ATRIAL FIBRILLATION CLASSIFICATION &

MANAGEMENT GUIDELINE

Dr. Rohan Sonawane

JR MD (Internal

medicine)

Dr. V. P. Sinha

MD, DM (Cardiology)

1) Introduction

2) Classification

3) Mechanism of AF

4) Causes & Clinical Features

5) Diagnostic Evaluation

6) Management Guidelines

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.

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

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

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.

CLASSIFICATION

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.

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

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

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.

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.

DIAGNOSTIC EVALUATION

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.

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

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.

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

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

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

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.

PHARMACOLOGICAL MANAGEMENT OF PATIENTS WITH NEWLY

DISCOVERED AF

PHARMACOLOGICAL MANAGEMENT OF PATIENTS WITH

RECURRENT PAROXYSMAL AF

PHARMACOLOGICAL MANAGEMENT OF PATIENTS WITH

RECURRENT PERSISTENT OR PERMANENT AF

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)

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

depolarized the heart, disrupting reenterant circuits and allowing sinus node to

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

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.

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

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

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

VernakalantIt 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.

DronaderoneIt 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.

PifenidoneThis is an antifibrotic drug which also potentiates L-type calcium channels has

been recently found to be effective and is under study

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

MANAGEMENT STRATEGIES FOR MAINTAINING SINUS

RHYTHM

NON PHARMACOLOGICAL METHODS

1) Catheter ablation

2) AV node ablation

3) Implanted defibrillator

4) Role of atrial pacing

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

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.

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.

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.

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

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.

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.

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

ANTITHROMBOTIC THERAPY IN PATIENTS

WITH ATRIAL FIBRILLATION

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

BLEEDING RISK SCORES VALIDATED IN AF PATIENTS

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

lesser effects from dietary factors

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.

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

ESRD on Dose NR (CrCl <15 NR (CrCl <15 NR

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

ACC/AHA NEW MANAGEMENT GUIDLINE

RECOMMENDATIONS FOR PREVENTION OF

THROMBOEMBOLISM IN PATIENTS WITH AF

RECOMMENDATIONS FOR RATE CONTROL

RECOMMENDATION FOR RHYTHM CONTROL

RECOMMENDATION FOR ANTIARRHYTHMIC

DRUGS TO MAINTAIN SINUS RHYTHM

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)

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)

MANAGEMENT OF AF IN SPECIAL GROUP OF PATIENTS