Therapeutics Atrial fibrillation - PowerPoint Presentation

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Therapeutics

Atrial fibrillation

Dr Sura Al ZoubiPhD,MClinPharm

Lecture 7

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Pharmacotherapy: A Pathophysiologic Approach, 10e

. Chapter 18: The Arrhythmias2014 AHA/ACC/HRS Guideline for the Management of

Patients With Atrial Fibrillation2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial FibrillationReferences

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Normal Conduction

Electrical activity is initiated by the sinoatrial (SA) node because it possesses the highest degree of

automaticity and moves through cardiac tissueGains entrance to the ventricle via the AV node and a large bundle of conducting tissue referred to as the bundle of HisFrom the bundle of His, the cardiac conduction system bifurcates into several (usually three) bundle branches

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Atrial Fibrillation

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Mechanisms and Background

AF is the most common sustained arrhythmia encountered in clinical practice

AF affect between 2.7 and 6.1 million AmericansThe overall prevalence of AF is 0.4% to 1%, and this increases with age (eg, approximately an 8% prevalence in patients greater than 80 years old) and with the increased severity of HF

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AF is characterized by extremely rapid (atrial rate

of 400 to 600 beats/min) and disorganized atrial activation.

With this disorganized atrial activity, there is a loss of the contribution of synchronized atrial contraction (atrial kick) to forward cardiac output. Supraventricular impulses penetrate the AV conduction system in variable degrees resulting in an irregular activation of the ventricles and an irregularly irregular pulse. The

AV junction will not conduct most of the supraventricular impulses, causing the ventricular response to be considerably slower (120 to 180 beats/min) than the atrial rate.

Long episodes are more difficult to terminate perhaps because of tachycardia-induced changes in atrial function (mechanical and/or electrical “remodeling”).Definitions

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Definitions

Acute AF: onset within 48

hours Paroxysmal AF: terminates spontaneously in less than 7 daysRecurrent AF: two or more episodes Persistent AF: duration longer than 7 days and does not terminate spontaneously

Permanent AF: does not terminate with attempts at pharmacologic or electrical cardioversion

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CLINICAL PRESENTATION

These arrhythmias are usually not directly life-threatening

and do not generally cause hemodynamic collapse or syncopePatients with underlying forms of heart disease who are heavily reliant on atrial contraction to maintain adequate cardiac output (eg, mitral stenosis, obstructive cardiomyopathy) display more severe symptoms of AF or AFl.

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Symptoms

Most often, patients complain of rapid heart rate/palpitations and/or worsening symptoms of HF (dyspnea, fatigue).

Medical emergencies are severe HF (ie, pulmonary edema, hypotension) or AF occurring in the setting of acute MI.9

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Diagnostic Tests/Signs (ECG)

AF is an irregularly irregular supraventricular rhythm

with no discernible, consistent atrial activity (P waves). Ventricular rate is usually 120 to 180 beats/min and the pulse is irregular10

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Management

The traditional approach to the treatment of AF can be organized into several sequential

goals; First, evaluate the need for acute treatment (usually administering drugs that slow ventricular rate). Next, contemplate methods to restore SR, taking into consideration the risks (

eg, thromboembolism).

Lastly, consider ways to prevent the long-term complications of AF such as arrhythmia recurrence and thromboembolism11

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ANTIARRHYTHMIC DRUGS

In a theoretical sense, drugs may have antiarrhythmic activity by directly altering conduction in several ways.

A drug may depress the automatic properties of abnormal pacemaker cells. A drug may do this by decreasing the slope of phase 4 depolarization and/or by

elevating threshold potential. If the rate of spontaneous impulse generation of the abnormally automatic foci becomes less than that of the SA node, normal cardiac rhythm can be restored.

Drugs may alter the conduction characteristics of the pathways of a reentrant loop.12

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AADs have specific electrophysiologic

actions that alter cardiac conduction in patients with or without heart disease. These actions form the basis

of grouping AADs into specific categories based on their electrophysiologic actions in vitro. Vaughan Williams proposed the most frequently used classification system (has been criticized)

ANTIARRHYTHMIC DRUGS

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Classification of Antiarrhythmic Drugs

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Class

Ia AADs

Quinidine, procainamide, and disopyramide, slow conduction velocity, prolong refractoriness, and decrease the automatic properties of sodium-dependent (normal and diseased) conduction tissue. Although class Ia AADs are primarily considered sodium channel blockers, their

electrophysiologic actions can also be attributed to blockade of potassium channels. In

reentrant tachycardias, these drugs generally depress conduction and prolong refractoriness, theoretically transforming the area of unidirectional block into a bidirectional block. Clinically, class Ia drugs are broad-spectrum AADs that are

effective for

both supraventricular and ventricular arrhythmias

.

Procainamide is

only available in the IV formulation

as

all of

its oral formulations have been discontinued.

These

AADs tend not to be used frequently in clinical practice for the management of

either supraventricular

or ventricular arrhythmias primarily because of their

limited

efficacy

and significant toxicities

.

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Class Ib AADs

The class Ib AADs lidocaine,

mexiletine, and phenytoin are considerably more effective in ventricular arrhythmias than supraventricular arrhythmias. As a group, these drugs are relatively weak sodium channel blockers (at normal stimulation rates).

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Class Ic AADs

The class Ic AADs,

propafenone and flecainide, are extremely potent sodium channel blockers, profoundly slowing conduction velocity while leaving refractoriness relatively unaltered. The class Ic AADs theoretically eliminate reentry by slowing conduction to a point where the impulse is

extinguished and cannot propagate further. Although the class

Ic AADs are effective for both ventricular and supraventricular arrhythmias, their use for ventricular arrhythmias has been limited by the risk of proarrhythmia

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Class II AADs

The β-blockers are classified as class II AADs.

For the most part, the clinically relevant acute antiarrhythmic mechanisms of the β-blockers result from their antiadrenergic actions. Because the SA and AV nodes are heavily influenced by adrenergic innervation, β-blockers would be most useful in tachycardias

in which these nodal tissues are abnormally automatic or are a portion of a reentrant loop. These

drugs are also helpful in slowing ventricular response in atrial arrhythmias (eg, AF) by their effects on the AV node. Furthermore, some tachycardias are exercise-related or precipitated by states of high sympathetic tone (perhaps through triggered activity), and β-blockers may be useful in these instances.

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Class II AADs

β-Adrenergic stimulation results in increased conduction velocity, shortened refractoriness, and increased automaticity of the nodal tissues; β-blockers will antagonize

these effects. In the nodal tissues, β-blockers interfere with calcium entry into the cell by altering catecholamine-dependent channel integrity and gating kinetics. In sodium-dependent atrial and ventricular tissues, β-blockers shorten repolarization somewhat but otherwise have little direct effect.

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The antiarrhythmic

properties of β-blockers observed with long-term, chronic therapy in patients with heart disease are less well understood. Although

it is clear that β-blockers decrease the likelihood of SCD (presumably arrhythmic death) after MI, the mechanism for this benefit remains unclear but may relate to the complex interplay of changes in sympathetic tone, damaged myocardium, and ventricular conduction. In patients with

HF, drugs such as β-blockers, angiotensin-converting enzyme inhibitors, and angiotensin II receptor blockers may prevent arrhythmias such as AF by attenuating

the structural and/or electrical remodeling process in the myocardiumClass II AADs21

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Class III AADs

The class III AADs include those agents that specifically prolong refractoriness in atrial and ventricular tissues.

This class includes amiodarone, dronedarone, sotalol, ibutilide, and dofetilide; these drugs share the common effect of delaying repolarization by blocking potassium channels.

Amiodarone and sotalol are effective in most supraventricular and ventricular arrhythmias

. Amiodarone displays electrophysiologic characteristics of all four Vaughan Williams classes; it is a sodium channel blocker with relatively “fast on-off” kinetics, has nonselective β-blocking actions,

blocks potassium

channels, and also has a small degree of calcium channel blocking

activity

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Class III AADs

Unlike amiodarone and sotalol

, dronedarone, ibutilide, and dofetilide are only approved for the treatment of supraventricular arrhythmias. Both ibutilide (only available IV) and

dofetilide (only available orally) can be used for the acute conversion of AF or AFl to SR

Dofetilide can also be used to maintain SR in patients with AF or AFl of longer than 1 week’s duration who have been converted to SR. Dronedarone is approved to reduce the risk of cardiovascular (CV) hospitalization in patients with a history of paroxysmal or persistent AF who are currently in SR.

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Class IV AADs

The non-DHP CCBs, verapamil and diltiazem, are categorized as class IV AADs.

At least two types of calcium channels are operative in SA and AV nodal tissues: an L-type channel and a T-type channel. Both L-type channel blockers (verapamil and diltiazem) will slow conduction, prolong refractoriness, and decrease automaticity (eg,

due to EADs or LADs) of the calcium-dependent tissue in the SA and AV nodes. Therefore, these agents are effective

in automatic or reentrant tachycardias which arise from or use the SA or AV nodes. 24

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Class IV AADs

In supraventricular arrhythmias (eg

, AF or AFl), these drugs can slow ventricular response by slowing AV nodal conduction. Furthermore, because calcium entry seems to be integral to exercise-related tachycardias and/or tachycardias caused by some forms of triggered automaticity, these agents may be

effective in the treatment of these types of arrhythmias. The

DHP CCBs (eg, nifedipine) do not have significant antiarrhythmic activity as they do not affect AV nodal conduction.

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Side

Effects of Antiarrhythmic Drugs

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Amiodarone Monitoring

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Typical Maintenance Doses of

Oral Antiarrhythmic Drugs

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IV

Antiarrhythmic Dosing

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Algorithm for the treatment of AF and

AFl

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Algorithm for the treatment of AF and

AFl

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Acute Management

Hemodynamically instable

patients: severe hypotension, angina, or pulmonary edema. Medical emergencyDirect current cardioversion (DCC) is indicated as first-line therapy in an attempt to immediately restore SR (without regard to the risk of thromboembolism).AF

often requires high energy levels (ie, greater than 200 J).

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Rate control

Hemodynamically stable patient

 there is no emergent need to restore SRFocus should be directed toward controlling the patient’s ventricular rateDrugs that

slow conduction and increase refractoriness in the AV node (eg, β-blockers, non-DHP CCBs, or digoxin) should be used as initial therapy

IV β-blockers and non-DHP CCBs have a relatively quick onset and can effectively control the ventricular rate at rest and during exercise. β-Blockers are also effective for controlling ventricular rate under conditions of increased sympathetic tone

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Use of

digoxin for this purpose has been declined especially in patients with normal LV systolic function due to:

Its relatively slow onset Its inability to control the ventricular rate during exercise.

Although an initial decrease in the ventricular rate can sometimes be observed within 1 hour of IV administration of digoxin, full control (heart rate less than 80 beats/min at rest and less than 100 beats/min during exercise) is usually not achieved for 24 to 48 hours.

It tends to be ineffective for controlling ventricular rate under conditions of increased sympathetic tone (ie, surgery, thyrotoxicosis) because it slows AV nodal conduction primarily

through

vagotonic

mechanisms.

The

use of digoxin in patients with AF has been associated with a significant increase

in the

risk of mortality

.

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The

selection of a drug to control ventricular rate in the acute setting should be primarily based on the patient’s LV function

Normal LV functionIn patients with LVEF greater than 40%, an IV β-blocker (propranolol, metoprolol, esmolol) or non-DHP CCB (diltiazem or verapamil) is recommended as first-line therapy to control ventricular

rateHFrEF

In patients with LVEF less than or equal to 40%, both IV diltiazem and verapamil should be avoided because of their potent negative inotropic effects. IV β-blockers should be used with caution

in this patient population and should be avoided if patients are in the midst of an episode

of decompensated

HF.

In

those patients who are having an exacerbation of HF symptoms

, IV administration of either digoxin or amiodarone

should

be

used as first-line therapy to achieve ventricular rate

control

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IV amiodarone can also be used in patients who are refractory to or have

contraindications to β-blockers, non-DHP CCBs, and digoxin. However, clinicians should be aware that the use of amiodarone for controlling ventricular rate may

also stimulate the conversion of AF to SR and place the patient at risk for a TE event, especially if the AF has persisted for at least 48 hours or is of unknown duration. In patients with stable HFpEF, either IV diltiazem or verapamil is recommended to acutely control ventricular rate; however, these

agents should be avoided in these patients if they are experiencing decompensated HF

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Summary of Recommendations for Rate Control (

2014 AHA/ACC/HRS Guideline)

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Doses

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Algorithm for the treatment of AF and

AFl

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The distinction between

nonvalvular and valvular AF has confused clinicians

Valvular AF generally refers to AF in the setting of moderate-to-severe mitral stenosis (potentially requiring surgical intervention) or in

the presence of an artificial (mechanical) heart valve.

Valvular AF is considered an indication for long-term anticoagulation with warfarin. In contrast, nonvalvular AF does not imply the absence of valvular

heart disease

. Instead, as used in the present focused update

,

nonvalvular

AF is

AF in the absence of moderate- to-severe mitral stenosis or a mechanical heart valve

.

This

is because in most AF NOAC clinical trials

, up

to approximately 20% of patients were

enrolled with

various

valvular

defects, including mild

mitral stenosis

, mitral regurgitation, aortic stenosis,

aortic regurgitation

, and tricuspid

regurgitation.

PREVENTION OF THROMBOEMBOLISM, Selecting

an Anticoagulant

Regimen (

2019 AHA/ACC/HRS Focused

Update)

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PREVENTION OF THROMBOEMBOLISM

When initiating chronic antithrombotic therapy to prevent stroke in patients with AF, selection of the appropriate regimen is based on the patient’s stroke risk as determined by the

CHA2DS2-VASc risk scoring system.41

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CHA2DS

2-VASc

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Recommendations for Selecting an Anticoagulant

Regimen—Balancing Risks and Benefits

Class IFor patients with AF and an elevated CHA2DS2-VASc score of 2 or greater in men or 3 or greater in women, oral anticoagulants are recommended. (Options include: Warfarin, Dabigatran, Rivaroxaban, Apixaban or

Edoxaban).NOACs (dabigatran, rivaroxaban, apixaban

, and edoxaban) are recommended over warfarin in NOAC-eligible patients with AF (except with moderate-to-severe mitral stenosis or a mechanical heart valve).Among patients treated with warfarin, the international normalized ratio (INR)

should be

determined at least weekly

during initiation

of anticoagulant therapy and

at least

monthly when anticoagulation (INR

in range

) is

stable

In patients with AF (except with

moderate to-severe

mitral stenosis or a

mechanical heart

valve), the CHA2DS2-VASc score

is recommended

for assessment of

stroke risk.

For patients with AF who

have mechanical

heart valves, warfarin

is recommended

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Class I

Selection of anticoagulant therapy should be based on the risk of thromboembolism, irrespective of whether the AF pattern is paroxysmal, persistent, or permanentRenal function and hepatic function should be evaluated before initiation of a NOAC and should be

reevaluated at least annually.In patients with AF, anticoagulant therapy should be individualized on the basis of shared decision-making after discussion of the absolute risks and relative risks of stroke and bleeding, as well as the patient’s

values and preferences.Reevaluation of the need for and choice of anticoagulant

therapy at periodic intervals is recommended to reassess stroke and bleeding risks.For patients with AF (except with moderate-to-severe mitral stenosis or a mechanical heart valve) who are unable to maintain a therapeutic

INR level

with warfarin, use of a NOAC

is recommended.

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Class

IIaFor patients with AF (except with moderate to-severe mitral stenosis or a mechanical heart valve) and a CHA2DS2-VASc score of 0 in men or 1 in women, it is reasonable to omit anticoagulant

therapyClass IIbFor patients with AF who have a CHA2DS2-VASc score of 2 or greater in men or 3 or greater in women and who have end-stage chronic kidney disease (CKD; creatinine clearance [CrCl] <15 mL/min) or are on dialysis, it might be reasonable to prescribe warfarin (INR 2.0 to 3.0) or apixaban for oral anticoagulation

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Class

IIbFor patients with AF (except with moderate to-severe mitral stenosis or a

mechanical heart valve) and moderate-to-severe CKD (serum creatinine ≥1.5 mg/dL [apixaban], CrCl 15 to 30 mL/min [dabigatran], CrCl ≤50 mL/min [rivaroxaban], or

CrCl 15 to 50 mL/min [edoxaban]) with an elevated CHA2DS2-VASc

score, treatment with reduced doses of direct thrombin or factor Xa inhibitors may be considered (eg, dabigatran, rivaroxaban, apixaban, or edoxaban).

For patients with AF (except with

moderate to-severe

mitral stenosis or a

mechanical heart

valve) and a CHA2DS2-VASc score of

1 in

men and 2 in women, prescribing an

oral anticoagulant

to reduce

thromboembolic stroke

risk may be

considered

Class III

In

patients with AF and

end-stage CKD

or on dialysis, the direct

thrombin inhibitor

dabigatran or the factor

Xa

inhibitors

rivaroxaban or

edoxaban

are not

recommended because of the lack

of evidence

from clinical trials that

benefit exceeds

risk

.

The direct thrombin inhibitor

dabigatran should

not be used in patients with AF

and a

mechanical heart valve

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Recommendations for Interruption and Bridging

Anticoagulation (2019 AHA/ACC/HRS Focused Update)

Class IBridging therapy with unfractionated heparin or low-molecular-weight heparin is recommended for patients with AF and a mechanical heart valve undergoing procedures that require interruption

of warfarin. Decisions on bridging therapy should balance the risks of stroke and bleeding.

For patients with AF without mechanical heart valves who require interruption of warfarin for procedures, decisions about bridging therapy (unfractionated heparin or low-molecular-weight heparin) should balance the risks of stroke and bleeding and the duration of time a patient will not

be anticoagulated.

Idarucizumab

is recommended for

the reversal

of dabigatran in the event

of life-threatening

bleeding or an

urgent procedure.

Class

IIa

Andexanet

alfa

can be useful for the reversal

of rivaroxaban

and

apixaban

in the event of

lifethreatening

or

uncontrolled

bleeding

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Algorithm for the treatment of AF and

AFl

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Rhythm control

After treatment with AV nodal blocking drugs and a subsequent decrease in the ventricular rate, the patient should be evaluated for the possibility

of restoring SR if AF persists.50

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Several

factors should be considered;Many patients spontaneously convert to

SR without intervention (complication of cardiac surgery)Restoring SR is not a necessary or realistic goal in some patients (overall mortality is not statistically different between rate control and rhythm control)

Because a rhythm-control strategy does not offer any significant advantage over a rate-control strategy in the management of patients with persistent or recurrent AF (including those with concomitant HFrEF), it is acceptable to allow patients to remain in AF

, while being chronically treated not only with AV nodal blocking drugs to achieve adequate ventricular rate control but also with appropriate antithrombotic therapy to prevent TE complications.

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Adequate ventricular rate control was previously considered to be achieving a heart rate less than

80 beats/min at rest and less than 100 beats/min during exercise, evidence from the RACE II trial has suggested that selecting a more lenient rate-control strategy (resting heart rate less than 110 beats/min) may be a reasonable approach for certain patients with AF (persistent AF provided that patients are

asymptomatic and have preserved LV systolic function; LVEF >40%)Electrical or pharmacologic cardioversion should be considered for those patients with AF who; Remain symptomatic despite having adequate ventricular rate

controlAdequate ventricular

rate control cannot be achievedAre experiencing their first episode of AF if they are likely to convert to and remain in SRYounger age

Presence of tachycardia-induced cardiomyopathy

AF

precipitated by acute

illness

Patient

preference.

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PREVENTION OF THROMBOEMBOLISM,

Electrical and Pharmacological Cardioversion of AF and Atrial Flutter (2019 AHA/ACC/HRS Focused

Update)Class IFor patients with AF or atrial flutter of 48 hours’ duration or longer, or when the duration of AF is unknown, anticoagulation with

warfarin (INR 2.0 to 3.0), a factor Xa inhibitor, or direct thrombin inhibitor is recommended for at least 3 weeks

before and at least 4 weeks after cardioversion, regardless of the CHA2DS2-VASc score or the method (electrical or pharmacological) used to restore sinus rhythmFor patients with AF or atrial flutter of more than 48 hours’ duration

or unknown

duration that requires

immediate cardioversion

for hemodynamic instability

, anticoagulation

should be initiated

as soon

as possible and continued for

at least

4 weeks after cardioversion

unless contraindicated

After cardioversion for AF of

any duration

, the decision about

long-term anticoagulation

therapy should be

based on

the thromboembolic risk profile

and bleeding

risk

profile

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PREVENTION OF THROMBOEMBOLISM,

Electrical and Pharmacological Cardioversion of AF and Atrial Flutter (2019 AHA/ACC/HRS Focused

Update)Class IIaFor patients with AF or atrial flutter of less than 48 hours’ duration with a CHA2DS2-VASc score of 2 or greater in men and 3

or greater in women, administration of heparin, a factor Xa inhibitor, or a direct

thrombin inhibitor is reasonable as soon as possible before cardioversion, followed by long-term anticoagulation therapyFor patients with AF or atrial flutter of 48 hours’ duration or longer or of unknown duration who have not been anticoagulated for the preceding 3 weeks, it is reasonable

to perform

transesophageal

echocardiography before

cardioversion and proceed

with cardioversion

if no left atrial thrombus

is identified

, including in the LAA,

provided that

anticoagulation is achieved

before

transesophageal

echocardiography

and maintained

after cardioversion for at least

4 weeks.

Class

IIb

For patients with AF or atrial flutter of

less than

48 hours’ duration with a

CHA2DS2-VASc

score of 0 in men or 1 in women

, administration

of heparin, a factor

Xa

inhibitor

, or a direct thrombin inhibitor

, versus

no anticoagulant therapy, may

be considered

before cardioversion,

without the

need for

postcardioversion

oral anticoagulation

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Electrical and Pharmacological Cardioversion

After prior anticoagulation (or

after transesophageal echocardiography demonstrated absence of a thrombus, obviating need for warfarin), methods for restoring sinus rhythm are Electrical (DCC); is quick and more often successful, but it requires prior sedation or anesthesia and has a small risk of serious complications, such as sinus arrest or ventricular arrhythmias.

Pharmacologic cardioversion; effective agent may be determined in case long-term therapy is required. Disadvantages are significant side effects, such as drug-induced

TdP, drug–drug interactions, and lower cardioversion rate for drugs compared with DCC.There is good evidence for efficacy of class III pure Ik blockers (ibutilide and dofetilide), class Ic

drugs (

eg

, flecainide and

propafenone

), and amiodarone (oral or IV).

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Overall, when considering pharmacologic cardioversion, the selection of an AAD should be based on whether the patient has SHD (

eg, LV dysfunction, CAD, valvular heart disease, LV hypertrophy

).In the absence of any type of SHD, the use of a single, oral loading dose of flecainide or propafenone is a reasonable approach for cardioversion. Ibutilide can also be used as an alternative in this patient population; however, use of this agent is restricted

to a monitored setting in the hospital because it requires QT interval monitoring. Additionally, it should be remembered that a patient’s ventricular rate should be adequately controlled with AV nodal blocking drugs prior to administering a class Ic

AAD for cardioversion. The class Ic AADs may paradoxically increase ventricular response. The most likely mechanism for this effect is that by slowing atrial conduction, the class Ic AADs decrease the number of impulses reaching the AV node. Consequently, the AV node paradoxically allows more impulses to gain entrance to the ventricular conduction system, thereby increasing ventricular rate.In patients with underlying SHD, flecainide,

propafenone

, and

ibutilide

should

be avoided because of the increased risk of

proarrhythmia

;

amiodarone or

dofetilide

should be used instead.

Although

amiodarone can

be administered

safely on an outpatient basis because of its low

proarrhythmic

potential,

dofetilide

therapy can only be initiated in the hospital (for

QT interval

monitoring and assessment of renal function).

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Electrical and

Pharmacological Cardioversion

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Long-Term Complications

There are two forms of therapy that the clinician must consider in each patient with AF: long-term antithrombotic therapy to prevent stroke

Long-term AADs to prevent recurrences of AF58

Slide59

Algorithm for the treatment of AF and

AFl

59

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Long-term AADs

According to the most recent AHA/ACC/HRS treatment guidelines for AF, the class Ic or III AADs are reasonable to consider to maintain patients in

SR.Selection of an antiarrhythmic drug to maintain sinus rhythm should be based primarily on whether the patient has SHD. 60

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Dosage and Safety Considerations for Maintenance of Sinus Rhythm in AF

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Dosage and Safety Considerations for Maintenance of Sinus Rhythm in AF

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Recommendations for AF Complicating ACS

Class I

For patients with ACS and AF at increased risk of systemic thromboembolism (based on CHA2DS2-VASc risk score of 2 or greater), anticoagulation is recommended unless the bleeding risk exceeds the expected benefit.Urgent direct-current cardioversion

of new-onset AF in the setting of ACS is recommended for patients with hemodynamic

compromise, ongoing ischemia, or inadequate rate control.Intravenous beta blockers are recommended to slow a rapid ventricular response to AF in patients with ACS who do not display HF, hemodynamic

instability, or bronchospasm.

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Upstream Therapy

Class

IIaAn ACE inhibitor or angiotensin-receptor blocker (ARB) is reasonable for primary prevention of new-onset AF in patients with HF with reduced LVEF. (Level of Evidence: B)

Class IIbTherapy

with an ACE inhibitor or ARB may be considered for primary prevention of new-onset AF in the setting of hypertension. (Level of Evidence: B)Statin therapy may be reasonable for primary prevention of new-onset AF after coronary artery surgery. (Level of

Evidence: A

)

Class

III: NO

BENEFIT

Therapy

with an ACE inhibitor, ARB, or statin is not

beneficial for

primary prevention of AF in patients without

cardiovascular disease.

(Level of Evidence: B)

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EVALUATION OF THERAPEUTIC OUTCOMES

The most important monitoring parameters include:

Mortality (total and due to arrhythmic death),Arrhythmia recurrence (duration, frequency, and symptoms),

Hemodynamic consequences (heart rate, blood pressure, and symptoms), and

Treatment complications (side effects or need for alternative or additional drugs, devices, or surgery).

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Thank You

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