This document provides guidelines for the classification and management of atrial fibrillation (AF). It discusses the introduction, classification, mechanisms, causes and features of AF. The diagnostic evaluation and management guidelines cover rate control versus rhythm control strategies, pharmacological and electrical cardioversion options, and drugs used for rate and rhythm control. The goals are to control the heart rate, prevent thromboembolism, and restore normal sinus rhythm when possible. Management is individualized based on the frequency, duration and symptoms of AF and patient characteristics.

1. ATRIAL FIBRILLATION CLASSIFICATION
&
MANAGEMENT GUIDELINE
Dr. Rohan Sonawane
JR MD (Internal
medicine)
Dr. V. P. Sinha
MD, DM (Cardiology)

2. 1) Introduction
2) Classification
3) Mechanism of AF
4) Causes & Clinical Features
5) Diagnostic Evaluation
6) Management Guidelines

3. INTRODUCTION
- Atrial fibrillation (AF) is a supraventricular arrhythmia
which is disorganised, rapid & uncoordinated atrial
activation characterized electrocardiographically by
low-amplitude baseline oscillations (fibrillatory or f
waves) and an irregularly irregular ventricular rhythm.
- The f waves have a rate of 300 to 600 beats/min
and are variable in amplitude, shape, and timing.
- The Ventricular rate during AF typically is100 –
160/min which can exceed > 250 beats/min in Wolf-
Parkinson-White Syndrome due to conduction over
accessory pathway.

4. Comparison between f waves of AF(top panel) and flutter waves of atrial
flutter(bottom panel). Here f waves are variable in rate ,shape and amplitude
whereas flutter waves are constant in rate and all aspects of morphology

5. AF with prominent f waves in V₁ that mimic atrial flutter waves. But the typical f
waves are present in leads II and V₅, which establish the diagnosis of AF

6. A 12-lead ECG of AF in which f waves are not discernible. The irregularly
irregular ventricular rate indicates that this is AF and not a junctional rhythm.

7. CLASSIFICATION

8. TERM DEFINATION
Paroxysmal AF - AF that terminates spontaneously or with intervention
within 7 days of onset. (most < 24 hours)
· Episodes may recur with variable frequency.
Persistent AF -Continuous AF that is sustained >7 days.
Longstanding
persistent AF
-Continuous AF of >12 months duration.
Permanent AF -Continuous AF >12 months refractory to cardioverson
-Permanent AF is used when there has been a joint
decision by the patient and clinician to cease further
attempts to restore and/or maintain sinus rhythm.
Nonvalvular AF AF in the absence of rheumatic mitral stenosis, a
mechanical or bioprosthetic heart valve, or mitral valve
repair.
Lone AF -Individuals under 60 years old without clinical or
echocardiographic evidence of cardiopulmonary
disease,including hypertension
-These patients have a favorable prognosis with respect to
thromboembolism and mortality.

9. Paroxysmal AF
Vagotonic AF Adrinergic AF Mixed or random
-25% of paroxysmal
AF
-Initiated in setting
of high vagol tone
typically in evening
when pt is relaxing
or during sleep
-10 - 15% of
paroxysmal AF
-- in setting of high
sympathetic tone
like strenuous
exercise

10. MECHANISM OF ARTIAL FIBRILLATION
Various phenotypes of AF have different electro physiologic
characteristics because of remodelling and different clinical modulators that
affect the substrate, such as heart failure, atrial stretch and ischemia,
sympatho-vagal influences, inflammation and fibrosis.
Electrophysiological mechanism:
-- One or more automatic, triggered or micro-re entrant foci, so
called drivers, which fires at rapid rates and cause fibrillation. Rapid
discharges from pulmonary veins are the most common triggers of AF more
so in Paroxysmal AF than in Persistent AF
-- Multiple re-entrant circuits wondering throughout the artia,
destroying and reforming wavelets that cause fibrillation.
-- Other mechanism that seen in Persistent is change in atrial
substrate, including interstitial fibrosis that causes slow, discontinuous and
anisotropic conduction, may give rise to Complex Fractionated Atrial Electro
gram ( CFAEs ) and re-entry

13. CAUSES & CLINICAL FEATURES
Causes of AF:
• Hypertension
• Ischemic heart disease
• Mitral valve disease
• Hypertrophic Cardiomyopathy
• Less common causes like restrictive cardiomyopathies like
amyloidosis, constrictive pericarditis, Cardiac tumours and sever
pulmonary hypertension, Thoracic or cardiac surgery.
• Wolf- Parkinson-White syndrome may degenerate in to AF
• Obesity- Atrial dilatation and increased systemic inflammatory
factors like CRP are responsible for AF
• Obstructive sleep apnoea- Hypoxia, surge in autonomic tone and
Hypertension are responsible for AF
• Temporary or reversible causes like Alcohol intake called
“Holiday heart”.
• Most common correctible cause is hyperthyroidism.

14. Clinical Features:
AF has a wide range of symptoms from none to severe disabling
symptoms. The most common symptoms of AF are
- Palpitation
- Fatigue
- Dypsnea
- Effort intolerance
- Light-headedness
- Syncope- is an uncommon symptoms, most often
caused by long sinus pause of AF in a patient with sick
sinus syndrome or Drop in blood
pressure due to sudden reduction in cardiac output in
structurally heart diseases.
- Some time asymptomatic patient does not seek medical
care and directly present with stroke or heart failure.

15. DIAGNOSTIC EVALUATION

16. MANAGEMENT OF AF
Management of AF depends on Patient present in emergency with
AF with rapid ventricular rate or patient haemodynamically stable or
unstable, but overall Management of patients with AF involves 3, not
mutually exclusive,
objectives—rate control,
prevention of thromboembolism and
correction of the rhythm disturbance.
Regardless of whether the rate control or rhythm control strategy is
pursued, attention must also be directed to antithrombotic therapy for
prevention of thromboembolism.

17. RATE CONTROL VERSUS RHYTHM CONTROL
The AFFIRM study and RACE trial have convincingly demonstrated
that rate control is no inferior to rhythm control especially in
asymptomatic or minimally symptomatic patients of age> 65yrs
Decision of a rate control strategy v/s a rhythm control strategy is to
be individualized taking several factors into account which include:
1) Nature
2) Frequency
3) Severity of symptoms
4) Length of time of AF
5) Left atrial size (>5.0 cm)
6) Other co morbidities
7) Response to prior cardioversion
8) Age
9) Side effects and efficacy of drugs used
10) Patient’s preference

18. RATE CONTROL
An excessively rapid ventricular rate during AF results in
uncomfortable symptoms and decrease effect intolerance and can cause a
tachycardia induced cardiomyopathy if it is sustained for several weeks to
month. Heart rate control must be assessed both at rest and during exertion.
The goals of rate control according to AHA/ACC recommendations
are as follows to achieve our desired heart rates:
1) At rest :- 60-80 beats/min
2) Mild to moderate exertion :- 90-115 beats/min
3) During strenuous exercise :- 120-160 beats/min
But recent randomized control trials have given 2 ways of rate control
targets and comparative analysis of both of them :
1) Lenient rate control
Target was focused on getting the heart rate at < 110 beats /min
2) Strict rate control
Target was same as discussed above i.e. < 80 beats/min at rest
and <110 beats/min with moderate exercise
And finally it was found that lenient rate control was easier to achieve and was
no inferior to strict rate control along with lesser mortality.

19. INTRAVENOUS AND ORAL RATE CONTROL AGENTS USED IN
ATRIAL FIBRILLATION
DRUGS INTRAVENOUS ADMINISTRATION ORAL
ADMINISTRATION
BETA BLOCKER:
Metoprolol tartrate 2.5–5.0 mg IV bolus over 2 min; up to 3
doses
25–100 mg BID
Metoprolol XL
(succinate)
N/A 50–400 mg QD
Atenolol N/A 25–100 mg QD
Esmolol 500 mcg/kg IV bolus over 1 min, then
50–300 mcg/kg/min
IV
N/A
Propranolol 1 mg IV over 1 min, up to 3 doses at 2
min intervals
10–40 mg TID or QID
Nodalol N/A 10-240 mg QD
Carvedilol N/A 3.125- 25 mg BID
Bisoprolol N/A 2.5 – 10 mg QD

20. Nondihydropyridine calcium channel antagonists:
Verapamil (0.075-0.15 mg/kg) IV bolus over 2 min, may
give an additional 10.0 mg after 30 min if no
response, then 0.005 mg/kg/min infusion
180 – 480 mg QD
(ER)
Diltiazem 0.25 mg/kg IV bolus over 2 min, then 5-15
mg/h
120 – 360 mg QD
(ER)
Digitalis Glycosides :
Digoxin 0.25 mg IV bolus repeat dosing to a maximum
of 1.5 mg over 24 hours
0.125 – 0.25 mg QD
Others :
Amiodarone 300 mg IV over 1 hour, then 10 – 15 mg/h over
24 hours
100-200 mg QD

21. RHYTHM CONTROL
In patient with persistent AF it is reasonable to attempt to restore
sinus rhythm at least in once in patients <65 yr old or in patients > 65 years
old who are symptomatic from AF despite heart rate control. If the AF has
been continuous for more than 1 year or if the left atrial diameter is very large (
> 5 cm), there is high probability of an early recurrence.
It all depends on the attending clinician about the method of rhythm
control to be applied to the patient which are:
1) DC cardiversion
2) Pharmacological cardioversion
3) Hybrid therapy

22. Hybrid therapy is one in which early rhythm control is achieved by
electrical cardioversion and concurrently after that patient is put on
antiarrhythmic drugs to maintain sinus rhythm
 Treatment by cardioversion without daily antiarrhythmic drug therapy is
appropriate if episodes of AF are separated by at least 6 months.
 Treatment with a rhythm control drug is appropriate when AF recurs
within a few months of cardioversion
 The most realistic goal of antiarrythmic drug therapy in patient with
persistent AF is to delay the onset of next episode by at least for several
months, not for several years.

23. PHARMACOLOGICAL MANAGEMENT OF PATIENTS WITH NEWLY
DISCOVERED AF

24. PHARMACOLOGICAL MANAGEMENT OF PATIENTS WITH
RECURRENT PAROXYSMAL AF

25. PHARMACOLOGICAL MANAGEMENT OF PATIENTS WITH
RECURRENT PERSISTENT OR PERMANENT AF

26. If the patient is hemodynamically unstable then early transthoracic DC
cardioversion is needed because a delay in cardioversion is never appropriate
in setting of severe cardiovascular decompensation.
If the patient is hemodynamically stable who present with AF that does
not appear to be self limiting following management decisions to be made:
Early Cardioversion:
- Performed if AF duration is <48 hours
- rapid relief of symptoms
- Avoidance of need of thansoesophageal echocardiography
- Avoidance of therapeutic anticoagulation for 3-4 weeks
- Lower risk of early AF recurrence because of less atrial
remodeling
Delayed Caedioversion:
- Duration of AF is >48 hours
- Duration is unclear in non anticoagulated patient
- Transoesophageal echocardiography not available
- Left Atrial thrombus by TEE
- Correctable causes of AF ( hyperthyroidism, achoholism)

27. In case if immediate cardioversion is needed then shock is to be
given after loading dose of unfractionated heparin followed by continuous
maintenance infusion as early as possible.
But if delayed cardioversion is to be done then protocol to be
used is
3 weeks anticoagulation cardioversion 4 weeks
anticoagulation
Post cardioversion anticoagulation is needed to prevent
thromboembolism related to atrial stunning as atria take some time to gain its
normal functioning.
For DC cardioversion an appropriate first shock strength using a
biphasic waveform is 150 - 200 J followed by higher output shocks if needed. But
if a 360-J biphasic shock is unsuccessful then ibutilide is to be given before
another shock to lower the defibrillation energy required and improve the success
rate.
Properly timed DC current with pads on anterior and posterior chest

28. There are two types of failure :
1) Complete failure
Here sinus rhythm has not been restored so increasing the shock
strength or ibutilide enhancement may turn it to be successful
1) Incomplete failure
Here sinus rhythm is attained after shock with immediate recurrence of
AF within a few seconds. In this case increasing the shock strength is
useless, ibutilide infusion may help out

29. PHARMACOLOGICAL CARDIOVERSION
Early pharmacological cardioversion can be tried in
hemodynamically stable patients as it has advantage of not requiring
anesthesia or deep sedation as well as lower probability of immediate
recurrence of AF.
“pill-in-the-pocket” i.e. episodic drug therapy was developed for
patients with relatively infrequent episodes of AF by using flecainide(100-
200mg) or propafenone(300-600 mg) including a short acting beta blocker or
CCB for rate control.

30. DOSES AND SAFETY CONSIDERATION OF DRUGS USED
FOR PHARMACOLOGICAL CARDIOVERSION
Drugs Doses Exclude/ use with caution
Vaughan Williams Class IA :
Disopyramide Immediate release: 100- 200 mg
once every 6 hr
Extended release: 200 – 400 mg
once every 12 hr
HF, Prolonged QT interval,
Glaucoma,
Quinidine 324 – 648 mg every 8 hr Prolonged QT interval,
Diarrhoea
Procainamide 0.5 – 1 gm oral or IM F/B 0.25-0.5
gm every 2 hr or 500mg IV loading
F/B 2mg/kg/hr.
Maintenance dose 0.5gm every 4-6
hr
Prolonged QT interval,
SLE

31. Vaughan Williams Class IC
Flecainide 50-200 mg once every 12 hr Sinus or V node
dysfunction, HF, CAD,
Atrial Flutter,Liver
desease
Propafenone Immediate release 150-300 mg once
every 8hr.
Extended release 225-425mg once every
12hr
Sinus or V node
dysfunction, HF, CAD,
Atrial Flutter,Liver
desease
Vaughan Williams Class III
Amiodarone Oral: 400-600 mg daily in divided doses
for 2-4 wk; maintenance typically 100-200
mg QD,
IV: 150 mg over 10 min then 1 mg/min for
6 hours then 0.5 mg /min for 18 hours or
change to oral dosing, after 24 hours
consider decreasing dose to 0.25mg/min
Sinus/AV node
dysfunction, infranodal
conduction disease,
lung disease,
prolonged QT interval
Dofetilide 125-500 mcg once every 12 hours Prolonged QT interval,
Renal disease,
Hypokalemia, Avoid
other QT interval
prolonging drugs

32. Dronedarone 400 mg once every 12 hours Bradycardia, HF,
Long standing AF/
flutter, Liver disease,
Prolonged QT interval
Sotalol 40-160 mg every 12 hours Prolonged Qt interval,
Renal Disease,
Hypokalemia, HF,
Asthma, Sinus / AV
nodal dysfunction

33. Vernakalant
It is an atrial selective antiarrythmic drug specially designed to block potassium
channels at the atrial level without any proarrythmic effects at the ventricular level
and is recommended for i.v. use.
Its use has been advocated by European Society of Cardiology for rapid
conversion of AF.
But ACT-5 trial was suspended regarding the adverse effects of vernakalant
which were hypotension, complete AV block and cardiogenic shock. Since then a
lot of controversies are prevailing regarding its use and is still in PHASE- III trial.
Dronaderone
It has been associated with increased mortality in patients even with minimal heart
failure which was well documented by ANDROMEDA trial . It is used only in europe now
where also ESC does not considers it in heart failure.
Pifenidone
This is an antifibrotic drug which also potentiates L-type calcium channels has
been recently found to be effective and is under study

34. ROLE OF STATINS, ACE INHIBITORS AND ARBS, OMEGA-
3 FATTY ACIDS, AND RANOLAZINE
Statins prevent AF because of their anti-inflammatory effects. But meta-analysis of
randomized trials have concluded that statins do not prevent AF, except after open heart
surgery
ACE inhibitors and ARBs have favourable effects on electrical and structural
remodeling and so prevent AF which is only limited to patients with left ventricular
systolic dysfunction or hypertrophy
Ranolazine blocks atrial selective late sodium channels and also inhibits L – type
calcium channels as well as RyR2 receptor

35. MANAGEMENT STRATEGIES FOR MAINTAINING SINUS
RHYTHM

36. NON PHARMACOLOGICAL METHODS
1) Catheter ablation
2) AV node ablation
3) Implanted defibrillator
4) Role of atrial pacing

37. CATHETER ABLATION
It is difficult as AF arrhythmia substrate is usually widespread. But success
rate is more than 95% if arrhythmia substrate is well defined, localized and
temporally stable
Ideal candidate is one with lone AF or only minimal structural heart disease
and the person has symptomatic AF that is affecting quality of life and that has
not adequately responded to drug therapy.
Less successful if left atrium is markedly dilated or in case of persistent AF of
more than 4 yrs duration
Most commonly used technique is radiofrequency ablation using a 3.5 mm
irrigated tip or an 8 mm tip catheter which includes electrical isolation of
pulmonary veins which is accomplished by either ostial ablation or wide area
ablation 1 to 2 cm away from the ostia, in the antral region of pulmonary veins
Risk: Cardiac tamponade, Pulmonary vain stenosis, cerebral
thromboembolism, atrioesophageal fistula

38. Different ablation strategies are :
1) Linear ablation across the left atrial roof, mitral isthmus or cavotricuspid
isthmus
2) Ablation of CFAEs in left atrium, coronary sinus,or right atrium
3) Combination of linear ablation and CFAEs ablation
4) Ablation of ganglionated plexi
 Newer ablation tools have been discovered to cut short the lengthy
procedure of point by point ablation required at large number of sites.
These are :
1) Cryobaloon catheter
2) Laser balloon catheter
3) High-density focused ultrasound balloon catheter
4) High density mesh ablator
Out of this cryoballoon catheter is most commonly used.

39. AV Node ablation
AV node ablation result in complete AV nodal block and substitute a regular,
paced rhythm for an irregular and rapid rhythm. Advantage with this is its
usefulness in tachycardia induced cardiomyopathy by improving left ventricular
ejection fraction, and disadvantage lies in lifelong need for ventricular pacing
and no restoration of AV synchrony.
Implanted defibrillator
Most appropriate candidates for an implanted atrial defibrillator are patients
with relatively infrequent episodes of poorly tolerated AF who do not respond
well to pharmacological therapy, who are not good candidates for catheter
ablation, and who qualify for an ICD.
 Limitations of atrial defibrillation are painful shocks and the potential for
immediate recurrences of AF after cardioversion.

40. Atrial pacing
Dual right atrial pacing of the interatrial septum in the region of Bachmann
bundle prevents AF
Different algorithms of pacing are to :
1) Overdrive sinus rhythm
2) Burst pacing
3) Suppression of post extrasystolic pauses
4) Acceleration of atrial pacing rate when repetitive premature atrial
complexes are sensed.
Antitachycardia pacing(ATP) which consists of a burst of rapid atrial pacing at
the onset of AF may be useful for terminaton of atrial flutter or an atrial
tachycardia, but is rarely if ever effective for AF. So due to insufficient evidence
atrial pacing is not indicated for prevention of AF in patients without
bradycardia.

41. SURGICAL TECHNIQUES
MAZE PROCEDURE
It is the most effective used surgical technique for AF. It is a cut-and-sew
procedure in which 12 atrial incisions are given to isolate pulmonary veins and
to create lines of block in the left atrium and right atrium. This procedure
requires cardiopulmonary bypass and is technically difficult to perform so is not
widely used. So gradual modifications were adopted in this technique with use
of different types of energy for surgical ablation such as radiofrequency
energy, cryoenergy, microwave, and high intensity focussed ultrasound.
THE CORRIDOR PROCEDURE
In this procedure an isolated strip of muscle is created which links the SA node
and AV node, thus driving ventricle rate via AV node – His bundle complex.
MINIMALLY INVASIVE PROCEDURES
 Complete endoscopic ablation with microwave energy
 Thoracoscopic or robotic assisted off pump epicardial microwave
ablation
 Bilateral minithoracoscopic video assisted pulmonary vein ablation
usiing bipolar radiofrequency, and others

42. PREVENTION OF THROMBOEMBOLIC COMPLICATION
Major goal of therapy in patients with AF is to prevent thromboembolic
complications notably stroke. But for this proper risk stratification and condition
is needed to be identified for an appropriate anticoagulant or any other therapy.
METHODS
• Anticoagulation
• Non-pharmacological
The strongest predictors of ischemic stroke and systemic
thromboembolism are history of stroke or TIA and mitral stenosis. For this a
simple scheme form risk stratification was developed known as CHADS₂ score.
But apart from this renal failure has also been considered as an
independent risk factor.

44. In 2010 European guidelines proposed another way of risk stratification by
recommending 3 additional risk factors as mentioned in CHADS₂ and was
considered as CHA₂DS₂-VASc.
Additional risk factors considered were presence of vascular disease, age 65-
74 yrs and female gender with one score for each.
Here total score was 9 and if score was ≥ 2 then oral anticoagulation was
needed and if score was 1 then oral anticoagulation or aspirin should be used
after risk benefit analysis.

45. CHA2DS2-VASc Score
Congestive HF 1
Hypertension 1
Age > 75 years 2
Diabetes Mellitus 1
Stroke/TIA/TE 2
Vascular disease (prior MI, PAD, or aortic 1
plaque)
Age 65–74 y 1
Sex category (i.e., female sex) 1
Maximum Score 9

46. ANTITHROMBOTIC THERAPY IN PATIENTS
WITH ATRIAL FIBRILLATION

47. RISK ASSESSMENT FOR BLEEDING
Estimation of bleeding risk is a crucial step in the management of
patients with atrial fibrillation (AF). Three bleeding risk–prediction schemes
have been derived and validated exclusively in AF populations:
1) HEMORR2HAGES
2) HAS-BLED, and
3) ATRIA
Out of these most commonly used is the HAS-BLED score which has been
discussed here

48. BLEEDING RISK SCORES VALIDATED IN AF PATIENTS

50. DRUGS FOR PREVENTION OF THROMBOEMBOLIC
COMPLICATIONS
•Warfarin: It acts by interfering with synthesis of Vit-K dependent clotting factors
in liver.It reduced risk of stroke by 61%. Target International normalized
ratio 2-3. even relatively small decrease in INR level from 2 to 1.7 more than
doubles the risk of stroke.
•Low- molecular weight heparin: Heparin, especially low-molecular weight
heparin is typically used as a temporary bridge therapy to therapeutic
anticoagulation when therapy with warfarin is initiated or in high-risk patients
for a few days before and after a medical or dental procedurewhen
anticoagulation with warfarin has been suspended
No advantage on combination of warfarin and unfractionated heparin was
noted .
•Direct thrombin inhibiters:
Dabigatran- an oral direct thrombin inhibitor at a dose of 110mg twice
daily was recently shown to have similar efficacy to warfarin (RELY trial) but
lower rate of major hemorrage, also with an advantage of a fixed dosing and

51. Factor Xa inhibitors:
Rivaroxaban- an oral factor Xa inhibitor was approved by FDA in 2011 for
stroke prevention in atrial fibrillation based on the conclusions of ROCKET-
AF trial in which it was non inferior to warfarin in stroke prevention and had
substantially less intracranial hemorrhage. It is dosed at 20 mg once a day
with dose reduction to 15 mg in patients with creatinine clearance < 50
ml/min
Apixaban- another oral factor Xa inhibitor is yet to be approved for atrial
fibrillation. In ARISTOTLE trial I has shown a lower risk of major bleeding.
According to AVERROES trial in patients not suitable for warfarin
,apixaban was shown to be well tolerated and superior to aspirin. It is
dosed at 5 mg twice daily with dose reductions in high risk category.
ACTIVE-A trial advocated for combination of aspirin and clopidogrel for patients
unable to take warfarin but it was associated with slightly increased risk of
bleeding.

52. DOSE SELECTION OF ORAL ANTICOAGULANTS IN
PATIENTS WITH CHRONIC KIDNEY DISEASE
Renal
Function
Warfarin Dabigatran Rivaroxaban Apixaban
Normal/ mild
impairment
Dose
adjusted for
INR 2-3
150 mg BID
CrCl >30ml/min
20 mg
HS(CrCL
>50ml/min)
5 or 2.5 mg
BID
Mod
impairment
Dose
adjusted for
INR 2-3
150 mg BID or
75 mg BID (
CrCl >
30ml/min
15 mg HS
(CrCL 30-
50ml/min)
5 or 2.5 mg
BID
Sever
impairment
Dose
adjusted for
INR 2-3
75 mg BID
(CrCl 15-30
ml/min)
15 mg HS
(CrCl 15-30
ml/min)
NR
ESRD not on
Dialysis
Dose
adjusted for
INR 2-3
NR (CrCl <15
ml/min)
NR (CrCl <15
ml/min)
NR

53. NON-PHARMACOLOGICAL METHODS
1) EXCISION OF LEFT ATRIAL APPENDAGE
2) CLOSURE OF LEFT ATRIAL APPENDAGE
Approximately 90% of left atrial thrombi form in the left atrial appendage, so
its better to remove the source.
Both of these two techniques were compared and final conclusion was in
favour of excision of the appendage as compared to percutaneous closure.
 In PROTECT AF trial they considered percutaneous closure of left atrial
appendage with a filter device (watchman) which was found to be
noninferior to warfarin for stroke prevention

54. ACC/AHA NEW MANAGEMENT GUIDLINE

56. RECOMMENDATIONS FOR PREVENTION OF
THROMBOEMBOLISM IN PATIENTS WITH AF

59. RECOMMENDATIONS FOR RATE CONTROL

61. RECOMMENDATION FOR RHYTHM CONTROL

64. RECOMMENDATION FOR ANTIARRHYTHMIC
DRUGS TO MAINTAIN SINUS RHYTHM

65. Class I
1. Before initiating antiarrhythmic drug therapy, treatment of
precipitating or reversible causes of AF is recommended. (Level of Evidence: C)
2. The following antiarrhythmic drugs are recommended in patients with
AF to maintain sinus rhythm, depending on underlying heart disease and
comorbidities (Level of Evidence: A):
a. Amiodarone
b. Dofetilide
c. Dronedarone
d. Flecainide
e. Propafenone
f. Sotalol
3. The risks of the antiarrhythmic drug, including proarrhythmia, should
be considered before initiating therapy with each drug. (Level of Evidence: C)
4. Owing to its potential toxicities, amiodarone should only be used
after consideration of risks and when other agents have failed or are
contraindicated. (Level of Evidence: C)

66. Class IIa
1. A rhythm-control strategy with pharmacological therapy can be useful in
patients with AF for the treatment of tachycardia-induced cardiomyopathy. (Level of
Evidence: C)
Class IIb
1. It may be reasonable to continue current antiarrhythmic drug therapy in the
setting of infrequent, well-tolerated recurrences of AF, when the drug has reduced the
frequency or symptoms of AF. (Level of Evidence: C)
Class III: Harm
1. Antiarrhythmic drugs for rhythm control should not be continued when AF
becomes permanent (Level of Evidence: C) including dronedarone (Level of Evidence:
B)
2. Dronedarone should not be used for treatment of AF in patients with New
York Heart Association (NYHA) class III and IV HF or patients who have had an episode
of decompensated HF in the past 4 weeks . (Level of Evidence: B)

67. MANAGEMENT OF AF IN SPECIAL GROUP OF PATIENTS