogrel, 0.89; 95% confidence interval [CI], 0.81 to 0.98; P=0.01). The addition of clopidogrel to aspirin alone reduced the risk of stroke by 28% (from 3.3% to 2.4%, p<0.001) and reduced the risk of MI by 22% (from 0.9% per year to 0.7% per year, p=0.08). The risk of major bleeding among patients treated with aspirin and clopidogrel was 2.0% per year whereas it was 1.3% per year among patients treated with aspirin alone (relative risk, 1.57; 95% CI, 1.29 to 1.92; P<0.001). If 1000 patients were treated for 3 years, the combination of aspirin plus clopidogrel would prevent 28 strokes (17 disabling or fatal), and 6 myocardial infarctions, at a cost of 20 major bleeds compared to aspirin alone.

2010 ACCF/ACG/AHA Expert Consensus Document on the Concomitant Use of Proton Pump Inhibitors and Thienopyridines- Summary of Findings and Consensus Recommendations[12] (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.
 ”

Oral Anticoagulation (Coumadin) versus Dual Antiplatelet Therapy (ASA/Clopidogrel)

In the ACTIVE W trial, dual antiplatelet therapy with aspirin(75-100 mg per day) and clopidogrel (75 mg per day) was found to be statistically inferior to coumadin therapy (target INR 2.0 to 3.0) in the management of patients with atrial fibrillation who had one or more risk factors for stroke[13]. The primary endpoint of ACTIVE W was the first occurrence of stroke, non-CNS systemic embolus, myocardial infarction, or vascular death. The annual risk in the coumadin group was 3.93% per year, and in the Aspirin/Clopidogrel group it was 5.60% per year yielding a relative risk of 1.44 (1.18-1.76; p=0.0003). The efficacy was not as great among patients who were coumadin naive, although the p-value for the interaction was negative. There was no excess bleeding among patients treated with coumadin, and in fact there was an excess of minor bleeds among patients treated with ASA and clopidogrel (13.6% / yr vs 11.5% year, p=0.0009).

When examining the data from atrial fibrillation trials, it is critical to evaluate the results in patients who were previously treated with coumadin separate from those patients who were naive to coumadin. Patients previously treated with coumadin are likely to be those patients who best tolerate coumadin and have passed their "bleeding stress test" and have a lower rate of bleeding on coumadin. Those patients who bleed while on coumadin have already been culled out from the population. When the data in ACTIVE W were evaluated including only those patients previously treated with coumadin(again a population to be anticipated to be at low risk of bleeding), the risk of major bleeding was indeed statistically significantly lower among patients previously treated with coumadin (p=0.03) than patients not previously treated.

The majority of the reduction in events was due to a reduction in stroke and non-CNS emolization associated with [[coumadin therapy. The pathophysiology of stroke among patients with atrial fibrillation is thought to be embolization from clot in the left atrium. The data from ACTIVE W suggest that platelet activation and its treatment may not play a pivotal role in the treatment of mural thrombus and embolization in atrial fibrillation. Coumadin was more effective in the reduction of non-disabling stroke rather than disabling stroke. There were more fatal hemorrhagic strokes (which may more often be fatal), and this may explain in part why coumadin was not associated with a reduction in mortality in the study.

While clopidogrel plus aspirin has been found to reduce the risk of recurrent myocardial infarction among patients with presumed plaque rupture and acute coronary syndromes, it is notable in ACTIVE W that the risk of myocardial infarction tended to be higher among patients treated with aspirin plus clopidogrel versus coumadin (0.86% vs 0.55%,p=0.09)[14].

2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation (DO NOT EDIT)[15]

Preventing Thromboembolism (DO NOT EDIT)[15]

Class I
"1. Antithrombotic therapy to prevent thromboembolism is recommended for all patients with AF, except those with lone AF or contraindications. (Level of Evidence: A) "
"2. The selection of the antithrombotic agent should be based upon the absolute risks of stroke and bleeding and the relative risk and benefit for a given patient. (Level of Evidence: A) "
"3. For patients without mechanical heart valves at high risk of stroke, chronic oral anticoagulant therapy with a vitamin K antagonist is recommended in a dose adjusted to achieve the target intensity INR of 2.0 to 3.0, unless contraindicated. Factors associated with highest risk for stroke in patients with AF are prior thromboembolism (stroke, TIA, or systemic embolism) and rheumatic mitral stenosis. (Level of Evidence: A) "
"4. Anticoagulation with a vitamin K antagonist is recommended for patients with more than 1 moderate risk factor. Such factors include age 75 y or greater, hypertension, HF, impaired LV systolic function (ejection fraction 35% or less or fractional shortening less than 25%), and diabetes mellitus. (Level of Evidence: A) "
"5. INR should be determined at least weekly during initiation of therapy and monthly when stable. (Level of Evidence: A) "
"6. Aspirin, 81–325 mg daily, is recommended in low-risk patients or in those with contraindications to oral anticoagulation. (Level of Evidence: A) "
"7. For patients with AF who have mechanical heart valves, the target intensity of anticoagulation should be based on the type of prosthesis, maintaining an INR of at least 2.5. (Level of Evidence: B) "
"8. Antithrombotic therapy is recommended for patients with atrial flutter as for those with AF. (Level of Evidence: C) "
"9. Dabigatran is useful as an alternative to warfarin for the prevention of stroke and systemic thromboembolism in patients with paroxysmal to permanent AF and risk factors for stroke or systemic embolization who do not have a prosthetic heart valve or hemodynamically significant valve disease, severe renal failure (creatinine clearance <15 mL/ min) or advanced liver disease (impaired baseline clotting function). (Level of Evidence: B) "
Class III
"1. Long-term anticoagulation is not recommended for primary stroke prevention in patients below age 60 years without heart disease (lone AF). (Level of Evidence: C) "
Class IIa
"1. For primary prevention of thromboembolism in patients with nonvalvular AF who have just 1 of the following validated risk factors, antithrombotic therapy with either aspirin or a vitamin K antagonist is reasonable, based upon an assessment of the risk of bleeding complications, ability to safely sustain adjusted chronic anticoagulation, and patient preferences: age greater than or equal to 75 y (especially in female patients), hypertension, HF, impaired LV function, or diabetes mellitus. (Level of Evidence: A) "
"2. For patients with nonvalvular AF who have 1 or more of the following less well-validated risk factors, antithrombotic therapy with either aspirin or a vitamin K antagonist is reasonable for prevention of thromboembolism: age 65 to 74 y, female gender, or CAD. The choice of agent should be based upon the risk of bleeding complications, ability to safely sustain adjusted chronic anticoagulation, and patient preferences. (Level of Evidence: B) "
"3. It is reasonable to select antithrombotic therapy using the same criteria irrespective of the pattern (paroxysmal, persistent, or permanent) of AF. (Level of Evidence: B) "
"4. In patients with AF without a mechanical heart valve, it is reasonable to interrupt anticoagulation for up to 1 wk for procedures that carry a risk of bleeding. (Level of Evidence: C) "
"5. It is reasonable to re-evaluate the need for anticoagulation at regular intervals. (Level of Evidence: C) "
Class IIb
"1. In patients 75 years of age and older at risk of bleeding but without contraindications to anticoagulant therapy, and in patients who are unable to safely tolerate standard anticoagulation (INR 2.0 to 3.0), a lower INR target (2.0;

range 1.6 to 2.5) may be considered for primary prevention of stroke and systemic embolism. (Level of Evidence: C) "

"2. When surgical procedures require interruption of oral anticoagulant therapy for longer than 1 wk in high-risk patients, unfractionated heparin may be administered or low-molecular-weight heparin given by subcutaneous injection, although the efficacy of these alternatives in this situation is uncertain. (Level of Evidence: C) "
"3. Following percutaneous coronary intervention or revascularization surgery in patients with AF, low-dose aspirin (less than 100 mg per d) and/or clopidogrel (75 mg per d) may be given concurrently with anticoagulation to prevent myocardial ischemic events, but these strategies have not been thoroughly evaluated and are associated with an increased risk of bleeding. (Level of Evidence: C) "
"4. In patients undergoing percutaneous coronary intervention, anticoagulation may be interrupted to prevent bleeding at the site of peripheral arterial puncture, but the vitamin K antagonist should be resumed as soon as possible after the procedure and the dose adjusted to achieve an INR in the therapeutic range. Aspirin may be given temporarily during the hiatus, but the maintenance regimen should then consist of the combination of clopidogrel, 75 mg daily, plus warfarin (INR 2.0 to 3.0). Clopidogrel should be given for a minimum of 1 mo after implantation of a bare metal stent, at least 3 mo for a sirolimus-eluting stent, at least 6 mo for a paclitaxel-eluting stent, and 12 mo or longer in selected patients, following which warfarin may be continued as monotherapy in the absence of a subsequent coronary event. When warfarin is given in combination with clopidogrel or low-dose aspirin, the dose intensity must be carefully regulated. (Level of Evidence: C) "
"5. In patients with AF younger than 60 y without heart disease or risk factors for thromboembolism (lone AF), the risk of thromboembolism is low without treatment and the effectiveness of aspirin for primary prevention of stroke relative to the risk of bleeding has not been established. (Level of Evidence: C) "
"6. In patients with AF who sustain ischemic stroke or systemic embolism during treatment with low-intensity anticoagulation (INR 2.0 to 3.0), rather than add an antiplatelet agent, it may be reasonable to raise the intensity of anticoagulation to a maximum target INR of 3.0 to 3.5. (Level of Evidence: B) "

Combining Anticoagulant With Antiplatelet Therapy (DO NOT EDIT) [16]

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) "

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Guideline Resources

References

  1. ↑ 1.0 1.1 1.2 Hart RG, Benavente O, McBride R, Pearce LA (1999). "Antithrombotic therapy to prevent stroke in patients with atrial fibrillation: a meta-analysis". Ann. Intern. Med. 131 (7): 492–501. Unknown parameter |month= ignored (help)
  2. ↑ Gorter JW (1999). "Major bleeding during anticoagulation after cerebral ischemia: patterns and risk factors. Stroke Prevention In Reversible Ischemia Trial (SPIRIT). European Atrial Fibrillation Trial (EAFT) study groups". Neurology. 53 (6): 1319–27. PMID 10522891. Unknown parameter |month= ignored (help)
  3. ↑ Hylek EM, Singer DE (1994). "Risk factors for intracranial hemorrhage in outpatients taking warfarin". Ann. Intern. Med. 120 (11): 897–902. PMID 8172435. Unknown parameter |month= ignored (help)
  4. ↑ Hart RG, Halperin JL (1999). "Atrial fibrillation and thromboembolism: a decade of progress in stroke prevention". Ann. Intern. Med. 131 (9): 688–95. PMID 10577332. Unknown parameter |month= ignored (help)
  5. ↑ Hylek EM, Skates SJ, Sheehan MA, Singer DE (1996). "An analysis of the lowest effective intensity of prophylactic anticoagulation for patients with nonrheumatic atrial fibrillation". N. Engl. J. Med. 335 (8): 540–6. PMID 8678931. Unknown parameter |month= ignored (help)
  6. ↑ "Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation: Stroke Prevention in Atrial Fibrillation III randomised clinical trial". Lancet. 348 (9028): 633–8. 1996. PMID 8782752. Unknown parameter |month= ignored (help)
  7. ↑ "Optimal oral anticoagulant therapy in patients with nonrheumatic atrial fibrillation and recent cerebral ischemia. The European Atrial Fibrillation Trial Study Group". N. Engl. J. Med. 333 (1): 5–10. 1995. PMID 7776995. Unknown parameter |month= ignored (help)
  8. ↑ 8.0 8.1 Hart RG (1998). "Intensity of anticoagulation to prevent stroke in patients with atrial fibrillation". Ann. Intern. Med. 128 (5): 408. PMID 9490603. Unknown parameter |month= ignored (help)
  9. ↑ "The efficacy of aspirin in patients with atrial fibrillation. Analysis of pooled data from 3 randomized trials. The Atrial Fibrillation Investigators". Arch. Intern. Med. 157 (11): 1237–40. 1997. PMID 9183235. Unknown parameter |month= ignored (help)
  10. ↑ Miller VT, Rothrock JF, Pearce LA, Feinberg WM, Hart RG, Anderson DC (1993). "Ischemic stroke in patients with atrial fibrillation: effect of aspirin according to stroke mechanism. Stroke Prevention in Atrial Fibrillation Investigators". Neurology. 43 (1): 32–6. PMID 8423907. Unknown parameter |month= ignored (help)
  11. ↑ Hart RG, Pearce LA, Miller VT; et al. (2000). "Cardioembolic vs. noncardioembolic strokes in atrial fibrillation: frequency and effect of antithrombotic agents in the stroke prevention in atrial fibrillation studies". Cerebrovasc. Dis. 10 (1): 39–43. PMID 10629345.
  12. ↑ 12.0 12.1 Abraham NS, Hlatky MA, Antman EM, Bhatt DL, Bjorkman DJ, Clark CB; et al. (2010). "ACCF/ACG/AHA 2010 Expert Consensus Document on the concomitant use of proton pump inhibitors and thienopyridines: a focused update of the ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents". Circulation. 122 (24): 2619–33. doi:10.1161/CIR.0b013e318202f701. PMID 21060077.
  13. ↑ The ACTIVE Writing Group on behalf of the ACTIVE Investigators. Lancet 2006;367:1903-12.
  14. ↑ The ACTIVE Writing Group on behalf of the ACTIVE Investigators. Lancet 2006;367:1903-12.
  15. ↑ 15.0 15.1 Wann LS, Curtis AB, Ellenbogen KA, Estes NA, Ezekowitz MD, Jackman WM; et al. (2011). "2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on Dabigatran): a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines". Circulation. 123 (10): 1144–50. doi:10.1161/CIR.0b013e31820f14c0. PMID 21321155.
  16. ↑ ACTIVE Investigators. Connolly SJ, Pogue J, Hart RG, Hohnloser SH, Pfeffer M; et al. (2009). "Effect of clopidogrel added to aspirin in patients with atrial fibrillation". N Engl J Med. 360 (20): 2066–78. doi:10.1056/NEJMoa0901301. PMID 19336502. Review in: Ann Intern Med. 2009 Sep 15;151(6):JC3-8
  17. ↑ Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA et al. (2006) ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation 114 (7):e257-354. DOI:10.1161/CIRCULATIONAHA.106.177292 PMID: 16908781
  18. ↑ Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA et al. (2011) 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 123 (10):e269-367. DOI:10.1161/CIR.0b013e318214876d PMID: 21382897
  19. ↑ Estes NA, Halperin JL, Calkins H, Ezekowitz MD, Gitman P, Go AS et al. (2008) ACC/AHA/Physician Consortium 2008 clinical performance measures for adults with nonvalvular atrial fibrillation or atrial flutter: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures and the Physician Consortium for Performance Improvement (Writing Committee to Develop Clinical Performance Measures for Atrial Fibrillation): developed in collaboration with the Heart Rhythm Society. Circulation 117 (8):1101-20. DOI:10.1161/CIRCULATIONAHA.107.187192 PMID: 18283199

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