Atrial fibrillation pharmacological treatment
| Conduction | ||
Sinus rhythm  |
Atrial fibrillation  | |
| Atrial fibrillation | |
 | |
|---|---|
| The P waves, which represent depolarization of the atria, are irregular or absent during atrial fibrillation. | |
| ICD-10 | I48 |
| ICD-9 | 427.31 |
| DiseasesDB | 1065 |
| MedlinePlus | 000184 |
| eMedicine | med/184 emerg/46 |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
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Synonyms and related keywords: AF, Afib, fib
Pharmacological treatment of atrial fibrillation
The main goals of treatment of atrial fibrillation are to prevent temporary circulatory instability and to prevent stroke. Rate and rhythm control are principally used to achieve the former, while anticoagulation may be required to decrease the risk of the latter.[1] In emergencies, when circulatory collapse is imminent due to uncontrolled tachycardia, immediate cardioversion may be indicated.[2]
The primary factors determining atrial fibrillation treatment are duration and evidence of hemodynamic instability. Cardioversion is indicated with new onset AF (for less than 48 hours) and with hemodynamic instability. If rate and rhythm control cannot be maintained by medication or cardioversion, electrophysiological studies with pathway ablation may be required.[2]
Antithrombotic Strategies for Prevention of Ischemic Stroke and Systemic Embolism
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.[3]
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. [3][4][5] [3][6] 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.[7][8] [9][10]
ACC / AHA Guidelines- Preventing Thromboembolism (DO NOT EDIT) [11]
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Class I1. 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 anticoagulation is stable. (Level of Evidence: A) 6. Aspirin, 81–325 mg daily, is recommended as an alternative to vitamin K antagonists 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) Class IIa
Class IIb
Class III
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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
Newer agents that inhibit factor Xa are under investigation for the management of atrial fibrillation. These agents include apixabin and rivaroxaban.
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. [10] [10]
[12] 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. [13][14]
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.
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[15]. 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)[16].
Conversion to sinus rhythm and thromboembolism
Electrical & mechanical dissociation
Despite the restoration of sinus rhythm on the ECG following cardioversion (either spontaneous, pharmacologic or electrical or after radiofrequency catheter ablation of atrial flutter), in some patients there is a persistent lack of atrial contractility. This state is known as electrical mechanical dissociation and may be sue to mechanical stunning in the atrium and the atrial appendage. [17] [18][19][19][20][21][22] The lack of atrial contraction can be diagnosed on echocardiography by the appearance of spontaneous echo contrast. [17] In general, the longer the patient was in atrial fibrillation, the longer the time it takes for the recoery of atrial mechanical function. The period of recovery can be quite variable, and it can take several weeks in total. Recovery of mechanical function can be delayed for several weeks, depending in part on the duration of AF before restoration of sinus rhythm[23][24][25] This kind of electrical mechanical dissociation may explain in part the observation that some patients develop thromboembolic events following cardioversion despite the fact that they had no visible left atrial clot on TEE. [26] It has been hypothesized that the low shear state and turbulent nature of left atrial hemodynamics during this period leads to the development of clot which then embolizes once there is restoration of sufficient mechanical force.[27] It is in part due to the presence of atrial mechanical dissociation and the risk of clot formation and embolization that oral anticoagulation is recommended for 3 to 4 weeks following successful electrical cardioversion in patients in whom the duration of Afib is unknown or in whom the duration of atrial fibrillation has been documented to be longer than 48 hours. Among patients in whom the duration of atrial fibrillation is less than 48 hours, the necessity for anticoagulation is not as clear, although it should be noted that stroke has been observed in these patients as well. No matter what the duration of atrial fibrillation, if a patient becomes hemodynamically unstable, this is an indication for immediate cardioversion.
Management Strategies
New diagnosed or First Episode of Atrial Fibrillation
In patients who have self-limited episodes of paroxysmal AF, antiarrhythmic drugs to prevent recurrence are usually unnecessary, unless AF is associated with severe symptoms related to hypotension, myocardial ischemia, or HF. Whether these individuals require longterm or even short-term anticoagulation is not clear, and the decision must be individualized for each patient based on the intrinsic risk of thromboembolism.
Vagally mediated Atrial fibrillation
Adrenergically induced Atrial Fibrillation
Beta blockers (sotalol)
Congestive Heart Failure
amiodarone or dofetilide to maintain sinus rhythm.
Anticoagulation
Patients with atrial fibrillation, even lone atrial fibrillation without other evidence of heart disease, are at increased risk of stroke during long term follow up.[28] A systematic review of risk factors for stroke in patients with nonvalvular atrial fibrillation concluded that a prior history of stroke or TIA is the most powerful risk factor for future stroke, followed by advancing age, hypertension, diabetes.[29] The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.[30] The risk of systemic embolization (atrial clots migrating to other organs) depends strongly on whether there is an underlying structural problem with the heart (e.g. mitral stenosis) and on the presence of other risk factors, such as diabetes and high blood pressure. Finally, patients under 65 are much less likely to develop embolization compared with patients over 75. In young patients with few risk factors and no structural heart defect, the benefits of anticoagulation may be outweighed by the risks of hemorrhage (bleeding). Those at a low risk may benefit from mild (and low-risk) anticoagulation with aspirin (or clopidogrel in those who are allergic to aspirin). In contrast, those with a high risk of stroke derive most benefit from anticoagulant treatment with warfarin or similar drugs.
In the United Kingdom, the NICE guidelines recommend using a clinical prediction rule for this purpose.[31] The CHADS/CHADS2 score is the best validated clinical prediction rule for determining risk of stroke (and therefore who should be anticoagulated); it assigns points (totaling 0-6) depending on the presence or absence of co-morbidities such hypertension and diabetes. In a comparison of seven prediction rules, the best rules were the CHADS2 which performed similarly to the SPAF[32] and Framingham[33] prediction rules. [34]
To compensate for the increased risk of stroke, anticoagulants may be required. However, in the case of warfarin, if a patient has a yearly risk of stroke that is less than 2%, then the risks associated with taking warfarin outweigh the risk of getting a stroke. [35][36]
Acute anticoagulation
If anticoagulation is required urgently (e.g. for cardioversion), heparin or similar drugs achieve the required level of protection much quicker than warfarin, which may take several days to reach adequate levels.
In the initial stages after an embolic stroke, anticoagulation may be risky, as the damaged area of the brain is relatively prone to bleeding (hemorrhagic transformation).[37] As a result, a clinical practice guideline by National Institute for Health and Clinical Excellence recommends that anticoagulation should begin two weeks after stroke if no hemorrhage occurred.[31]
Chronic anticoagulation
Among patients with "non-valvular" atrial fibrillation, anticoagulation with warfarin can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. [38][39]. There is evidence that aspirin and clopidogrel are effective when used together, but the combination is still inferior to warfarin.[40]
Warfarin treatment requires frequent monitoring with a blood test called the international normalized ratio (INR); this determines whether the correct dose is being used. In atrial fibrillation, the usual target INR is between 2.0 and 3.0 (higher targets are used in patients with mechanical artificial heart valves, many of whom may also have atrial fibrillation). A high INR may indicate increased bleeding risk, while a low INR would indicate that there is insufficient protection from stroke.
An attempt was made to find a better method of implementing warfarin therapy without the inconvenience of regular monitoring and risk of intracranial hemorrhage. A combination of aspirin and fixed-dose warfarin (initial INR 1.2-1.5) was tried. Unfortunately, in a study of AF patients with additional risk factors for thromboembolism, the combination of aspirin and the lower dose of warfarin was significantly inferior to the standard adjusted-dose warfarin (INR 2.0-3.0), yet still had a similar risk of intracranial hemorrhage.[41]
Elderly patients
The very elderly (patients aged 75 years or more) may benefit from anticoagulation provided that their anticoaguation does not increase hemorrhagic complications, which is a difficult goal. Patients aged 80 years or more may be especially susceptible to bleeding complications, with a rate of 13 bleeds per 100 person-years.[42] A rate of 13 bleeds per 100 person years would seem to preclude use of warfarin; however, a randomized controlled trial found benefit in treating patients 75 years or over with a number needed to treat of 50.[43] Of note, this study had very low rate of hemorrhagic complications in the warfarin group.
Rate control versus rhythm control
AF can cause disabling and annoying symptoms. Palpitations, angina, lassitude (weariness), and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. Furthermore, AF with a persistent rapid rate can cause a form of heart failure called tachycardia induced cardiomyopathy. This can significantly increase mortality and morbidity, which can be prevented by early and adequate treatment of the AF.
There are two ways to approach these symptoms: rate control and rhythm control. Rate control treatments seek to reduce the heart rate to normal, usually 60 to 100 beats per minute. Rhythm control seeks to restore the normal heart rhythm, called normal sinus rhythm. Studies suggest that rhythm control is mainly a concern in newly diagnosed AF, while rate control is more important in the chronic phase. Rate control with anticoagulation is as effective a treatment as rhythm control in long term mortality studies, the AFFIRM Trial.[44]
The AFFIRM study showed no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic treatment, compared to those who have only rate control.[44]
Rate control
Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, effectively decreasing the number of impulses that conduct down into the ventricles. This can be done with:[2]
- Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, atenolol, bisoprolol)
- Cardiac glycosides (i.e. digoxin)
- Calcium channel blockers (i.e. diltiazem or verapamil)
In addition to these agents, amiodarone has some AV node blocking effects (particularly when administered intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension).
ACC / AHA Guidelines- Pharmacological Rate Control During Atrial Fibrillation (DO NOT EDIT) [11]
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Class I1. Measurement of the heart rate at rest and control of the rate using pharmacological agents (either a beta blocker or non dihydropyridine calcium channel antagonist, in most cases) are recommended for patients with persistent or permanent AF. (Level of Evidence: B) 2. Intravenous administration of digoxin or amiodarone is recommended to control the heart rate in patients with AF and heart failure who do not have an accessory pathway. (Level of Evidence: B) 3. In patients who experience symptoms related to AF during activity, the adequacy of heart rate control should be assessed during exercise, adjusting pharmacological treatment as necessary to keep the rate in the physiological range. (Level of Evidence: C) 4. Digoxin is effective following oral administration to control the heart rate at rest in patients with AF and is indicated for patients with heart failure, LV dysfunction, or for sedentary individuals. (Level of Evidence: C) Class IIa1. A combination of digoxin and either a beta blocker or non dihydropyridine calcium channel antagonist is reasonable to control the heart rate both at rest and during exercise in patients with AF. The choice of medication should be individualized and the dose modulated to avoid bradycardia. (Level of Evidence: B) 2. It is reasonable to use ablation of the AV node or accessory pathway to control heart rate when pharmacological therapy is insufficient or associated with side effects. (Level of Evidence: B) 3. Intravenous amiodarone can be useful to control the heart rate in patients with AF when other measures are unsuccessful or contraindicated. (Level of Evidence: C) 4. When electrical cardioversion is not necessary in patients with AF and an accessory pathway, intravenous procainamide or ibutilide is a reasonable alternative. (Level of Evidence: C) Class IIb1. When the ventricular rate cannot be adequately controlled both at rest and during exercise in patients with AF using a [beta blocker]], non dihydropyridine calcium channel antagonist, or digoxin, alone or in combination, oral amiodarone may be administered to control the heart rate. (Level of Evidence: C) 2. Intravenous procainamide, disopyramide, ibutilide, or amiodarone may be considered for hemodynamically stable patients with AF involving conduction over an accessory pathway. (Level of Evidence: B) 3. When the rate cannot be controlled with pharmacological agents or tachycardia-mediated cardiomyopathy is suspected, catheter-directed ablation of the AV node may be considered in patients with AF to control the heart rate. (Level of Evidence: C) Class III1. Digitalis should not be used as the sole agent to control the rate of ventricular response in patients with paroxysmal AF. (Level of Evidence: B) 2. Catheter ablation of the AV node should not be attempted without a prior trial of medication to control the ventricular rate in patients with AF. (Level of Evidence: C) 3. In patients with decompensated HF and AF, intravenous administration of a non dihydropyridine calcium channel antagonist may exacerbate hemodynamic compromise and is not recommended. (Level of Evidence: C) 4. Intravenous administration of digitalis glycosides or non dihydropyridine calcium channel antagonists to patients with AF and a pre-excitation syndrome may paradoxically accelerate the ventricular response and is not recommended. (Level of Evidence: C) |
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Cardioversion
Rhythm control methods include electrical and chemical cardioversion:[2]
- Electrical cardioversion involves the restoration of normal heart rhythm through the application of a DC electrical shock.
- Chemical cardioversion is performed with drugs, such as amiodarone, dronedarone[45], procainamide, ibutilide, propafenone or flecainide.
The main risk of cardioversion is systemic embolization of a thrombus (blood clot) from the previously fibrillating left atrium. Cardioversion should not be performed without adequate anticoagulation in patients with more than 48 hours of atrial fibrillation. Cardioversion may be performed in instances of AF lasting more than 48 hours if a transesophogeal echocardiogram (TEE) demonstrates no evidence of clot within the heart.[2]
Whichever method of cardioversion is used, approximately 50% of patient relapse within one year, although the continued daily use of oral antiarrhythmic drugs may extend this period. The key risk factor for relapse is duration of AF, although other risk factors that have been identified include the presence of structural heart disease, and increasing age.
Maintenance of sinus rhythm
The mainstay of maintaining sinus rhythm is the use of antiarrhythmic agents. Recently, other approaches have been developed that promise to decrease or eliminate the need for antiarrhythmic agents.
Antiarrhythmic agents
The anti-arrhythmic medications often used in either pharmacological cardioversion or in the prevention of relapse to AF alter the flux of ions in heart tissue, making them less excitable, setting the stage for spontaneous and durable cardioversion. These medications are often used in concert with electrical cardioversion.
Sources
- The ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation [46]
References
- ↑ Prystowsky EN (2000). "Management of atrial fibrillation: therapeutic options and clinical decisions". Am J Cardiol. 85 (10A): 3D–11D. PMID 10822035
- ↑ 2.0 2.1 2.2 2.3 2.4
- ↑ 3.0 3.1 3.2 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ "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) - ↑ "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) - ↑ 10.0 10.1 10.2 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) - ↑ 11.0 11.1 Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207
- ↑ "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) - ↑ 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) - ↑ 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.
- ↑ The ACTIVE Writing Group on behalf of the ACTIVE Investigators. Lancet 2006;367:1903-12.
- ↑ The ACTIVE Writing Group on behalf of the ACTIVE Investigators. Lancet 2006;367:1903-12.
- ↑ 17.0 17.1 Fatkin D, Kuchar DL, Thorburn CW, Feneley MP (1994). "Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: evidence for "atrial stunning" as a mechanism of thromboembolic complications". J. Am. Coll. Cardiol. 23 (2): 307–16. PMID 8294679. Unknown parameter
|month=ignored (help) - ↑ Antonielli E, Pizzuti A, Bassignana A; et al. (1999). "Transesophageal echocardiographic evidence of more pronounced left atrial stunning after chemical (propafenone) rather than electrical attempts at cardioversion from atrial fibrillation". Am. J. Cardiol. 84 (9): 1092–6, A9–10. PMID 10569673. Unknown parameter
|month=ignored (help) - ↑ 19.0 19.1 Falcone RA, Morady F, Armstrong WF (1996). "Transesophageal echocardiographic evaluation of left atrial appendage function and spontaneous contrast formation after chemical or electrical cardioversion of atrial fibrillation". Am. J. Cardiol. 78 (4): 435–9. PMID 8752189. Unknown parameter
|month=ignored (help) - ↑ Bellotti P, Spirito P, Lupi G, Vecchio C (1998). "Left atrial appendage function assessed by transesophageal echocardiography before and on the day after elective cardioversion for nonvalvular atrial fibrillation". Am. J. Cardiol. 81 (10): 1199–202. PMID 9604945. Unknown parameter
|month=ignored (help) - ↑ Harjai K, Mobarek S, Abi-Samra F; et al. (1998). "Mechanical dysfunction of the left atrium and the left atrial appendage following cardioversion of atrial fibrillation and its relation to total electrical energy used for cardioversion". Am. J. Cardiol. 81 (9): 1125–9. PMID 9605054. Unknown parameter
|month=ignored (help) - ↑ Sparks PB, Jayaprakash S, Vohra JK; et al. (1998). "Left atrial "stunning" following radiofrequency catheter ablation of chronic atrial flutter". J. Am. Coll. Cardiol. 32 (2): 468–75. PMID 9708477. Unknown parameter
|month=ignored (help) - ↑ Mitusch R, Garbe M, Schmücker G, Schwabe K, Stierle U, Sheikhzadeh A (1995). "Relation of left atrial appendage function to the duration and reversibility of nonvalvular atrial fibrillation". Am. J. Cardiol. 75 (14): 944–7. PMID 7733009. Unknown parameter
|month=ignored (help) - ↑ Manning WJ, Silverman DI, Katz SE; et al. (1995). "Temporal dependence of the return of atrial mechanical function on the mode of cardioversion of atrial fibrillation to sinus rhythm". Am. J. Cardiol. 75 (8): 624–6. PMID 7887393. Unknown parameter
|month=ignored (help) - ↑ Grimm RA, Leung DY, Black IW, Stewart WJ, Thomas JD, Klein AL (1995). "Left atrial appendage "stunning" after spontaneous conversion of atrial fibrillation demonstrated by transesophageal Doppler echocardiography". Am. Heart J. 130 (1): 174–6. PMID 7611109. Unknown parameter
|month=ignored (help) - ↑ Black IW, Fatkin D, Sagar KB; et al. (1994). "Exclusion of atrial thrombus by transesophageal echocardiography does not preclude embolism after cardioversion of atrial fibrillation. A multicenter study". Circulation. 89 (6): 2509–13. PMID 8205657. Unknown parameter
|month=ignored (help) - ↑ Berger M, Schweitzer P (1998). "Timing of thromboembolic events after electrical cardioversion of atrial fibrillation or flutter: a retrospective analysis". Am. J. Cardiol. 82 (12): 1545–7, A8. PMID 9874066. Unknown parameter
|month=ignored (help) - ↑ Brand FN, Abbott RD, Kannel WB, Wolf PA (1985). "Characteristics and prognosis of lone atrial fibrillation. 30-year follow-up in the Framingham Study". JAMA. 254 (24): 3449–53. PMID 4068186.
- ↑ "Independent predictors of stroke in patients with atrial fibrillation: a systematic review". Neurology. 69 (6): 546–54. 2007. doi:10.1212/01.wnl.0000267275.68538.8d. PMID 17679673.
- ↑ Kopecky SL, Gersh BJ, McGoon MD; et al. (1987). "The natural history of lone atrial fibrillation. A population-based study over three decades". N. Engl. J. Med. 317 (11): 669–74. PMID 3627174.
- ↑ 31.0 31.1 National Institute for Health and Clinical Excellence (June 2006). "Clinical Guideline 36 - Atrial fibrillation". Retrieved 2007-08-15.
- ↑ Hart RG, Pearce LA, McBride R, Rothbart RM, Asinger RW (1999). "Factors associated with ischemic stroke during aspirin therapy in atrial fibrillation: analysis of 2012 participants in the SPAF I-III clinical trials. The Stroke Prevention in Atrial Fibrillation (SPAF) Investigators". Stroke. 30 (6): 1223–9. PMID 10356104.
- ↑ Wang TJ, Massaro JM, Levy D; et al. (2003). "A risk score for predicting stroke or death in individuals with new-onset atrial fibrillation in the community: the Framingham Heart Study". JAMA. 290 (8): 1049–56. doi:10.1001/jama.290.8.1049. PMID 12941677.
- ↑ Baruch L, Gage BF, Horrow J; et al. (2007). "Can patients at elevated risk of stroke treated with anticoagulants be further risk stratified?". Stroke. 38 (9): 2459–63. doi:10.1161/STROKEAHA.106.477133. PMID 17673721.
- ↑ van Walraven C, Hart RG, Singer DE; et al. (2002). "Oral anticoagulants vs aspirin in nonvalvular atrial fibrillation: an individual patient meta-analysis". JAMA. 288 (19): 2441&ndash, 48. PMID 12435257.
- ↑ Gage BF, Cardinalli AB, Owens D. (1998). "Cost-effectiveness of preference-based antithrombotic therapy for patients with nonvalvular atrial fibrillation". Stroke. 29: 1083&ndash, 91. PMID 9626276.
- ↑ Paciaroni M, Agnelli G, Micheli S, Caso V (2007). "Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials". Stroke. 38 (2): 423–30. doi:10.1161/01.STR.0000254600.92975.1f. PMID 17204681. ACP JC synopsis
- ↑ Hart RG, Pearce LA, Aguilar MI (2007). "Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation". Ann Intern Med. 146 (12): 857–67. PMID 17577005.
- ↑ Aguilar M, Hart R, Pearce L (2007). "Oral anticoagulants versus antiplatelet therapy for preventing stroke in patients with non-valvular atrial fibrillation and no history of stroke or transient ischemic attacks". Cochrane Database Syst Rev. 3: CD006186. doi:10.1002/14651858.CD006186.pub2. PMID 17636831.
- ↑ Connolly S, Pogue J, Hart R; et al. (2006). "Clopidogrel plus aspirin versus oral anticoagulation for atrial fibrillation in the Atrial fibrillation Clopidogrel Trial with Irbesartan for prevention of Vascular Events (ACTIVE W): a randomised controlled trial". Lancet. 367 (9526): 1903–12. doi:10.1016/S0140-6736(06)68845-4. PMID 16765759.
- ↑ "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): 633–638. 1996. doi:10.1016/S0140-6736(96)03487-3. PMID 8782752.
- ↑ Hylek EM, Evans-Molina C, Shea C, Henault LE, Regan S (2007). "Major hemorrhage and tolerability of warfarin in the first year of therapy among elderly patients with atrial fibrillation". Circulation. 115 (21): 2689–96. doi:10.1161/CIRCULATIONAHA.106.653048. PMID 17515465.
- ↑ Mant J; et al. (2007). "Warfarin versus aspirin for stroke prevention in an elderly community population with atrial fibrillation (the Birmingham Atrial Fibrillation Treatment of the Aged Study, BAFTA): a randomised controlled trial". Lancet. 370: 493–503. doi:10.1016/S0140-6736(07)61233-1.
- ↑ 44.0 44.1 Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD (2002). "A comparison of rate control and rhythm control in patients with atrial fibrillation". N Engl J Med. 347 (23): 1825–33. PMID 12466506
- ↑ Singh BN, Connolly SJ, Crijns HJ; et al. (2007). "Dronedarone for maintenance of sinus rhythm in atrial fibrillation or flutter". N. Engl. J. Med. 357 (10): 987–99. doi:10.1056/NEJMoa054686. PMID 17804843.
- ↑ Fuster V, Ryden LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey JY, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann S. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation- Executive Summary: executive summary: 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 Guidlines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006; 114: 700-752. PMID 16908781
Further Readings
- Fuster V, Rydén LE, Cannom DS, 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.
- Estes NAM 3rd, Halperin JL, Calkins H, Ezekowitz MD, Gitman P, Go AS, McNamara RL, Messer JV, Ritchie JL, Romeo SJW, Waldo AL, Wyse DG. ACC/AHA/Physician Consortium 2008 clinical performance measures for adults with non valvular 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 Performance Measures for Atrial Fibrillation). Circulation 2008; 117:1101–1120
- Braunwald's Heart Disease, Libby P, 8th ed., 2007, ISBN 978-1-41-604105-4
- Hurst's the Heart, Fuster V, 12th ed. 2008, ISBN 978-0-07-149928-6
- Willerson JT, Cardiovascular Medicine, 3rd ed., 2007, ISBN 978-1-84628-188-4
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