Atrial fibrillation overview of treatment: Difference between revisions

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{| border="1" style="border-collapse:collapse" cellpadding="3" align="right"
{{Atrial fibrillation}}
| colspan="3" align="center" bgcolor="#ABCDEF" | Conduction
{{CMG}} {{AOEIC}} {{Mitra}}
|-
| <small>Sinus rhythm</small> [[Image:Heart conduct sinus.gif|none|230px]]
| <small>Atrial fibrillation</small> [[Image:Heart conduct atrialfib.gif|none|230px]]
|}
{{Infobox_Disease |
  Name          = Atrihttp://miles.wikidoc.org/skins/common/images/button_bold.pngal fibrillation |
  Image          = SinusRhythmLabels.png  |
  Caption        = The P waves, which represent depolarization of the atria, are irregular or absent during atrial fibrillation. |
  DiseasesDB    = 1065 |
  ICD10          = {{ICD10|I|48||i|30}} |
  ICD9          = {{ICD9|427.31}} |
  ICDO          = |
  OMIM          = |
  MedlinePlus    = 000184 |
  eMedicineSubj  = med |
  eMedicineTopic = 184 |
  eMedicine_mult = {{eMedicine2|emerg|46}} |
}}
{{SI}}
 
{{CMG}}
 
'''Associate Editor-In-Chief:''' {{CZ}}
 
{{Editor Join}}
 
'''Synonyms and related keywords''': AF, Afib, fib


==Goals of Atrial Fibrillation Treatment==
==Goals of Atrial Fibrillation Treatment==
The primary goals in the management of patients with [[atrial fibrillation]] include:


The two main goals in managing the patient with atrial fibrillation are:
* '''1) Achieving adequate rate control during [[AF]]''':
 
**[[Beta-blockers]]
#'''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.<ref name="pmid16908781"/>
**[[Nondihydropyridine calcium channel blockers]]:
#'''Prevent embolic [[stroke]].''' [[Anticoagulation]] with [[antiplatelets]] such as [[aspirin]] and/or [[clopidogrel]] or [[antithrombin]]s such as [[warfarin]] or [[dabigatran]] are used to reduce the risk of embolic stroke.<ref>{{cite journal | author=Prystowsky EN | title=Management of atrial fibrillation: therapeutic options and clinical decisions | journal=Am J Cardiol | year=2000 | pages=3D-11D | volume=85 | issue=10A }} PMID 10822035</ref>
***[[Verapamil]]
***[[Diltiazem]]
**[[Digoxin]]
**[[AV junction]] [[ablation]] plus [[pacemaker]]
*'''2) Prevention from [[thromboembolism]] and [[stroke]]''':
**[[Anticoagulation]]
**Occlusion or resection of [[atrial appendage]]
*'''3) Treatment of reversible risk factors for [[AF]]''' including:
**[[Hypertension]]
**[[Hyperlipidemia]]
**[[Diabetes mellitus]]
**[[Obesity]]
**[[Sleep apnea]]
**Excessive [[alcohol]] use
*'''4) Long-term strategies for management of [[symptoms]]''' (reduction or elimination):
**Maintenance of [[sinus rhythm]]:
***[[Antiarrhythmic]] medication
***[[Catheter ablation]]
**Surgery ([[Maze procedure]])
**Management of continuous [[AF]]


==General Principals of Atrial Fibrillation Treatment==
==General Principals of Atrial Fibrillation Treatment==
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#'''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.  
#'''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.  
#'''Risk of systemic embolization and risk of bleeding.'''  The risk of stroke can be ascertained using the [[CHADS Score|CHADS<sub>2</sub> Score]] or the more sophisticated [[CHA2DS2-VASc Score|CHA<sub>2</sub>DS<sub>2</sub>-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.
#'''Risk of systemic embolization and risk of bleeding.'''  The risk of stroke can be ascertained using the [[CHADS Score|CHADS<sub>2</sub> Score]] or the more sophisticated [[CHA2DS2-VASc Score|CHA<sub>2</sub>DS<sub>2</sub>-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.
#'''Durability of rate and rhythm control.''' If rate and rhythm control cannot be maintained by medication or cardioversion, [[Cardiac electrophysiology|electrophysiological studies]] with [[Radiofrequency ablation|ablation]] may be required.<ref name="pmid16908781"/>
#'''Durability of rate and rhythm control.''' If rate and rhythm control cannot be maintained by medication or cardioversion, [[Cardiac electrophysiology|electrophysiological studies]] with [[Radiofrequency ablation|ablation]] may be required.<ref name="pmid16908781">{{cite journal |author=Fuster V, Rydén 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, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL |title=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 |journal=[[Circulation]] |volume=114 |issue=7 |pages=e257–354 |year=2006 |month=August |pmid=16908781 |doi=10.1161/CIRCULATIONAHA.106.177292 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=16908781 |issn=}}</ref>


==Cardioversion==
==Cardioversion==
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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. <ref name="pmid8294679">{{cite journal |author=Fatkin D, Kuchar DL, Thorburn CW, Feneley MP |title=Transesophageal  echocardiography before and during direct current cardioversion of  atrial fibrillation: evidence for "atrial stunning" as a mechanism of  thromboembolic complications |journal=J. Am. Coll. Cardiol. |volume=23 |issue=2 |pages=307–16 |year=1994 |month=February |pmid=8294679 |doi= |url=}}</ref> <ref name="pmid10569673">{{cite journal |author=Antonielli E, Pizzuti A, Bassignana A, ''et al''  |title=Transesophageal echocardiographic evidence of more pronounced  left atrial stunning after chemical (propafenone) rather than electrical  attempts at cardioversion from atrial fibrillation |journal=Am. J.  Cardiol. |volume=84 |issue=9 |pages=1092–6, A9–10 |year=1999  |month=November |pmid=10569673 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914999005081}}</ref><ref name="pmid8752189">{{cite journal |author=Falcone  RA, Morady F, Armstrong WF |title=Transesophageal echocardiographic  evaluation of left atrial appendage function and spontaneous contrast  formation after chemical or electrical cardioversion of atrial  fibrillation |journal=Am. J. Cardiol. |volume=78 |issue=4 |pages=435–9  |year=1996 |month=August |pmid=8752189 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(96)00333-5}}</ref><ref name="pmid8752189">{{cite journal |author=Falcone  RA, Morady F, Armstrong WF |title=Transesophageal echocardiographic  evaluation of left atrial appendage function and spontaneous contrast  formation after chemical or electrical cardioversion of atrial  fibrillation |journal=Am. J. Cardiol. |volume=78 |issue=4 |pages=435–9  |year=1996 |month=August |pmid=8752189 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(96)00333-5}}</ref><ref name="pmid9604945">{{cite journal |author=Bellotti  P, Spirito P, Lupi G, Vecchio C |title=Left atrial appendage function  assessed by transesophageal echocardiography before and on the day after  elective cardioversion for nonvalvular atrial fibrillation |journal=Am.  J. Cardiol. |volume=81 |issue=10 |pages=1199–202 |year=1998 |month=May  |pmid=9604945 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(98)00089-7}}</ref><ref name="pmid9605054">{{cite journal |author=Harjai K, Mobarek S, Abi-Samra F, ''et al''  |title=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 |journal=Am.  J. Cardiol. |volume=81 |issue=9 |pages=1125–9 |year=1998 |month=May  |pmid=9605054 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914998001416}}</ref><ref name="pmid9708477">{{cite journal |author=Sparks PB, Jayaprakash S, Vohra JK, ''et al''  |title=Left atrial "stunning" following radiofrequency catheter  ablation of chronic atrial flutter |journal=J. Am. Coll. Cardiol.  |volume=32 |issue=2 |pages=468–75 |year=1998 |month=August |pmid=9708477  |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(98)00253-8}}</ref> The lack of atrial contraction can be diagnosed on echocardiography by the appearance of spontaneous echo contrast. <ref name="pmid8294679">{{cite journal |author=Fatkin D, Kuchar DL, Thorburn CW, Feneley MP |title=Transesophageal  echocardiography before and during direct current cardioversion of  atrial fibrillation: evidence for "atrial stunning" as a mechanism of  thromboembolic complications |journal=J. Am. Coll. Cardiol. |volume=23 |issue=2 |pages=307–16 |year=1994 |month=February |pmid=8294679 |doi= |url=}}</ref>  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]]<ref name="pmid7733009">{{cite journal |author=Mitusch  R, Garbe M, Schmücker G, Schwabe K, Stierle U, Sheikhzadeh A  |title=Relation of left atrial appendage function to the duration and  reversibility of nonvalvular atrial fibrillation |journal=Am. J.  Cardiol. |volume=75 |issue=14 |pages=944–7 |year=1995 |month=May  |pmid=7733009 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S000291499980695X}}</ref><ref name="pmid7887393">{{cite journal |author=Manning WJ, Silverman DI, Katz SE, ''et al''  |title=Temporal dependence of the return of atrial mechanical function  on the mode of cardioversion of atrial fibrillation to sinus rhythm  |journal=Am. J. Cardiol. |volume=75 |issue=8 |pages=624–6 |year=1995  |month=March |pmid=7887393 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914999806328}}</ref><ref name="pmid7611109">{{cite journal |author=Grimm  RA, Leung DY, Black IW, Stewart WJ, Thomas JD, Klein AL |title=Left  atrial appendage "stunning" after spontaneous conversion of atrial  fibrillation demonstrated by transesophageal Doppler echocardiography  |journal=Am. Heart J. |volume=130 |issue=1 |pages=174–6 |year=1995  |month=July |pmid=7611109 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0002-8703(95)90253-8}}</ref>  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]]. <ref name="pmid8205657">{{cite journal |author=Black IW, Fatkin D, Sagar KB, ''et al''  |title=Exclusion of atrial thrombus by transesophageal echocardiography  does not preclude embolism after cardioversion of atrial fibrillation. A  multicenter study |journal=Circulation |volume=89 |issue=6  |pages=2509–13 |year=1994 |month=June |pmid=8205657 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8205657}}</ref>  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.<ref name="pmid9874066">{{cite journal |author=Berger  M, Schweitzer P |title=Timing of thromboembolic events after electrical  cardioversion of atrial fibrillation or flutter: a retrospective  analysis |journal=Am. J. Cardiol. |volume=82 |issue=12 |pages=1545–7, A8  |year=1998 |month=December |pmid=9874066 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S000291499800705X}}</ref>  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.   
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. <ref name="pmid8294679">{{cite journal |author=Fatkin D, Kuchar DL, Thorburn CW, Feneley MP |title=Transesophageal  echocardiography before and during direct current cardioversion of  atrial fibrillation: evidence for "atrial stunning" as a mechanism of  thromboembolic complications |journal=J. Am. Coll. Cardiol. |volume=23 |issue=2 |pages=307–16 |year=1994 |month=February |pmid=8294679 |doi= |url=}}</ref> <ref name="pmid10569673">{{cite journal |author=Antonielli E, Pizzuti A, Bassignana A, ''et al''  |title=Transesophageal echocardiographic evidence of more pronounced  left atrial stunning after chemical (propafenone) rather than electrical  attempts at cardioversion from atrial fibrillation |journal=Am. J.  Cardiol. |volume=84 |issue=9 |pages=1092–6, A9–10 |year=1999  |month=November |pmid=10569673 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914999005081}}</ref><ref name="pmid8752189">{{cite journal |author=Falcone  RA, Morady F, Armstrong WF |title=Transesophageal echocardiographic  evaluation of left atrial appendage function and spontaneous contrast  formation after chemical or electrical cardioversion of atrial  fibrillation |journal=Am. J. Cardiol. |volume=78 |issue=4 |pages=435–9  |year=1996 |month=August |pmid=8752189 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(96)00333-5}}</ref><ref name="pmid8752189">{{cite journal |author=Falcone  RA, Morady F, Armstrong WF |title=Transesophageal echocardiographic  evaluation of left atrial appendage function and spontaneous contrast  formation after chemical or electrical cardioversion of atrial  fibrillation |journal=Am. J. Cardiol. |volume=78 |issue=4 |pages=435–9  |year=1996 |month=August |pmid=8752189 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(96)00333-5}}</ref><ref name="pmid9604945">{{cite journal |author=Bellotti  P, Spirito P, Lupi G, Vecchio C |title=Left atrial appendage function  assessed by transesophageal echocardiography before and on the day after  elective cardioversion for nonvalvular atrial fibrillation |journal=Am.  J. Cardiol. |volume=81 |issue=10 |pages=1199–202 |year=1998 |month=May  |pmid=9604945 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(98)00089-7}}</ref><ref name="pmid9605054">{{cite journal |author=Harjai K, Mobarek S, Abi-Samra F, ''et al''  |title=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 |journal=Am.  J. Cardiol. |volume=81 |issue=9 |pages=1125–9 |year=1998 |month=May  |pmid=9605054 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914998001416}}</ref><ref name="pmid9708477">{{cite journal |author=Sparks PB, Jayaprakash S, Vohra JK, ''et al''  |title=Left atrial "stunning" following radiofrequency catheter  ablation of chronic atrial flutter |journal=J. Am. Coll. Cardiol.  |volume=32 |issue=2 |pages=468–75 |year=1998 |month=August |pmid=9708477  |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(98)00253-8}}</ref> The lack of atrial contraction can be diagnosed on echocardiography by the appearance of spontaneous echo contrast. <ref name="pmid8294679">{{cite journal |author=Fatkin D, Kuchar DL, Thorburn CW, Feneley MP |title=Transesophageal  echocardiography before and during direct current cardioversion of  atrial fibrillation: evidence for "atrial stunning" as a mechanism of  thromboembolic complications |journal=J. Am. Coll. Cardiol. |volume=23 |issue=2 |pages=307–16 |year=1994 |month=February |pmid=8294679 |doi= |url=}}</ref>  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]]<ref name="pmid7733009">{{cite journal |author=Mitusch  R, Garbe M, Schmücker G, Schwabe K, Stierle U, Sheikhzadeh A  |title=Relation of left atrial appendage function to the duration and  reversibility of nonvalvular atrial fibrillation |journal=Am. J.  Cardiol. |volume=75 |issue=14 |pages=944–7 |year=1995 |month=May  |pmid=7733009 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S000291499980695X}}</ref><ref name="pmid7887393">{{cite journal |author=Manning WJ, Silverman DI, Katz SE, ''et al''  |title=Temporal dependence of the return of atrial mechanical function  on the mode of cardioversion of atrial fibrillation to sinus rhythm  |journal=Am. J. Cardiol. |volume=75 |issue=8 |pages=624–6 |year=1995  |month=March |pmid=7887393 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914999806328}}</ref><ref name="pmid7611109">{{cite journal |author=Grimm  RA, Leung DY, Black IW, Stewart WJ, Thomas JD, Klein AL |title=Left  atrial appendage "stunning" after spontaneous conversion of atrial  fibrillation demonstrated by transesophageal Doppler echocardiography  |journal=Am. Heart J. |volume=130 |issue=1 |pages=174–6 |year=1995  |month=July |pmid=7611109 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0002-8703(95)90253-8}}</ref>  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]]. <ref name="pmid8205657">{{cite journal |author=Black IW, Fatkin D, Sagar KB, ''et al''  |title=Exclusion of atrial thrombus by transesophageal echocardiography  does not preclude embolism after cardioversion of atrial fibrillation. A  multicenter study |journal=Circulation |volume=89 |issue=6  |pages=2509–13 |year=1994 |month=June |pmid=8205657 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8205657}}</ref>  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.<ref name="pmid9874066">{{cite journal |author=Berger  M, Schweitzer P |title=Timing of thromboembolic events after electrical  cardioversion of atrial fibrillation or flutter: a retrospective  analysis |journal=Am. J. Cardiol. |volume=82 |issue=12 |pages=1545–7, A8  |year=1998 |month=December |pmid=9874066 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S000291499800705X}}</ref>  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==
==Maintenance of Rhythm Control==
Avoidance of stimulants such as [[caffeine]], [[Alcoholism|alcohol]] withdrawal, [[binge drinking]], and [[holiday heart syndrome]] may be critical in reducing the recurrence of atrial fibrillation. Drugs such as [[digoxin]] and [[hyperthyroidism]], [[hypokalemia]], [[sleep apnea]] and [[pheochromocytoma]] are all associated with atrial fbrillation. Antiarrhythmics may also be critical to maintaining [[normal sinus rhythm]].  Recommendations for specific populations of patients are provided below:


===New diagnosed or First Episode of Atrial Fibrillation===
===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.
In patients who have self-limited episodes of paroxysmal AF, antiarrhythmic drugs to prevent recurrence are usually unnecessary, unless the AF is associated with severe symptoms related to [[hypotension]], [[myocardial ischemia]], or [[heart failure]]. 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. Recommendations for specific patient populations follow:


=== Vagally mediated Atrial fibrillation===
=== Vagally mediated Atrial fibrillation===
[[Disopyramide]] or [[flecainide]]
[[Disopyramide]] or [[flecainide]] are recommended.


=== Adrenergically induced Atrial Fibrillation===
=== Adrenergically induced Atrial Fibrillation===
[[Beta blockers]] including [[sotalol]]
[[Beta blockers]] including [[sotalol]] are recommended.


=== Congestive Heart Failure ===
=== Congestive Heart Failure ===
[[Amiodarone]] or [[dofetilide]] to maintain [[sinus rhythm]].
[[Amiodarone]] or [[dofetilide]] are recommended.
 
==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.<ref name="pmid4068186">{{cite journal |author=Brand FN, Abbott RD, Kannel WB, Wolf PA |title=Characteristics and prognosis of lone atrial fibrillation. 30-year follow-up in the Framingham Study |journal=JAMA |volume=254 |issue=24 |pages=3449-53 |year=1985 |pmid=4068186 |doi=}}</ref>  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.<ref name="pmid17679673">{{cite journal |author= |title=Independent predictors of stroke in patients with atrial fibrillation: a systematic review |journal=Neurology |volume=69 |issue=6 |pages=546-54 |year=2007 |pmid=17679673 |doi=10.1212/01.wnl.0000267275.68538.8d}}</ref> The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.<ref name="pmid3627174">{{cite journal |author=Kopecky SL, Gersh BJ, McGoon MD, ''et al'' |title=The natural history of lone atrial fibrillation. A population-based study over three decades |journal=N. Engl. J. Med. |volume=317 |issue=11 |pages=669-74 |year=1987 |pmid=3627174 |doi=}}</ref>  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 [[National Institute for Health and Clinical Excellence|NICE]] guidelines recommend using a [[clinical prediction rule]] for this purpose.<ref name="nice">{{cite web |author=National Institute for Health and Clinical Excellence|url=http://guidance.nice.org.uk/CG36 |title=Clinical Guideline 36 - Atrial fibrillation | date=June 2006 | accessdate=2007-08-15 |format= |work=}}</ref> The ''[[CHADS Score|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 [[clinical prediction rule|prediction rule]]s, the best rules were the [[CHADS Score|CHADS2]] which performed similarly to the SPAF<ref name="pmid10356104">{{cite journal |author=Hart RG, Pearce LA, McBride R, Rothbart RM, Asinger RW |title=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 |journal=Stroke |volume=30 |issue=6 |pages=1223–9 |year=1999 |pmid=10356104 |doi=}}</ref> and [[Framingham Heart Study|Framingham]]<ref name="pmid12941677">{{cite journal |author=Wang TJ, Massaro JM, Levy D, ''et al'' |title=A  risk score for predicting stroke or death in individuals with new-onset  atrial fibrillation in the community: the Framingham Heart Study |journal=JAMA |volume=290 |issue=8 |pages=1049–56 |year=2003 |pmid=12941677 |doi=10.1001/jama.290.8.1049}}</ref> [[clinical prediction rule|prediction rule]]s. <ref name="pmid17673721">{{cite journal |author=Baruch L, Gage BF, Horrow J, ''et al'' |title=Can patients at elevated risk of stroke treated with anticoagulants be further risk stratified? |journal=Stroke |volume=38 |issue=9 |pages=2459–63 |year=2007 |pmid=17673721 |doi=10.1161/STROKEAHA.106.477133}}</ref>
 
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. <ref>{{cite journal | author=van Walraven C, Hart RG, Singer DE, ''et al.''  | title=Oral anticoagulants vs aspirin in nonvalvular atrial  fibrillation: an individual patient meta-analysis | journal=JAMA |  year=2002 | volume=288 | issue=19 | pages=2441&ndash;48 | url=http://jama.ama-assn.org/cgi/content/abstract/288/19/2441|id=PMID 12435257}}</ref><ref>{{cite journal |  author=Gage BF, Cardinalli AB, Owens D. | title=Cost-effectiveness of  preference-based antithrombotic therapy for patients with nonvalvular  atrial fibrillation | journal=Stroke | year=1998 | volume=29 |  pages=1083&ndash;91 | url=http://stroke.ahajournals.org/cgi/content/abstract/29/6/1083|id=PMID 9626276 }}</ref>
 
===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).<ref name="pmid17204681">{{cite journal  |author=Paciaroni M, Agnelli G, Micheli S, Caso V |title=Efficacy  and safety of anticoagulant treatment in acute cardioembolic stroke: a  meta-analysis of randomized controlled trials |journal=Stroke |volume=38  |issue=2 |pages=423-30 | year=2007 |pmid=17204681 |doi=10.1161/01.STR.0000254600.92975.1f }} [http://www.acpjc.org/Content/147/1/issue/ACPJC-2007-147-1-017.htm ACP JC synopsis ]</ref> 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.<ref name=nice/>
 
===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%. <ref name="pmid17577005">{{cite journal |author=Hart RG, Pearce LA, Aguilar MI |title=Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation |journal=Ann Intern Med |volume=146 |issue=12 |pages=857–67 |year=2007 |pmid=17577005 |doi=}}</ref><ref name="pmid17636831">{{cite journal |author=Aguilar M, Hart R, Pearce L |title=Oral  anticoagulants versus antiplatelet therapy for preventing stroke in  patients with non-valvular atrial fibrillation and no history of stroke  or transient ischemic attacks |journal= Cochrane Database Syst Rev |volume=3 |issue= |pages=CD006186 |year=2007 |pmid=17636831 |doi=10.1002/14651858.CD006186.pub2}}</ref>. There is evidence that [[aspirin]] and [[clopidogrel]] are effective when used together, but the combination is still inferior to [[warfarin]].<ref name="pmid16765759">{{cite journal |author=Connolly S, Pogue J, Hart R, ''et al'' |title=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 |journal=Lancet |volume=367 |issue=9526 |pages=1903–12 |year=2006 |pmid=16765759 |doi=10.1016/S0140-6736(06)68845-4}}</ref>
 
Warfarin treatment requires frequent monitoring with a blood test called the [[Prothrombin time|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 valve]]s,  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.<ref>{{cite journal |  title=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 |  journal=Lancet | volume=348 | issue=9028 | pages=633–638 | year=1996  |url=http://www.thelancet.com/journals/lancet/article/PIIS0140673696034873/abstract | pmid=8782752 | doi=10.1016/S0140-6736(96)03487-3}}</ref>
==Use of the CHADS Score to Risk Stratify Patients and Determine the Appropriate Anticoagulation Strategy==
==Use of the CHADS Score to Risk Stratify Patients and Determine the Appropriate Anticoagulation Strategy==


==Method==
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
!
!Condition
!Points
|-
| &nbsp;'''C'''&nbsp;
| &nbsp;[[Congestive heart failure]]
| <center>1</center>
|-
| &nbsp;'''H'''
| &nbsp;[[Hypertension]]: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)
| <center>1</center>
|-
| &nbsp;'''A'''
| &nbsp;Age >/=75 years
| <center>1</center>
|-
| &nbsp;'''D'''
| &nbsp;[[Diabetes Mellitus]]
| <center>1</center>
|-
| &nbsp;'''S<sub>2</sub>''' 
| &nbsp;Prior [[Stroke]] or [[Transient ischemic attack | TIA]] 
| <center>2</center>
|}
 
'''CHADS score''' or '''CHADS<sub>2</sub> score''' is a [[clinical prediction rule]] for estimating the risk of [[stroke]] in patients with [[rheumatic fever|non-rheumatic]] [[atrial fibrillation| atrial&nbsp;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,<ref name="pmid15477396 ">{{cite journal |  title=Selecting patients with atrial fibrillation for anticoagulation:  stroke risk stratification in patients taking aspirin |  journal=Circulation | year=2004 | volume=110 | issue=16 |  pages=2287&ndash;92 | author=Gage BF, van Walraven C, Pearce L, ''et al.'' | pmid=15477396 | doi=10.1161/01.CIR.0000145172.55640.93 | url=http://circ.ahajournals.org/cgi/content/full/110/16/2287}}</ref> since AF can cause stasis of blood in the upper [[Heart chamber|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 CHADS<sub>2</sub> score corresponds to a greater risk of stroke, while a low CHADS<sub>2</sub> score corresponds to a lower risk of stroke. The CHADS<sub>2</sub>  score was validated by a study of nonrheumatic atrial fibrillation  patients aged 65 to 95 who were not prescribed the anticoagulant [[warfarin]].<ref name=Gage2001>{{cite journal |author=Gage  BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ  |title=Validation of clinical classification schemes for predicting  stroke: results from the National Registry of Atrial Fibrillation  |journal=JAMA |volume=285 |issue=22 |pages=2864–70 |year=2001 |url=http://jama.ama-assn.org/cgi/content/full/285/22/2864 |pmid=11401607 |doi=}}</ref>
 
===How to Calculate the CHADS<sub>2</sub> Score===
The CHADS<sub>2</sub> scoring table is shown above:<ref> {{cite web|url=http://www.cardiology.org/tools/risk_of_stroke_AF.html  |title=Risk of Stroke with AF |accessdate=2007-09-14 |publisher=VA Palo  Alto Medical Center and at Stanford University: the Sportsmedicine  Program and the Cardiomyopathy Clinic }}</ref><br />
The CHADS<sub>2</sub> scoring table is shown above:<ref> {{cite web|url=http://www.cardiology.org/tools/risk_of_stroke_AF.html  |title=Risk of Stroke with AF |accessdate=2007-09-14 |publisher=VA Palo  Alto Medical Center and at Stanford University: the Sportsmedicine  Program and the Cardiomyopathy Clinic }}</ref><br />


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<br>
<br>


==Risk of stroke==
===Risk of stroke===
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
|+Annual Stroke Risk<ref name=Gage2001 />
|+Annual Stroke Risk<ref name=Gage2001 />
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| <center>10.5–27.4</center>
| <center>10.5–27.4</center>
|}
|}
According to the findings of the validation study, the risk of stroke as a percentage per year is:
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:


However, warfarin has its own stroke risk<ref name='Steiner2006'> {{cite journal|title=Intracerebral  hemorrhage associated with oral anticoagulant therapy: current  practices and unresolved  questions.|journal=Stroke|year=2006|first=Thorsten|last=Steiner|coauthors=Jonathan  Rosand, Michael Diringer|volume=37|issue=1|pages=256–62|id=PMID  16339459 {{doi|10.1161/01.STR.0000196989.09900.f8}}|url=http://stroke.ahajournals.org/cgi/reprint/37/1/256|format=|accessdate= }}</ref> and other drawbacks, which were considered in developing the recommendations of the next section.
While the CHADS<sub>2</sub>  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<ref name='Steiner2006'> {{cite journal|title=Intracerebral  hemorrhage associated with oral anticoagulant therapy: current  practices and unresolved  questions.|journal=Stroke|year=2006|first=Thorsten|last=Steiner|coauthors=Jonathan  Rosand, Michael Diringer|volume=37|issue=1|pages=256–62|id=PMID  16339459 {{doi|10.1161/01.STR.0000196989.09900.f8}}|url=http://stroke.ahajournals.org/cgi/reprint/37/1/256|format=|accessdate= }}</ref> (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 CHADS<sub>2</sub> score has various limitations, which have been debated <ref>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.</ref>.  Notably, many stroke risk factors  have not been included, and whilst simple, the score has only modest  predictive value for thromboembolism.
The CHADS<sub>2</sub> score has various limitations, which have been debated <ref>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.</ref>.  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 CHADS<sub>2</sub> score and to incorporate additional stroke risk factors, the [[CHA2DS2-VASc score]] has been proposed <ref>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.</ref>.  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. 


To complement the CHADS<sub>2</sub> score, by the inclusion of additional 'stroke risk modifier' risk factors, the [http://www.ganfyd.org/index.php?title=CHA2DS2-VASc_score CHA2DS2-VASc score] has been proposed <ref>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.</ref>.  These additional 'clinically  relevant non-major' stroke risk factors include age 65-74, female gender  and vascular disease.  In the [http://www.ganfyd.org/index.php?title=CHA2DS2-VASc_score CHA2DS2-VASc score] score, 'age 75 and above' also has extra weight, with 2 points. 
The [[CHA2DS2-VASc score]] has been used in the new [http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/atrial-fibrillation.aspx European Society of Cardiology guidelines for the management of atrial fibrillation] <ref>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.</ref>.
 
The [http://www.ganfyd.org/index.php?title=CHA2DS2-VASc_score CHA2DS2-VASc score] has been used in the new [http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/atrial-fibrillation.aspx European Society of Cardiology guidelines for the management of atrial fibrillation] <ref>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.</ref>.


The European Society of Cardiology (ESC) guidelines recommend that if the patient has a CHADS<sub>2</sub> score of 2 and above, oral anticoagulation therapy (OAC, eg. with warfarin(INR2-3) or one of the new OAC drugs, such as dabigatran)should  be prescribed.   
The European Society of Cardiology (ESC) guidelines recommend that if the patient has a CHADS<sub>2</sub> 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 CHADS<sub>2</sub> score is 0-1, other stroke risk modifiers should be considered: (i) If we have 2 or more risk factors (essentially a [http://www.ganfyd.org/index.php?title=CHA2DS2-VASc_score CHA2DS2-VASc score] score of 2 or more), OAC is recommended; and (ii) If we have 1 risk factor (essentially a [http://www.ganfyd.org/index.php?title=CHA2DS2-VASc_score CHA2DS2-VASc score] score=1), antithrombotic therapy with OAC or aspirin (OAC preferred) is recommended, and patient values and preferences should be considered.  
If the CHADS<sub>2</sub> 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 [http://www.ganfyd.org/index.php?title=CHA2DS2-VASc_score CHA2DS2-VASc score] score=0, such patients are ‘truly low risk’<ref>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.</ref>, and thus, the ESC guideline recommendation  is to prescribe either aspirin or no antithrombotic therapy, but 'no antithrombotic therapy' is preferred<ref>Lip  GY, Halperin JL. Improving stroke risk stratification in atrial  fibrillation. Am J Med. 2010 Jun;123(6):484-8. </ref>.
If patients have a [[CHA2DS2-VASc score]] of 0, then such patients are ‘truly low risk’<ref>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.</ref>. The ESC guidelines recommend either aspirin or no antithrombotic therapy, but 'no antithrombotic therapy' is preferred<ref>Lip  GY, Halperin JL. Improving stroke risk stratification in atrial  fibrillation. Am J Med. 2010 Jun;123(6):484-8. </ref>.


==Anticoagulation based on the CHADS<sub>2</sub> score ==
===Anticoagulation based on the CHADS<sub>2</sub> score ===
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
|-
|-
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| Moderate
| Moderate
| Aspirin or Warfarin
| Aspirin or Warfarin
| Aspirin daily or raise [[International normalized ratio|INR]] to 2.0-3.0, depending on factors such as patient preference  
| Aspirin daily or [[International normalized ratio|INR]] to 2.0-3.0, depending on factors such as patient preference  
|-
|-
| '''2 or greater'''
| '''2 or greater'''
| Moderate or High  
| Moderate or High  
| [[Warfarin]]
| [[Warfarin]]
| Raise [[International normalized ratio|INR]] to 2.0-3.0, unless contraindicated (e.g. clinically significant GI bleeding, inability to obtain regular INR screening)
| [[International normalized ratio|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 to the right:<ref name="pmid15477396 " /><ref name=Gage2001 />
The following treatment strategies were recommended in the table entitled Anticoagulation based on the CHADS2 score:<ref name="pmid15477396 " /><ref name=Gage2001 />


For detailed recommendations on how the treatment recommendations based on the CHADS<sub>2</sub> score are modified by considering additional 'stroke risk modifier' risk factors using the CHA2DS2-VASc score, see [http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/atrial-fibrillation.aspx ESC guideline] recommendations.
For detailed recommendations on how the treatment recommendations based on the CHADS<sub>2</sub> score are modified by considering additional 'stroke risk modifier' risk factors using the CHA2DS2-VASc score, see [http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/atrial-fibrillation.aspx ESC guideline] recommendations.
<br>
<br>


==Assessment of Bleeding Risk with Anticoagulation==
The decision to anticoagulate a patient should also be based upon an assessment of the risk of bleeding using a score such as the [[HAS-BLED score]].


==Anticoagulation in Special Populations==
===Elderly patients===
The very elderly (patients aged 75 years or more) may benefit from anticoagulation provided that their anticoagulation 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.<ref name="pmid17515465">{{cite journal |author=Hylek EM, Evans-Molina C, Shea C, Henault LE, Regan S |title=Major hemorrhage and tolerability of warfarin in the first year of therapy among elderly patients with atrial fibrillation |journal=Circulation |volume=115 |issue=21 |pages=2689-96 |year=2007 |pmid=17515465 |doi=10.1161/CIRCULATIONAHA.106.653048}}</ref> 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.<ref name="pmidpendingMant"> {{cite journal  |author=Mant J et al |title=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 |journal=Lancet |volume=370  |issue= |pages=493-503 | year=2007 |pmid= |doi=10.1016/S0140-6736(07)61233-1}}</ref> Of note, this study had very low rate of hemorrhagic complications in the warfarin group.


===Anticoagulation===
==Treatment of Modifiable Risk Factors==
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.<ref name="pmid4068186">{{cite journal |author=Brand FN, Abbott RD, Kannel WB, Wolf PA |title=Characteristics and prognosis of lone atrial fibrillation. 30-year follow-up in the Framingham Study |journal=JAMA |volume=254 |issue=24 |pages=3449-53 |year=1985 |pmid=4068186 |doi=}}</ref>  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.<ref name="pmid17679673">{{cite journal |author= |title=Independent predictors of stroke in patients with atrial fibrillation: a systematic review |journal=Neurology |volume=69 |issue=6 |pages=546-54 |year=2007 |pmid=17679673 |doi=10.1212/01.wnl.0000267275.68538.8d}}</ref> The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.<ref name="pmid3627174">{{cite journal |author=Kopecky SL, Gersh BJ, McGoon MD, ''et al'' |title=The natural history of lone atrial fibrillation. A population-based study over three decades |journal=N. Engl. J. Med. |volume=317 |issue=11 |pages=669-74 |year=1987 |pmid=3627174 |doi=}}</ref> 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.
The treatment of modifiable risk factors in patients with AF may help in maintaining the sinus rhythm. <ref name="pmid24240932">{{cite journal| author=Abed HS, Wittert GA, Leong DP, Shirazi MG, Bahrami B, Middeldorp ME | display-authors=etal| title=Effect of weight reduction and cardiometabolic risk factor management on symptom burden and severity in patients with atrial fibrillation: a randomized clinical trial. | journal=JAMA | year= 2013 | volume= 310 | issue= 19 | pages= 2050-60 | pmid=24240932 | doi=10.1001/jama.2013.280521 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24240932  }} </ref>  <ref name="pmid32148086">{{cite journal| author=Chung MK, Eckhardt LL, Chen LY, Ahmed HM, Gopinathannair R, Joglar JA | display-authors=etal| title=Lifestyle and Risk Factor Modification for Reduction of Atrial Fibrillation: A Scientific Statement From the American Heart Association. | journal=Circulation | year= 2020 | volume= 141 | issue= 16 | pages= e750-e772 | pmid=32148086 | doi=10.1161/CIR.0000000000000748 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32148086  }} </ref> <ref name="pmid29401239">{{cite journal| author=Rienstra M, Hobbelt AH, Alings M, Tijssen JGP, Smit MD, Brügemann J | display-authors=etal| title=Targeted therapy of underlying conditions improves sinus rhythm maintenance in patients with persistent atrial fibrillation: results of the RACE 3 trial. | journal=Eur Heart J | year= 2018 | volume= 39 | issue= 32 | pages= 2987-2996 | pmid=29401239 | doi=10.1093/eurheartj/ehx739 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29401239  }} </ref>
A recent scientific statement by the American Heart Association suggested weight reduction for achieving a [[BMI]] of <27 kg/m2 along with regular moderate exercise and management of [[diabetes]], [[hyperlipidemia]] and [[sleep apnea]], smoking cessation, and reduction of alcohol intake for reduction of [[atrial fibrillation]]. <ref name="pmid32148086">{{cite journal| author=Chung MK, Eckhardt LL, Chen LY, Ahmed HM, Gopinathannair R, Joglar JA | display-authors=etal| title=Lifestyle and Risk Factor Modification for Reduction of Atrial Fibrillation: A Scientific Statement From the American Heart Association. | journal=Circulation | year= 2020 | volume= 141 | issue= 16 | pages= e750-e772 | pmid=32148086 | doi=10.1161/CIR.0000000000000748 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32148086  }} </ref>


In the United Kingdom, the [[National Institute for Health and Clinical Excellence|NICE]] guidelines recommend using a [[clinical prediction rule]] for this purpose.<ref name="nice">{{cite web |author=National Institute for Health and Clinical Excellence|url=http://guidance.nice.org.uk/CG36 |title=Clinical Guideline 36 - Atrial fibrillation | date=June 2006 | accessdate=2007-08-15 |format= |work=}}</ref> The ''[[CHADS Score|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 [[clinical prediction rule|prediction rule]]s, the best rules were the [[CHADS Score|CHADS2]] which performed similarly to the SPAF<ref name="pmid10356104">{{cite journal |author=Hart RG, Pearce LA, McBride R, Rothbart RM, Asinger RW |title=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 |journal=Stroke |volume=30 |issue=6 |pages=1223–9 |year=1999 |pmid=10356104 |doi=}}</ref> and [[Framingham Heart Study|Framingham]]<ref name="pmid12941677">{{cite journal |author=Wang TJ, Massaro JM, Levy D, ''et al'' |title=A risk score for predicting stroke or death in individuals with new-onset atrial fibrillation in the community: the Framingham Heart Study |journal=JAMA |volume=290 |issue=8 |pages=1049–56 |year=2003 |pmid=12941677 |doi=10.1001/jama.290.8.1049}}</ref> [[clinical prediction rule|prediction rule]]s. <ref name="pmid17673721">{{cite journal |author=Baruch L, Gage BF, Horrow J, ''et al'' |title=Can patients at elevated risk of stroke treated with anticoagulants be further risk stratified? |journal=Stroke |volume=38 |issue=9 |pages=2459–63 |year=2007 |pmid=17673721 |doi=10.1161/STROKEAHA.106.477133}}</ref>
==Vote on and Suggest Revisions to the Current Guidelines==
 
* [[The Living Guidelines: Diagnosis and Management of Atrial Fibrillation | The AF Living Guidelines: Vote on current recommendations and suggest revisions to the guidelines]]
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. <ref>{{cite journal | author=van Walraven C, Hart RG, Singer DE, ''et al.'' | title=Oral anticoagulants vs aspirin in nonvalvular atrial fibrillation: an individual patient meta-analysis | journal=JAMA | year=2002 | volume=288 | issue=19 | pages=2441&ndash;48 | url=http://jama.ama-assn.org/cgi/content/abstract/288/19/2441|id=PMID 12435257}}</ref><ref>{{cite journal | author=Gage BF, Cardinalli AB, Owens D. | title=Cost-effectiveness of preference-based antithrombotic therapy for patients with nonvalvular atrial fibrillation | journal=Stroke | year=1998 | volume=29 | pages=1083&ndash;91 | url=http://stroke.ahajournals.org/cgi/content/abstract/29/6/1083|id=PMID 9626276 }}</ref>
 
====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).<ref name="pmid17204681">{{cite journal  |author=Paciaroni M, Agnelli G, Micheli S, Caso V |title=Efficacy and safety of anticoagulant treatment in acute cardioembolic stroke: a meta-analysis of randomized controlled trials |journal=Stroke |volume=38  |issue=2 |pages=423-30 | year=2007 |pmid=17204681 |doi=10.1161/01.STR.0000254600.92975.1f }} [http://www.acpjc.org/Content/147/1/issue/ACPJC-2007-147-1-017.htm ACP JC synopsis ]</ref> 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.<ref name=nice/>
 
====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%. <ref name="pmid17577005">{{cite journal |author=Hart RG, Pearce LA, Aguilar MI |title=Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation |journal=Ann Intern Med |volume=146 |issue=12 |pages=857–67 |year=2007 |pmid=17577005 |doi=}}</ref><ref name="pmid17636831">{{cite journal |author=Aguilar M, Hart R, Pearce L |title=Oral anticoagulants versus antiplatelet therapy for preventing stroke in patients with non-valvular atrial fibrillation and no history of stroke or transient ischemic attacks |journal= Cochrane Database Syst Rev |volume=3 |issue= |pages=CD006186 |year=2007 |pmid=17636831 |doi=10.1002/14651858.CD006186.pub2}}</ref>. There is evidence that [[aspirin]] and [[clopidogrel]] are effective when used together, but the combination is still inferior to [[warfarin]].<ref name="pmid16765759">{{cite journal |author=Connolly S, Pogue J, Hart R, ''et al'' |title=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 |journal=Lancet |volume=367 |issue=9526 |pages=1903–12 |year=2006 |pmid=16765759 |doi=10.1016/S0140-6736(06)68845-4}}</ref>
 
Warfarin treatment requires frequent monitoring with a blood test called the [[Prothrombin time|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 valve]]s, 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.<ref>{{cite journal | title=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 | journal=Lancet | volume=348 | issue=9028 | pages=633–638 | year=1996 |url=http://www.thelancet.com/journals/lancet/article/PIIS0140673696034873/abstract | pmid=8782752 | doi=10.1016/S0140-6736(96)03487-3}}</ref>
 
===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.<ref name="pmid17515465">{{cite journal |author=Hylek EM, Evans-Molina C, Shea C, Henault LE, Regan S |title=Major hemorrhage and tolerability of warfarin in the first year of therapy among elderly patients with atrial fibrillation |journal=Circulation |volume=115 |issue=21 |pages=2689-96 |year=2007 |pmid=17515465 |doi=10.1161/CIRCULATIONAHA.106.653048}}</ref> 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.<ref name="pmidpendingMant"> {{cite journal  |author=Mant J et al |title=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 |journal=Lancet |volume=370  |issue= |pages=493-503 | year=2007 |pmid= |doi=10.1016/S0140-6736(07)61233-1}}</ref> 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====
==Guideline Resources==
{{main|Antiarrhythmic agent}}
*[http://content.onlinejacc.org/cgi/reprint/48/4/e149.pdf ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation] <ref name="pmid16908781">Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA et al. (2006) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=16908781 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. [http://dx.doi.org/10.1161/CIRCULATIONAHA.106.177292 DOI:10.1161/CIRCULATIONAHA.106.177292] PMID: [http://pubmed.gov/16908781 16908781]</ref>
The [[antiarrhythmic agent|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==
*[http://circ.ahajournals.org/content/123/10/e269.full.pdf 2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation] <ref name="pmid21382897">Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA et al. (2011) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=21382897 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. [http://dx.doi.org/10.1161/CIR.0b013e318214876d DOI:10.1161/CIR.0b013e318214876d] PMID: [http://pubmed.gov/21382897 21382897]</ref>
* [[The Living Guidelines: Diagnosis and Management of Atrial Fibrillation | The AF Living Guidelines: Vote on current recommendations and suggest revisions to the guidelines]]


==Sources==
*[http://circ.ahajournals.org/content/117/8/1101.full.pdf ACC/AHA/Physician Consortium 2008 clinical performance measures for adults with nonvalvular atrial fibrillation or atrial flutter] <ref name="pmid18283199">Estes NA, Halperin JL, Calkins H, Ezekowitz MD, Gitman P, Go AS et al. (2008) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=18283199 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. [http://dx.doi.org/10.1161/CIRCULATIONAHA.107.187192 DOI:10.1161/CIRCULATIONAHA.107.187192] PMID: [http://pubmed.gov/18283199 18283199]</ref>
* The ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation <ref name="Fuster"> 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 </ref>


==References==
==References==
{{reflist|2}}
{{reflist|2}}
==Further Readings==
{{refbegin|2}}
* 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
{{refend}}
{{Electrocardiography}}
{{Circulatory system pathology}}
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Latest revision as of 17:49, 23 March 2022

Atrial Fibrillation Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Atrial Fibrillation from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Special Groups

Postoperative AF
Acute Myocardial Infarction
Wolff-Parkinson-White Preexcitation Syndrome
Hypertrophic Cardiomyopathy
Hyperthyroidism
Pulmonary Diseases
Pregnancy
ACS and/or PCI or valve intervention
Heart failure

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

EKG Examples
A-Fib with LBBB

Chest X Ray

Echocardiography

Holter Monitoring and Exercise Stress Testing

Cardiac MRI

Treatment

Rate and Rhythm Control

Cardioversion

Overview
Electrical Cardioversion
Pharmacological Cardioversion

Anticoagulation

Overview
Warfarin
Converting from or to Warfarin
Converting from or to Parenteral Anticoagulants
Dabigatran

Maintenance of Sinus Rhythm

Surgery

Catheter Ablation
AV Nodal Ablation
Surgical Ablation
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Atrial fibrillation overview of treatment On the Web

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Risk calculators and risk factors for Atrial fibrillation overview of treatment

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief: Mitra Chitsazan, M.D.[2]

Goals of Atrial Fibrillation Treatment

The primary goals in the management of patients with atrial fibrillation include:

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. [2] [3][4][4][5][6][7] The lack of atrial contraction can be diagnosed on echocardiography by the appearance of spontaneous echo contrast. [2] 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[8][9][10] 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. [11] 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.[12] 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.

Maintenance of Rhythm Control

Avoidance of stimulants such as caffeine, alcohol withdrawal, binge drinking, and holiday heart syndrome may be critical in reducing the recurrence of atrial fibrillation. Drugs such as digoxin and hyperthyroidism, hypokalemia, sleep apnea and pheochromocytoma are all associated with atrial fbrillation. Antiarrhythmics may also be critical to maintaining normal sinus rhythm. Recommendations for specific populations of patients are provided below:

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 the AF is associated with severe symptoms related to hypotension, myocardial ischemia, or heart failure. 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. Recommendations for specific patient populations follow:

Vagally mediated Atrial fibrillation

Disopyramide or flecainide are recommended.

Adrenergically induced Atrial Fibrillation

Beta blockers including sotalol are recommended.

Congestive Heart Failure

Amiodarone or dofetilide are recommended.

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.[13] 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.[14] The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.[15] 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.[16] 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[17] and Framingham[18] prediction rules. [19]

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. [20][21]

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).[22] 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.[16]

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%. [23][24]. There is evidence that aspirin and clopidogrel are effective when used together, but the combination is still inferior to warfarin.[25]

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.[26]

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,[27] 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.[28]

How to Calculate the CHADS2 Score

The CHADS2 scoring table is shown above:[29]

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[28]
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[30] (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 [31]. 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 [32]. 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 [33].

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’[34]. The ESC guidelines recommend either aspirin or no antithrombotic therapy, but 'no antithrombotic therapy' is preferred[35].

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:[27][28]

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.

Assessment of Bleeding Risk with Anticoagulation

The decision to anticoagulate a patient should also be based upon an assessment of the risk of bleeding using a score such as the HAS-BLED score.

Anticoagulation in Special Populations

Elderly patients

The very elderly (patients aged 75 years or more) may benefit from anticoagulation provided that their anticoagulation 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.[36] 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.[37] Of note, this study had very low rate of hemorrhagic complications in the warfarin group.

Treatment of Modifiable Risk Factors

The treatment of modifiable risk factors in patients with AF may help in maintaining the sinus rhythm. [38] [39] [40] A recent scientific statement by the American Heart Association suggested weight reduction for achieving a BMI of <27 kg/m2 along with regular moderate exercise and management of diabetes, hyperlipidemia and sleep apnea, smoking cessation, and reduction of alcohol intake for reduction of atrial fibrillation. [39]

Vote on and Suggest Revisions to the Current Guidelines

Guideline Resources

References

  1. ↑ 1.0 1.1 Fuster V, Rydén 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, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL (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. Unknown parameter |month= ignored (help)
  2. ↑ 2.0 2.1 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)
  3. ↑ 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)
  4. ↑ 4.0 4.1 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)
  5. ↑ 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)
  6. ↑ 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)
  7. ↑ 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)
  8. ↑ 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)
  9. ↑ 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)
  10. ↑ 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)
  11. ↑ 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)
  12. ↑ 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)
  13. ↑ 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.
  14. ↑ "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.
  15. ↑ 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.
  16. ↑ 16.0 16.1 National Institute for Health and Clinical Excellence (June 2006). "Clinical Guideline 36 - Atrial fibrillation". Retrieved 2007-08-15.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ "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.
  27. ↑ 27.0 27.1 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.
  28. ↑ 28.0 28.1 28.2 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.
  29. ↑ "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.
  30. ↑ 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)
  31. ↑ 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.
  32. ↑ 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.
  33. ↑ 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.
  34. ↑ 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.
  35. ↑ Lip GY, Halperin JL. Improving stroke risk stratification in atrial fibrillation. Am J Med. 2010 Jun;123(6):484-8.
  36. ↑ 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.
  37. ↑ 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.
  38. ↑ Abed HS, Wittert GA, Leong DP, Shirazi MG, Bahrami B, Middeldorp ME; et al. (2013). "Effect of weight reduction and cardiometabolic risk factor management on symptom burden and severity in patients with atrial fibrillation: a randomized clinical trial". JAMA. 310 (19): 2050–60. doi:10.1001/jama.2013.280521. PMID 24240932.
  39. ↑ 39.0 39.1 Chung MK, Eckhardt LL, Chen LY, Ahmed HM, Gopinathannair R, Joglar JA; et al. (2020). "Lifestyle and Risk Factor Modification for Reduction of Atrial Fibrillation: A Scientific Statement From the American Heart Association". Circulation. 141 (16): e750–e772. doi:10.1161/CIR.0000000000000748. PMID 32148086 Check |pmid= value (help).
  40. ↑ Rienstra M, Hobbelt AH, Alings M, Tijssen JGP, Smit MD, Brügemann J; et al. (2018). "Targeted therapy of underlying conditions improves sinus rhythm maintenance in patients with persistent atrial fibrillation: results of the RACE 3 trial". Eur Heart J. 39 (32): 2987–2996. doi:10.1093/eurheartj/ehx739. PMID 29401239.
  41. ↑ 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
  42. ↑ 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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