Atrial fibrillation overview of treatment

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Conduction
Sinus rhythm
Atrial fibrillation
Atrihttp://miles.wikidoc.org/skins/common/images/button_bold.pngal 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

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

Goals of Atrial Fibrillation Treatment

The two main goals in managing the patient with atrial fibrillation are:

  1. Prevent hemodynamic instability due to a low cardiac ouptut associated with poor ventricular filling as a result of rapid and chaotic contractions of the atrium. Rhythm control via antiarrhytmics is used to reduce the risk of developing recurrent atrial fibrillation, and rate control is used to reduce the heart rate when atrial fibrillation dues occur. If hemodynamic collapse has or is about to occur, then immediate cardioversion may be indicated.[1]
  2. Prevent embolic stroke. Anticoagulation with antiplatelets such as aspirin and/or clopidogrel or antithrombins such as warfarin or dabigatran are used to reduce the risk of embolic stroke.[2]

General Principals of Atrial Fibrillation Treatment

The primary determinants of the appropriate treatment of atrial fibrillation treatment are:

  1. Duration of atrial fibrillation and evidence of hemodynamic instability. Cardioversion is indicated if the AF is of new onset (the AF present for less than 48 hours) and if there is hemodynamic instability.
  2. Risk of systemic embolization and risk of bleeding. The risk of stroke can be ascertained using the CHADS2 Score or the more sophisticated CHA2DS2-VASC Score and the risk of bleeding can be asceratined using the HAS-BLED score as described below. The relative risk versus benefit of anticoagulation can then calculated.
  3. Durability of rate and rhythm control. If rate and rhythm control cannot be maintained by medication or cardioversion, electrophysiological studies with ablation may be required.[1]

Cardioversion

Risk of Cardioversion Due to Electrical and 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. [3] [4][5][5][6][7][8] The lack of atrial contraction can be diagnosed on echocardiography by the appearance of spontaneous echo contrast. [3] 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[9][10][11] 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. [12] 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.[13] 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 of Specific Scenarios

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

Disopyramide or flecainide

Adrenergically induced Atrial Fibrillation

Beta blockers including sotalol

Congestive Heart Failure

Amiodarone or dofetilide to maintain sinus rhythm.

Use of the CHADS Score to Risk Stratify Patients and Determine the Appropriate Anticoagulation Strategy

Condition Points
 C   Congestive heart failure
1
 H  Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)
1
 A  Age >/=75 years
1
 D  Diabetes Mellitus
1
 S2  Prior Stroke or TIA
2

CHADS score or CHADS2 score is a clinical prediction rule for estimating the risk of stroke in patients with non-rheumatic atrial fibrillation (AF), a common and serious heart arrhythmia associated with thromboembolic stroke. It is used to determine whether or not treatment is required with anticoagulation therapy or antiplatelet therapy,[14] since AF can cause stasis of blood in the upper heart chambers, leading to the formation of a mural thrombus that can dislodge into the blood flow, reach the brain, cut off blood supply to the brain, and cause a stroke. A high CHADS2 score corresponds to a greater risk of stroke, while a low CHADS2 score corresponds to a lower risk of stroke. The CHADS2 score was validated by a study of nonrheumatic atrial fibrillation patients aged 65 to 95 who were not prescribed the anticoagulant warfarin.[15]

How to Calculate the CHADS2 Score

The CHADS2 scoring table is shown above:[16]

Adding together the points that correspond to the conditions that a patient has will result in the CHADS2 score. This score is used in the next section to estimate stroke risk.

Risk of stroke

Annual Stroke Risk[15]
CHADS2 Score   Stroke Risk %       95% CI      
0
1.9
 1.2–3.0
1
2.8
 2.0–3.8
2
4.0
 3.1–5.1
3
5.9
 4.6–7.3
4
8.5
 6.3–11.1
5
12.5
 8.2–17.5
6
18.2
10.5–27.4

According to the findings of the validation study, the risk of stroke as a percentage per year is shown in the table titled Annual Stroke Risk:

While the CHADS2 score provides prognostic information regarding the natural history of non-valvular atrial fibrillation (NVAF) in the absence of warfarin therapy, it should be noted that warfarin therapy also has an associated stroke risk[17] (particularly hemorrhagic stroke) and a risk of major bleeding, and these considerations were taken into account in the development of the recommendations in the next section.

The CHADS2 score has various limitations, which have been debated [18]. Notably, many stroke risk factors have not been included, and whilst simple, the score has only modest predictive value for thromboembolism.

In order to improve upon the prognostic utility of the CHADS2 score and to incorporate additional stroke risk factors, the CHA2DS2-VASc score has been proposed [19]. These additional 'clinically relevant non-major' stroke risk factors include age 65-74, female gender and vascular disease. In the CHA2DS2-VASc score, 'age 75 and above' also has extra weight, with 2 points.

The CHA2DS2-VASc score has been used in the new European Society of Cardiology guidelines for the management of atrial fibrillation [20].

The European Society of Cardiology (ESC) guidelines recommend that if the patient has a CHADS2 score of 2 and above, oral anticoagulation (OAC) therapy is recommended. OAC options include warfarin with an INR target of 2-3 or dabigatran.

If the CHADS2 score is 0-1, other stroke risk modifiers should be considered: (i) If there are 2 or more risk factors (essentially a CHA2DS2-VASc score score of 2 or more), OAC is recommended; and (ii) If there is 1 risk factor (essentially a CHA2DS2-VASc score score=1), then antithrombotic therapy with either OAC or aspirin (OAC preferred) is recommended.

If patients have a CHA2DS2-VASc score of 0, then such patients are ‘truly low risk’[21]. The ESC guidelines recommend either aspirin or no antithrombotic therapy, but 'no antithrombotic therapy' is preferred[22].

Anticoagulation based on the CHADS2 score

Score Risk Anticoagulation Therapy Considerations
0 Low Aspirin Aspirin daily
1 Moderate Aspirin or Warfarin Aspirin daily or INR to 2.0-3.0, depending on factors such as patient preference
2 or greater Moderate or High Warfarin INR to 2.0-3.0, unless contraindicated (e.g. clinically significant GI bleeding, inability to obtain regular INR screening)

The following treatment strategies were recommended in the table entitled Anticoagulation based on the CHADS2 score:[14][15]

For detailed recommendations on how the treatment recommendations based on the CHADS2 score are modified by considering additional 'stroke risk modifier' risk factors using the CHA2DS2-VASc score, see ESC guideline recommendations.


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.[23] 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.[24] The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.[25] 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.[26] 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[27] and Framingham[28] prediction rules. [29]

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. [30][31]

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).[32] 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.[26]

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%. [33][34]. There is evidence that aspirin and clopidogrel are effective when used together, but the combination is still inferior to warfarin.[35]

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.[36]

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.[37] 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.[38] Of note, this study had very low rate of hemorrhagic complications in the warfarin group.

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

Main article: Antiarrhythmic agent

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.

See Also

Sources

  • The ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation [39]

References

  1. ↑ 1.0 1.1 Invalid <ref> tag; no text was provided for refs named pmid16908781
  2. ↑ Prystowsky EN (2000). "Management of atrial fibrillation: therapeutic options and clinical decisions". Am J Cardiol. 85 (10A): 3D–11D. PMID 10822035
  3. ↑ 3.0 3.1 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)
  4. ↑ 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)
  5. ↑ 5.0 5.1 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)
  6. ↑ 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)
  7. ↑ 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)
  8. ↑ 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)
  9. ↑ 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)
  10. ↑ 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)
  11. ↑ 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)
  12. ↑ 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)
  13. ↑ 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)
  14. ↑ 14.0 14.1 Gage BF, van Walraven C, Pearce L; et al. (2004). "Selecting patients with atrial fibrillation for anticoagulation: stroke risk stratification in patients taking aspirin". Circulation. 110 (16): 2287&ndash, 92. doi:10.1161/01.CIR.0000145172.55640.93. PMID 15477396.
  15. ↑ 15.0 15.1 15.2 Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ (2001). "Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation". JAMA. 285 (22): 2864–70. PMID 11401607.
  16. ↑ "Risk of Stroke with AF". VA Palo Alto Medical Center and at Stanford University: the Sportsmedicine Program and the Cardiomyopathy Clinic. Retrieved 2007-09-14.
  17. ↑ Steiner, Thorsten (2006). "Intracerebral hemorrhage associated with oral anticoagulant therapy: current practices and unresolved questions". Stroke. 37 (1): 256–62. PMID 16339459 doi:10.1161/01.STR.0000196989.09900.f8. Unknown parameter |coauthors= ignored (help)
  18. ↑ Karthikeyan G, Eikelboom JW. The CHADS2 score for stroke risk stratification in atrial fibrillation--friend or foe? Thromb Haemost. 2010 Jul 5;104(1):45-8.
  19. ↑ Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010 Feb;137(2):263-72.
  20. ↑ European Heart Rhythm Association; European Association for Cardio-Thoracic Surgery, Camm AJ, Kirchhof P, Lip GY, Schotten U, Savelieva I, Ernst S, Van Gelder IC, Al-Attar N, Hindricks G, Prendergast B, Heidbuchel H, Alfieri O, Angelini A, Atar D, Colonna P, De Caterina R, De Sutter J, Goette A, Gorenek B, Heldal M, Hohloser SH, Kolh P, Le Heuzey JY, Ponikowski P, Rutten FH. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Eur Heart J. 2010 Oct;31(19):2369-429.
  21. ↑ Van Staa TP, Setakis E, Di Tanna GL, Lane DA, Lip GY. A comparison of risk stratification schema for stroke in 79884 atrial fibrillation patients in general practice. J Thromb Haemost. 2010 Oct 1. doi: 10.1111/j.1538-7836.2010.04085.x. [Epub ahead of print] PubMed PMID: 21029359.
  22. ↑ Lip GY, Halperin JL. Improving stroke risk stratification in atrial fibrillation. Am J Med. 2010 Jun;123(6):484-8.
  23. ↑ 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.
  24. ↑ "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.
  25. ↑ 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.
  26. ↑ 26.0 26.1 National Institute for Health and Clinical Excellence (June 2006). "Clinical Guideline 36 - Atrial fibrillation". Retrieved 2007-08-15.
  27. ↑ 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.
  28. ↑ 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.
  29. ↑ 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.
  30. ↑ 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.
  31. ↑ 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.
  32. ↑ 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
  33. ↑ 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.
  34. ↑ 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.
  35. ↑ 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.
  36. ↑ "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.
  37. ↑ 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.
  38. ↑ 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.
  39. ↑ 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

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