atrial fibrilation

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Essentials of Diagnosis

Atr ia l f ib r i l l a t ion i s the mostcommon chron ic a r rhythmia , w i th aninc idence and preva lence that r i se w i thage, so that i t a f fect s approx imate ly10% o f ind iv idua l s over age 80 years .

i t may be the in i t i a l p resent ings ign in thyro tox icos is , and th iscond i t ion shou ld be exc luded w i th thein i t i a l ep isode .

:

● Irregularly irregular rhythm.● Absence of P waves on the electrocardiogram.

Irregularly irregular heart rhythm Tachycardia usually present Often associated with palpitations (acute onset) or fatigue (chronic) ECG shows atrial activity with irregular ventricular response

general considerations :

The most common chronic arrhythmia, affecting approximately 10% of individuals older than age 80The incidence increases significantly with age starting in the 7th decade of lifeRarely life-threateningIf the ventricular rate is rapid enough, it can precipitate hypotension, myocardial ischemia, or myocardialdysfunctionApproximately 60% of patients with a first episode will revert to sinus rhythm within 24 hours

It occurs in :

rheumatic and other forms of valvular heart disease,dilated cardiomyopathy,ASD,hypertension, andcoronary heart diseaseas well as in patients with no apparent cardiac disease;

The heart rate may range from quite slow toextremely rapid,

underlying complete heart block and a permanent

ventricular pacemaker is in place.

erratic [= πλανόδιος, εκκεντρικός, ασταθής, αλλοπρόσαλλος ]

but is uniformly irregular unless :

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The atrial activitymay be very fine anddifficult to detect on theECG, or quite courseand often mistaken foratrial flutter.

Atr ia l f ib r i l l a t ion o f ten appearsparoxysmal ly before becoming theestab l i shed rhythm.

The surface ECG

typically demonstrates erratic, disorganized atrial activity between discrete QRS complexesoccurring in an irregular pattern.

Pericarditis, chesttrauma, thoracic orcardiac surgery, thyroiddisorders, obstructivesleep apnea, orpulmonary disease (as well as medications such as theophylline and -adrenergicagonists) may cause attacks in patients with normal hearts. Acute alcohol excessand alcohol withdrawal—and, in predisposed individuals, even consumption of smallamounts of alcohol—may precipitate atrial fibrillation.

This latter presentation, which is often termed "holiday heart," is usually transientand self-limited.

Short-term rate control usually suffices as treatment.

Perhaps the most serious consequence of atrial fibrillation is thepropensity for thrombus formation due to stasis in the atria(particularly the left atrial appendage) and consequent embolization,most devastatingly to the cerebral circulation.

Overall, the rate of stroke is approximately 5 events per 100 patient-years of follow-up.

However, patients with

significant obstructive valvular disease,chronic heart failure or LV dysfunction,diabetes,hypertension, orage over 75 years andthose with a history of prior embolic events

ARE AT SUBSTANTIALLY HIGHER RISK (UP TO NEARLY 20 EVENTS PER 100PATIENT-YEARS IN PATIENTS WITH MULTIPLE RISK FACTORS)

A SIMPLE SCORE DERIVED FROM THE FRAMINGHAM STUDY TO ESTIMATE RISK OF STROKEIS AVAILABLE FOR PDA DOWNLOAD A THTTP://WWW.STATCODER.COM/A-FIB_STROKE.HTM.

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Complications

Propensity for stroke from embolization of an atrial thrombus

When to Refer

Symptomatic atrial fibrillation with or without rate controlAsymptomatic atrial fibrillation with poor rate control despite atrioventricular nodalblockers

When to Admit

Atrial fibrillation with rapid ventricular response resulting in hemodynamiccompromiseAtrial fibrillation resulting in acute heart failure

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Pat ients be low approx imate ly age65 who are " lone f ibr i l l a tors " (have noother card iac or sys temic d i sease) neednot rece ive ant i coagu la t ion un less therehas been a prev ious embol i sm.

Atr ia l f ib r i l l a t ion occurs whenthere a re mul t ip le , smal l a reas o f a t r ia lmyocard ium cont inuous ly d ischarg ingand cont rac t ing .

The Patient with Atrial Fibrillation :

In patients with this arrhythmia who

are older than age 65 years andin those of any age with valvular disease,

anticoagulation with warfarin is virtually mandated unless there is excessive risk because of

falling orhematologic disease.

Whether younger patients who have additional

vascular risk factors, such as

diabetes orhypertension,

benefit from anticoagulation is not known. If warfarin is to be discontinued for a necessary surgical procedure, it should be reinstated as soon as the surgeon deems it

safe, as this is a time of increased stroke vulnerability.

It has been the sense of many cardiologists that intermittent atrial fibrillation and fibrillation-flutter tachycardiasalso represent a risk of cerebral embolism, but there are no adequate studies to confirm this.

TINTINALLY : Atrial Fibrillation

There is no uniform atrial depolarization and contraction, butrather, only a quivering [= τρεμάμενος ] of the atrial wall.

Although the atrial rate is usually faster than 400 beats/min,

the ventricular rate is limited by the refractory period of the AV nodeor an accessory pathway.

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A more rap id vent r icu la rresponse may be seen in pa t ien ts w i thbypass [= πλάγ ια οδός , πάροδος ,παρακαμπτήρ ιος οδός ] t rac ts , Ventr i cu lar ra tes fa s ter than 300

beats /min are poss ib le and dangerous .

Atrial fibrillation canoccur in a paroxysmal or asustained manner.

The ECG characteristics of atrial fibrillation are

(1) fibrillatory waves of atrial activity, best seen in leads V1, V2, V3, and aVF; and(2) irregular ventricular response, usually around 170 to 180 beats/min in patients with a healthy AV node .

Disease or drugs (especially digoxin) may reduce AV node conduction and

markedly slow ventricular response.

and the rate in these patients has been suggested as a way

of estimating the refractory period of the accessory path.

In this case, because ventricular activation occurs by way of the bypass tract, the QRS complex is usually wide. The

configuration of the aberrancy [= απορρύθμιση ] may differ with the site of the accessory pathway.

Clinical Significance :

Predisposing factors for atrial fibrillation are :

increased atrial size and mass,increased vagal tone, andvariation in refractory periods between different parts of the atrial myocardium.

Atrial fibrillation is usually found in association with four disorders:

rheumatic heart disease,hypertension,ischemic heart disease, andthyrotoxicosis.

Less common causes are :

chronic lung disease,

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In patients with leftventricular failure, left atrialcontraction contributessignificantly to cardiac output.

A t r ia l f ib r i l l a t ion a lsopred isposes to per iphera l venous andat r ia l embol i , w i th the r isk o f pu lmonaryand sys temic a r te r ia l embol ism.

pericarditis,acute alcoholic intoxication,pulmonary embolus, andatrial septal defect.

. The loss of effective atrial contraction, as in atrial fibrillation, mayproduce heart failure in these patients.

Up to 15 percent of patients in chronic atrial fibrillation have at leastone embolic episode each year.

Conversion from chronic atrial fibrillation to sinus rhythm also carries a 1 to 2 percent risk of arterial embolism.

Patients with chronic atrial fibrillation are frequently anticoagulated.

Treatment :

The objectives of therapy include

(1) achieving rate control,(2) restoring sinus rhythm (where feasible), and(3) decreasing the risk of CVA.

The principles of treatment discussed largely follow those promulgated in the recent ACC/AHA/ESC guidelines.

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Management, Pharmacologic

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Source: American Heart Association/American College ofCardiology/European Society of Cardiology

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If, as is often the case—particularly in older individuals—

,

hemodynamic instability, or

evidence of important precipitating conditions (such as

silent myocardial infarction or ischemia,

decompensated heart failure,

pulmonary embolism, or

hemodynamically significant valvular disease),

hospitalization is usually not necessary. In most of these cases,atrial fibrillation is an unrecognized chronic or paroxysmal condition and should be managed accordingly

. For new onset atrial fibrillation, thyroid function tests and assessment for occult valvular or myocardial disease should beperformed.

Hemodynamically unstable patient

If the patient is hemodynamically unstable—usually as a result of

a rapid ventricular rate orassociated cardiac ornoncardiac conditions—

hospitalization and immediate treatment of atrial fibrillation are required.

Urgent cardioversion is usually indicated in patients with

shock or severe hypotension,pulmonary edema, orongoing myocardial infarction orischemia.

There is a potential risk of thromboembolism in patients undergoing cardioversion who havenot received anticoagulation therapy if atrial fibrillation has been present for > 48 hours;however, in hemodynamically unstable patients the need for immediate rate control outweighsthat risk.

the patient has no symptoms

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Electrical cardioversion is usually preferred in unstable patients.An initial shock with 100–200 J is administered in synchrony with theR wave. If sinus rhythm is not restored, an additional attempt with 360 J is indicated.

If this fails, cardioversion may be successful after loading with intravenous ibutilide

(1 mg over 10 minutes, repeated in 10 minutes if necessary).

In more stable patients or those at particularly high risk forembolism (ie, underlying mitral stenosis, a history of prior embolism,or severe heart failure), a strategy of rate control and anticoagulationis appropriate.

This is also true when the conditions that precipitated atrial fibrillation are likely to persist(such as following cardiac or noncardiac surgery, respiratory failure, or pericarditis) and whenthese conditions might resolve spontaneously over a period of hours to days (such as alcohol-induced atrial fibrillation, electrolyte or fluid imbalances, excessive exposure to theophylline orsympathomimetic agents, or some of the same previously cited conditions).

The choice of agent is guided by

the hemodynamic status of the patient,associated conditions, andthe urgency of achieving rate control.

Although both hypotension and heart failure may improve when the ventricular rate is slowed,calcium channel blockers and β-blockers may themselves precipitate hemodynamic deterioration.

Digoxin is less risky, but even when used aggressively (0.5 mg intravenously over 30minutes, followed by increments of 0.25 mg every 1–2 hours to a total dose of 1–1.5 mg over 24hours in patients not previously receiving this agent), rate control is rather slow and may beinadequate, particularly in patients with sympathetic activation.

In the setting of myocardial infarction or ischemia, β-blockers are the preferred agent.

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I f ra te contro l provesunsuccess fu l o r ear ly card iovers ion i scons idered necessary and the durat ionof a t r ia l f ib r i l l a t ion exceeds 2 –3 daysor i s unknown, a s t ra tegy o ft ransesophagea l echocard iography- gu idedcard iovers ion shou ld be cons idered.

The most frequently used agents are either

metoprolol (administered as a 5 mg intravenous bolus, repeated twice at intervals of 5 minutes and then given as

needed by repeat boluses or orally at total daily doses of 50–400 mg) or,

in very unstable patients,

esmolol (0.5 mg/kg intravenously, repeated if necessary, followed by a titrated infusion of 0.05–0.2 mg/kg/min).

If hypertension is present or β-blockers are contraindicated, calcium channel blockers are immediately effective.Diltiazem (20 mg bolus, repeated after 15 minutes if necessary, followed by a maintenance infusion of5–15 mg/h) is the preferred calcium blocker if hypotension or LV dysfunction is present.

Otherwise,

verapamil (5–10 mg intravenously over 2–3 minutes, repeated after 30 minutes if necessary) maybe used.

Amiodarone, even when administered intravenously, has a relatively slow onset but is often auseful adjunct when rate control with the previously cited agents is incomplete or contraindicated or whencardioversion is planned in the near future. However, amiodarone should not be used in this setting if long-termtherapy is planned with other antiarrhythmic agents.

By this approach, the presence of atrial thrombus isexcluded and electrical cardioversion can be attemptedwhile the patient remains under sedation.

If thrombus is present, the cardioversion is delayed untilafter a 4-week period of therapeutic anticoagulation.

In any case, because atrial contractile activity may not recover for several weeks after restoration of sinusrhythm in patients who have been in atrial fibrillation for more than several days, cardioversion is usuallyfollowed by anticoagulation for at least 1 month unless it is contraindicated.

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Up to two - th i rds o f pat ientsexper ienc ing a f i r s t ep i sode o f a t r ia lf ib r i l l a t ion wi l l spontaneous ly rever t tos inus rhythm wi th in 24 hours

Subsequent Management

. If atrial fibrillation persists or has been presentfor more than a week, spontaneous conversion isunlikely. In most cases early cardioversion is notrequired, so management consists of rate control andanticoagulation whether or not the patient has been admitted tohospital.

Rate control is usually relatively easy to achieve with

β-blockers,rate-slowing calcium blockers and, occasionally,digoxin,

used as single agents or more often in combination.

Good rate control should consist of a ventricular rate between 50and 100 beats/min with usual daily activities and a ventricular rate notexceeding 120 beats/min except with moderate to strenuous activity.

In older patients, who often have diminished AV nodal function and relatively limited activity, thiscan often be achieved with a single agent.

Most younger or more active individuals require a combination of two agents. Choice of theinitial medication is best based on the presence of accompanying conditions:

Hypertensive patients should be given β-blockers or calcium blockers;coronary patients should usually receive a β-blocker; andpatients with heart failure should be given a β-blocker with consideration of adding digoxin.

Adequacy of rate control should be evaluated by recording theapical pulse rate both at rest and with an appropriate level of activity(such as after brisk walking around the corridor or climbing stairs).

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Medications :

If atrial fibrillation persists for > 1 week

– Spontaneous conversion is unlikely– Management consists of rate control and anticoagulation with warfarin (goal INR of

2–3)

Rate control is defined as :

ventricular rate of 50–100 bpm with usual daily activities and

not exceeding 120 bpm except with moderate to strenuous activity

Conventional rate-control agents

used singly or,in younger adults, often in combination, include

– β-Blockers– Digoxin – Calcium channel blockers

In patients with

heart failure,coronary artery disease, orongoing ischemia,

β -blockers or digoxin are preferred

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Amiodarone (among other antiarrhythmic drugs) is useful

– When ra te cont ro l w i th o ther agents i s incomple te o r cont ra ind i ca ted– When card iovers ion i s ant i c ipa ted [= προβλέπω, προσδοκώ, προλαμβάνω

]

Do not use

if atrial fibrillation is associated with a known or suspected accessorypathway

Therapeutic Procedures

Urgent electrical cardioversion is recommended

in patients who are hemodynamically unstableeven if atrial fibrillation has been present for > 48 h

Elective electrical or pharmacologic cardioversion is recommended in patients

– With an initial episode of recent onset when there is an identifiable precipitating factor– Who remain symptomatic despite aggressive efforts at rate control

If cardioversion is planned and the duration of atrial fibrillation is unknown

digoxin, verapamil, or β-blockers

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– Perform a transesophageal echocardiography to exclude an atrial thrombus– Attempt electrical cardioversion while the patient remains sedated

If thrombus is present, delay cardioversion until therapeutic warfarinanticoagulation has been achieved for 4 weeks (goal INR of 2–3)

Use heparin

while awaiting therapeutic warfarin anticoagulation in atrial fibrillation with

mitral stenosis,

a history of embolic events, or

demonstrated thrombus on transesophageal echocardiography

After cardioversion, maintain therapeutic anticoagulation for at least 1–6 mo

Patients with atrial fibrillation who fail to convert

should receive anticoagulation therapy indefinitely

However, indefinite anticoagulation therapy is not indicated for those with

"lone atrial fibrillation," defined as

– AGE < 65– NO ASSOCIATED HEART DISEASE, HYPERTENSION, ATHEROSCLEROTIC VASCULARDISEASE, OR DIABETES MELLITUS

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Ora l qu in id ine or low-doseamiodarone can enhance ma in tenance o fs inus rhy thm.

For drug refractory, symptomatic atrial fibrillation, consider

radiofrequency catheter ablation orradiofrequency atrioventricular node ablation andpermanent pacing

1. Atrial fibrillation with a rapid ventricular response and acute hemodynamic deterioration should be treated with synchronized cardioversion.

More than 60 percent of patients can be converted with 100 J, andmore than 80 percent can be converted with 200 J.

Conversion to and retention in sinus rhythm are more likely when :

ATRIAL FIBRILLATION IS OF SHORT DURATION ANDTHE ATRIA ARE NOT GREATLY DILATED.

If initial cardioversion is unsuccessful, procainamide should be given intravenouslyto facilitate further cardioversion attempts.

Meta-analysis and decision analysis of postconversionantiarrhythmic treatment have found that the benefits of maintainingsinus rhythm with antiarrhythmics are partly

offset [= αντισταθμίζω, συμψιφίζω ] by an increase in suddendeath,

PRESUMABLYDUE TO THEPROARRHYTHMICPROPERTIES OFTHESE DRUGS.

Epidemiology :

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Approximately 4% ofthe population over age 60years has sustained anepisode of atrial fibrillation,with a particularly steepincrease in prevalence afterthe seventh decade of life

Risk factors for development of atrialfibrillation include

heart failure,hypertensive cardiovascular disease,coronary artery disease, andvalvular heart disease.

Moreover, both sustained and paroxysmal atrial fibrillation have important implications forthe development of a cerebrovascular accident (CVA) or other systemic emboli.

It is estimated that 15–20% of CVAs in nonrheumatic patients are due to atrial fibrillation.

In the ED setting,

all other causes of hypotension , such as acute blood loss,

should be ruled out before concluding that the rate is causing the hemodynamic deterioration. 2. In the more stable patient, the first priority is to achieve ventricular rate control. Diltiazem, 20 mg (0.25 mg/kg) given IV over 2 min,is extremely effective in achieving ventricular rate control, with the peak response seen

An infusion of 5 mg/h is usually started after the initial dose to maintain control, anda second dose of 25 mg (0.35 mg/kg) can be given after 15 min if rate control is not achieved.

Verapamil 5 to 10 mg IV is effective in slowing the ventricular response

in 60 to 70 percent of patients with atrial fibrillation andconverts 10 to 15 percent into sinus rhythm. Intravenous -adrenergic blockers (e.g., esmolol and propranolol)are effective, especially in patients with thyrotoxicosis or rheumatic mitral stenosis,but the depressive effects on myocardial contractility make them poor agents to use in patients with ventricular

failure.

in 2 to 7 min.

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Intravenous digoxin is an effective agent for this purpose, although the onset of action is slow,with a mean time longer than 11 h to achieve ventricular rate control.With a rapid digitalization protocol, an effect may be seen within 3 to 6 h. 3. Once ventricular rate control has been achieved, CHEMICAL CONVERSION CAN BE CONSIDERED with

procainamide,quinidine, orverapamil.

Intravenous procainamide has been used as a single agent to chemically convert atrial fibrillation of short duration into

sinus rhythm; however, ibutilide is being touted as a better agent. Amiodarone (300 mg IV 1h; 20 mg/kg over the next 24 h) has recently been shown to be a safe and highly effective first-choice drug for restoring sinus rhythm in patients with atrial fibrillation who present to an

ED.4 Because of the risk of intraatrial thrombi and arterial embolization,

patients with atrial fibrillation of more than 2 days' duration should be anticoagulated systemically for 1 to 3

weeksbefore attempts at chemical or electrical conversion. More recent work has indicated that there may be some increased risk of embolism even

with AF of less than 2 days' duration. An alternative to prolonged preanticoagulation is to exclude atrial thrombi by transesophageal echocardiography. Those without visible thrombi can be safely cardioverted following a loading dose of heparin and oral warfarin for

one month.5 4. Patients with a slow ventricular response not due to digitalis have AV node disease and probably a more generalized disorder of cardiac conduction

(second- or third-degree AV block is seen in these patients when in sinus rhythm).

These patients are at increased risk for profound bradycardias or asystole after cardioversion orantiarrhythmic drug therapy.

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5 . In some patients with a rapid ventricular response, conversion will reveal [= αποκαλύπτω, εμφανίζω ] a very slow rate ( tachybrady syndrome )

because of underlying disease of the pacemaker tissue (sick sinus syndrome).

Atrial fibrillation.

Rate Control

If the patient has

atrial fibrillation and

a rapid rate associated with

severe heart failure or

cardiogenic shock,

emergency direct-current cardioversion is indicated.

For patients with

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If rapid rate controlis desired, then calciumchannel blockers and β-blockers are far moreeffective than digitalis,which may require manyhours before rate controlis achieved.

atrial fibrillation associated ,

attempts to achieve acute rate control are indicated.

Drugs to slow the ventricular rate in patients with atrial fibrillation include

digitalis preparations,calcium channel blockers (verapamil or diltiazem), andβ-blockers.

In addition, a common misconception [= παρανόηση, εσφαλμένη αντίληψη,παρεξήγηση ] is that digitalis therapy is associated with acute conversion to sinusrhythm, but carefully controlled studies have shown that conversion to sinus rhythmis no more likely with digoxin than with placebo.

As emphasized later, digitalis and intravenous calcium channelblocker therapy are contraindicated in patients with

Wolff-Parkinson-White syndrome and

atrial fibrillation.

Intravenous diltiazem has been shown to be safe and effective

for patients with atrial fibrillation and a modest degree of heartfailure.

In patients with a known history of congestive heart failure,

use of intravenous -blockers or calcium channel blockers may aggravate the cardiac failure.

In this subset, digitalis or intravenous amiodarone would be the preferred agents for ratecontrol.

with rapid rate but with stable hemodynamics

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Two la rge randomized contro l ledt r ia l s ( the 4060 - pat ient At r ia lF ibr i l l a t ion Fo l low - up Inves t i ga t ion o fRhythm Management , or AFF IRM t r ia l ;and the Rate Contro l Versus E lect r i ca lCard iovers ion for Pers i s tent At r ia lF ibr i l l a t ion , or RACE t r i a l ) comparedst ra teg ies o f ra te contro l and rhythmcontro l

Of note is thatexercise tolerance andquality of life were notsignificantly better inthe rhythm controlgroup.

I n cases in wh ich e lect ivecard iovers ion i s requ i red, i t may beaccompl i shed e lect r i ca l l y (a s descr ibedabove) or pharmaco log ica l l y .

Rate Control or Elective Cardioversion

. In both, a strategy of rate control and long-termanticoagulation was associated with no higher rates ofdeath or stroke—both, if anything, favored rate control—andonly a modestly increased risk of hemorrhagic events than astrategy of restoring sinus rhythm and maintaining itwith antiarrhythmic drug therapy.

Nonetheless, thedecision as to whether to attempt to restore sinus rhythm following theinitial episode remains controversial.

Elective cardioversion following an appropriateperiod of anticoagulation is generally recommended for the initialepisode in patients in whom atrial fibrillation is thought to be of recentonset and when there is an identifiable precipitating factor.

Similarly, cardioversion is appropriate in patients who remain symptomatic from the rhythmdespite aggressive efforts to achieve rate control. However, it should be noted that even in patientsfor whom this is the initial episode of atrial fibrillation, the recurrence rate is sufficiently high that longer-term anticoagulation is generally appropriate until persistence of sinus rhythm can be confirmed for atleast 6 months.

Intravenous ibutilide may be used as describedabove in a setting in which the patient can undergocontinuous ECG monitoring for at least 3 hours followingadministration.

In patients in whom a decision has been made to continue antiarrhythmic therapy to maintain sinusrhythm (see next paragraph), cardioversion can be attempted with an agent that is being considered forlong-term use.

For instance, after therapeutic anticoagulation has been established, amiodarone can be initiatedon an outpatient basis (300–400 mg twice daily for 2 weeks, followed by 200 mg twice daily for at least a2–4 weeks and then a maintenance dose of 200 mg daily).

Because amiodarone increases the prothrombin time in patients taking warfarin and increasesdigoxin levels, careful monitoring of anticoagulation and drug levels is required.

Other agents that may be used for both cardioversion and maintenance therapy include

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propafenone (150–300 mg twice daily; should be avoided in patients with structural heartdisease),

flecainide (50–150 mg twice daily; should be avoided in patients with structural heart disease andshould be used in conjunction with an AV nodal blocking drug if there is a history of atrialflutter), and

dofetilide (500 mcg twice daily; downward dose adjustment is required with renal impairment anddosing must be initiated in hospital due to the potential risk of torsades de pointes).

Sotalol (80–160 mg twice daily; should be initiated in hospital in patients with structural heartdisease due to a risk of torsades de pointes) is not very effective for converting atrial fibrillation but canbe used to maintain sinus rhythm following cardioversion.

Unfortunately, sinus rhythm will persist in only 25% of patients who have had a sustained (lastingmore than several days) or recurrent episode of atrial fibrillation.

However, if the patient is treated long-term with an antiarrhythmic agent, sinus rhythm will persist inapproximately 50%.

The most commonly used medications are

amiodarone, sotalol, propafenone, flecainide, and dofetilide,

but the latter four agents are associated with a clear risk of proarrhythmia, and amiodaronefrequently causes other adverse effects.

Therefore, it may be prudent to determine whether atrialfibrillation recurs during a period of 6 months without antiarrhythmicdrugs during which anticoagulation is maintained.

If it does recur, the decision as to whether to restore sinus rhythm and initiate long-termantiarrhythmic therapy can be based on how well the patient tolerates atrial fibrillation. In such a patient,long-term anticoagulation is probably indicated in any case, because of the high rate of recurrence andthe likely occurrence of asymptomatic paroxysmal episodes.

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Long-Term Antiarrhythmic Therapy and Elective Cardioversion

For patients who have had

a single, initial episode of atrial fibrillationwith no significant hemodynamic problems,

no specific therapy is required because repeat episodes may not occur for many years.

In contrast, patients who manifest frequent recurrences

with

class IA (quinidine, procainamide, and disopyramide),class IC (propafenone and flecainide), orclass III (sotalol, amiodarone, and dofetilide) agents,

all of which are more effective than placebo in maintaining sinus rhythm

Antiarrhythmic Drug Therapy for Atrial Fibrillation

For patients with lone atrial fibrillation, use of any of the antiarrhythmic drugs listed is appropriate.

may be candidates for long-term antiarrhythmic therapy

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In addition, extracardiac factors are veryimportant in the choice ofantiarrhythmic drugs. Forexample, dose adjustmentsare mandatory for patientswith renal insufficiency.

Even w i th drug therapy ,recur rence ra tes fo r a t r ia l f ib r i l l a t ion

IN GENERAL, THE CLASS IC AGENTS (flecainide or propafenone) are the first choice in terms of efficacyand lowest incidence of side effects.

It would be wise, for example, to withhold [= παρακρατώ, αναχαιτίζω ] amiodarone as a first-line drug in view of thepotential for adverse effects.

Only two drugs have been proved safe for patients with severe congestive heart failure:

dofetilide andamiodarone.

For patients with atrial fibrillation ASSOCIATED WITH CORONARY ARTERY DISEASE,

consider use of sotalol as initial drug therapy.

This agent has class III antiarrhythmic effects and is a potent -blocker.

Class IC drugs should not be used in patients with significant structural cardiac disease or in those withischemic heart disease.

They have, however, been found to be safe and effective for patients with hypertension and atrial fibrillation.

This is especially true for

procainamide,sotalol, anddofetilide.

Dofetilide, for example, requires hospital admission, calculation of the creatinine clearance, and drug titrationaccording to the QT corrected for heart rate as well as renal function.

In addition, these agents may be associated with significant sideeffects.

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approach 50% per year (as opposed torecur rences w i th p lacebo therapy o f75% per year ) .

Great care must be exerc i sed inthe use o f these agents , ba lanc ing thebenef i t s aga ins t the potent ia l foradverse e f fect s .

Pat ien ts w i th s ign i f i cant s inusnode or a t r iovent r icu la r (AV) conduct iond isease may requ i re pacemaker therapybefore use o f an t ia r rhy thmic drugsbecause these drugs may fu r therdepress s inus node or AV conduct ion .

For class IA drugs, these include induction [= εγκαθίδρυση ] oftorsades de pointes, especially for those with congestive heart failure.

For example, a meta-analysiscompared quinidine with placebo for patients with atrial fibrillation andfound that death from all causes was higher in the groups treated withquinidine.

In addition, in the Stroke Prevention in Atrial Fibrillation (SPAF) trials,substantial numbers of patients were treated with antiarrhythmic agents; in patientswith heart failure, those treated with class I drugs had significantly increasedmortality rates compared with those not treated with antiarrhythmic drugs.

General rules include

avoidance of all class IA drugs or sotalol for patients withcongestive heart failure and

avoidance of class IC agents for patients with structural heart disease.

In addition, sotalol is contraindicated for patients with severe depression of the left ventricular ejection fraction and severe leftventricular hypertrophy.

The only drugs that appear to be both effective and safe forpatients with heart failure and atrial fibrillation are

amiodarone and dofetilide.

Amiodarone is associated with a host of both

cardiac (eg, severe sinus bradycardia or arrest or AV block) andnoncardiac (eg, thyroid abnormalities, pulmonary fibrosis) adverse effects,

but low-dose amiodarone (ie, 200 mg/day) appears to be effective and very well tolerated.

Dofetilide has a narrow therapeutic window and can cause life-threatening arrhythmias;

it can be used in patients with atrial fibrillation and congestive heart failure but requires a 2–3 day in-hospital stay formonitoring of the agent.

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Recent s tud ies have emphas izedthe use o f d rugs fo r acute convers ionof a t r ia l f ib r i l l a t ion . I t has been showntha t in t ravenous ibu t i l ide or in t ravenousdofe t i l ide (no t ava i lab le in the Un i tedSta tes ) a re e f fec t ive fo r convers ion o fapprox imate ly 35% o f pa t ien ts w i tha t r ia l f ib r i l l a t ion .

Chemical Cardioversion

It should be emphasized that this drug should beused only in a monitored environment.

The usual dose is 1 mg over 10 minutes, followed by a 10-minuteinterlude, followed by an additional 1 mg over 10 minutes if necessary.

Facilities with intravenous management, and a defibrillatorshould be readily available because the incidence of sustainedtorsades de pointes is 1–2%.

Ibutilide should be avoided for patients with severe heart failure or bradycardia.

Other Drugs for Chemical Cardioversion

Other drug combinations have also been found effective.

For example, it has been found that use of

large oral doses of either flecainide (300 mg) or propafenone (600 mg) may terminate up to80% of episodes of atrial fibrillation within 2 hours (pill-in-the-pocket).

This approach should be used only

in patients who are pretreated with -blocking drugs andin the absence of significant cardiac disease or heart failure.

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Anticoagulant Therapy

Management, Antithrombotic Therapy


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For pat ients w i th a t r ia lf ib r i l l a t ion , even when i t i s paroxysmalor occurs rare ly , ant i coagu la t ion wi thwar far in to an INR target o f 2 .0 –3 .0shou ld be es tab l i shed and mainta inedindef in i te ly for pat ients w i th nocontra ind icat ion to ant i coagu la t ion andat leas t one r i sk fac tor for s t roke

For patients unableto take warfarin,clopidogrel plus aspirin(versus aspirin alone)was shown to reducestroke risk by 28% inthe ACTIVE-A trial,although with anincreased risk ofbleeding.

Unfortunately, studies show that only about halfof patients with atrial fibrillation and an indication forwarfarin are receiving it, and even when they do, theyare out of the target INR range nearly half the time.Cardioversion, if planned, should be performed after at least4 weeks of anticoagulation at a therapeutic level.

Anticoagulation clinics with systematic managementof warfarin dosing and adjustment have been shown toresult in better maintenance of target anticoagulation

While there was hope that clopidogrel and aspirin might be reasonable alternatives for warfarin forsome patients, the ACTIVE-W trial was stopped early because of substantially lower rates of strokewith warfarin compared with the combination of clopidogrel and aspirin

Recently, dabigatran,

an oral direct thrombin inhibitor,

was compared with warfarin (in the RELY trial) for prevention of strokeand systemic embolism for patients with atrial fibrillation and at least oneadditional risk factor for stroke.

One dabigatran dose (110 mg orally twice daily)was noninferior to warfarin in stroke prevention andcaused significantly less bleeding, and a second

higher (150 mg orally twice daily) dose resulted in significantly fewerstrokes with similar bleeding rates.

Both doses of dabigatran caused substantially less intracerebral hemorrhage than warfarin.

While patients with kidney disease were excluded and there was a tendency for more myocardialinfarctions with dabigatran, dabigatran is a very attractive alternative to warfarin for many patientsbecause it eliminates the need for INR monitoring.

Exceptions to the need for anticoagulation is the patient with "lone atrial fibrillation" (eg, no evidence ofassociated heart disease, hypertension, atherosclerotic vascular disease, or diabetes mellitus) who is under age 65years or patients with low-risk profiles

Such patients should be treated with aspirin 81–325 mg daily or no antithrombotic therapy.

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The risk of CVA inpatients with nonrheumaticatrial fibrillation is 4–7% peryear.

The r i sks o f CVA are s imi la r inpat ients w i th paroxysmal versus chron icat r ia l f ib r i l l a t ion .

The ro le o f asp i r in therapy fo rpa t ien ts w i th a t r ia l f ib r i l l a t ion remainscont rovers ia l .

In a fo l low -up s tudy (SPAF I I ) ,the inc idence o f s t roke was h igher w i thasp i r in (4 .8%) compared w i th war fa r in(3 .6%) .

Patients at particularly high risk include those over age 70 years or withhypertension, a history of heart failure, increased left atrial size, diabetes, or priorCVA.

Numerous studies have documented the remarkable efficacyof warfarin in decreasing the risk of emboli by 45–85% in patientswith nonrheumatic atrial fibrillation with a low risk of significanthemorrhage, provided the international normalized ratio (INR) is in the range of 2.0 to 2.5. STILL CONTROVERSIAL ISTHE NEED FOR ANTICOAGULANT THERAPY IN YOUNGER PATIENTS WITH LONE ATRIALFIBRILLATION BECAUSE THE RISK OF EMBOLI IS VERY LOW IN THIS GROUP.

In one study, 75 mg of aspirin failed to decrease the stroke riskcompared with placebo (5.5%/year).

In contrast, the SPAF I trials showed that a higher dose of aspirin,325 mg, appeared to be of benefit in patients under 75 years of age.

The SPAF III trials demonstrated that ASPIRIN (325MG/DAY) AND FIXED LOW-DOSE WARFARIN (1, 2, OR 3 MG)WERE INEFFECTIVE FOR STROKE PREVENTION.

Therefore, the weight of current data favors use of warfarin with an INR of 2.0–3.0 as thebest strategy to prevent systemic embolization. A number of studies involving use of newer antithrombinagents, are in clinical trials.

Initial trials with ximelagatran in patients with atrial fibrillation

showed non-inferiority compared with warfarin butit failed FDA clearance because of hepatotoxicity.

The advantage of these agents will be to obviate the need for blood testing of INR levels.

Trials of aspirin and clopidogrel proved inferior to warfarin.

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Direct-currentcardioversion is a veryeffective technique forrestoration of sinusrhythm.

If the pat ient has a historyof recurrent episodes of atr ia lf ibr i l lat ion then he or she shouldbe pretreated with anantiarrhythmic agent becausereversion to atr ial f ibr i l lat ion aftershock therapy is very high.

One recommended opt ion fo rpa t ien ts w i th a t r ia l f ib r i l l a t ion o f morethan 48 hours dura t ion is to per formtransesophagea l echocard iography(TEE) , wh ich is exce l len t fo r de tec t ingc lo ts in the le f t a t r ium or the le f t a t r ia lappendage .

Direct-Current Cardioversion

Because of the benefits of sinus rhythm in terms of improved cardiac output and decreasedrisk of embolic phenomena, in general, at least one attempt should be made to restore sinusrhythm.

Several precautions [= πρόνοια, προφύλαξη ] are in order.

Use of antiarrhythmic drugs before direct-current shock,however, is inappropriate for the patient with an initial episodeof well-tolerated atrial fibrillation.

Unless urgent cardioversion is required because of

hemodynamic decompensation,severe ischemia, orcongestive heart failure,

it is imperative to follow one of several options for reducing the risk of systemic embolization:

a. For patients with atrial fibrillation of less than 48 hours duration

it would appear to be safe to proceed with application of direct-current shock.

b. If atrial fibrillation persists for more than 48 h,

then the risk of embolization increases and anticoagulants are required prior to ablation.

Evidence from several studies indicates that the finding of either aclot or spontaneous echocardiographic contrast in the left atrium isassociated with higher risks of systemic embolization.

In the absence of such findings on TEE, systemicemboli are rare. Therefore, patients with recent-onset atrial fibrillation

with no evidence of atrial clots or spontaneous contrast by TEE mayundergo direct-current cardioversion after initiation of

heparin therapy.

A recent report from the ACUTE trial showed that treatment of patients with atrial fibrillation treated on the basis ofTEE-guided therapy versus a group treated with a 3-week course of anticoagulant therapy

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had similar rates of thromboembolism (< 1%).

It must be appreciated that :

atrial function is depressed (atrial stunning) after cardioversion and thatanticoagulant therapy is recommended for at least 1 month after cardioversion.

This is true whether the duration of atrial fibrillation was either less than or greaterthan 48 hours.

For those patients with clot or dense spontaneous echocardiographic contrast with TEE,full anticoagulant therapy with an INR of 2.0–3.0 is recommended for at least 2–3 weeksbefore cardioversion.

c. An alternative approach is that patients with atrial fibrillation of greater than 48 hours

be fully anticoagulated for

at least 3 consecutive weeks before attempting direct-current cardioversion andfor about 4 weeks afterward to decrease the risk of an embolism after successful reversion to sinus rhythm.

This approach tends to be less efficient than the TEE-guided approach for recent-onset atrialfibrillation but is an acceptable alternative treatment for atrial fibrillation.

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Pads a re p laced in an an ter io r -poster io r o r ien ta t ion in o rder tomax imize cur ren t de l ivered to the a t r ium

Direct-currentexternal shock isusually performed in amonitored area undersupervision of ananesthesiologist.

. It is wise to check the arterialoxygen saturation, serumpotassium level, digoxin, orantiarrhythmic blood drug levels

before cardioversion.

DIRECT-CURRENT SHOCKS BEGINNING WITH AT LEAST 200 J ARE USED IN AN ATTEMPT TOACHIEVE SINUS RHYTHM. Multiple shocks of lesser energy are to be avoided .

If the patient fails to revert after maximal external shocks (360 J monophasic or 200 J biphasic), then successfulcardioversion can almost always be achieved either by the use of

A BIPHASIC WAVEFORM DEFIBRILLATOR ORSUPPLEMENTAL DOSES OF IBUTILIDE.

Ibutilide has been shown to lower the atrial defibrillation threshold.

An attempt at internal cardioversion using small energy shocks delivered between the coronarysinus and the right atrium is seldom necessary because the above-described treatments are almostalways effective.

The natural history of atrial fibrillation associated with

structural cardiac disease or

in patients with lone atrial fibrillation

is for spontaneous recurrence of the arrhythmia.

Unfortunately, no drug is universally effective, and the decision of how many drugs to trybefore a judgment is made to terminate antiarrhythmic drugs and focus on rate control dependson how symptomatic the patient is during atrial fibrillation.

If the episodes are poorly tolerated, then multiple drug trials or even various ablative proceduresmay be required (see section on Nonpharmacologic Treatment of Atrial Fibrillation).

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On the o ther hand , i f ra tecont ro l can be read i ly ach ieved w i thdrugs , such as d igox in , -b lockers , o rca lc ium antagon is ts

Becausepharmacologic therapyfor atrial fibrillation isnot ideal, a number ofnonpharmacologictreatment modalitieshave been introduced

: that block AV nodal conduction and the patient has agood symptomatic outcome, then an acceptable alternativeis :

to use drugs that control rate combined with long- termanticoagulant treatment.

A large, randomized trial (AFFIRM) compared the strategy of rate control and anticoagulation versus maintaining sinus rhythm withantiarrhythmic drugs. The AFFIRM trial randomized over 4000 patients with atrial fibrillation to either rate or rhythm control. The patientcohort consisted in large measure of older (mean age 69 years) patients who were not very symptomatic. They found no difference inmortality or quality of life between groups.

The rhythm control group had a higher incidence of hospitalizations and episodes of torsadesde pointes.

In addition, stroke risk was related to presence of no or inadequate anticoagulanttreatment.

This study showed that for most patients with atrial fibrillation, rate control was equallyeffective as rhythm control and that long-term anticoagulation therapy is required forboth groups.

Nonpharmacologic Treatment of Atrial Fibrillation

. For atrial fibrillation that proves refractory to drug management, onetime-tested approach is catheter ablation of the AV junction andpermanent pacemaker insertion.

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This dev ice has been shown tobe sa fe and e f fec t ive in convers ion o f

I t has been shown tha t a t r ia l -based pac ing sys tems wi l l decrease theinc idence o f a t r ia l f ib r i l l a t ion inpa t ien ts w i th the tachycard ia -bradycard ia syndrome

An innovativeapproach to the

Patients with persistent tachycardia may suffer from a tachycardia-induced cardiomyopathy

with left ventricular failure superimposed [= θέτω υπεράνω, θέτω επι τινός, υπερθέτω ] on their nativecardiac disease.

Hence, in the management of chronic atrial fibrillation, rate control is an important objective that must beachieved either

via AV nodal blocking drugs or, failing these,with catheter ablative procedures.

Catheter ablation of the AV junction involves insertion of an electrode catheter in the region of the His bundlewith application of radiofrequency energy in order to destroy AV conduction. The chief benefit of thistechnique is achievement of perfect rate control without need for drugs.

The drawbacks include the need for permanent pacing and a continued need for anticoagulant therapy.

For most of these patients, especially for those with left ventricular ejection fraction greaterthan 40%, single chamber pacing appears to be sufficient. In some patients, left ventricularfunction may deteriorate and biventricular pacing may be helpful (PAVE trial).

. In addition, pacing may allow for safe use ofantiarrhythmic drugs.

In patients with vagally mediated atrial fibrillation, atrial pacing may be effective in decreasing episodesof atrial fibrillation.

Experimental studies have shown that either dual-site atrial pacing (ie, from coronary sinusand right atrium) or from the atrial septum in conjunction with antiarrhythmic therapy, maysuppress atrial fibrillation, but this technique has not been shown to be clinically useful.

. The chief drawback isthat although the energy

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at r ia l f ib r i l l a t ion in 85% o f ins tances .

More recent t r i a l s haveemphas ized the use o f w ide areaab la t ive les ions around the pu lmonary

management of atrialfibrillation involves useof an internal atrialdefibrillator

I n some pat ients w i th paroxysmalat r ia l f ib r i l l a t ion , a rap id ly f i r ingectop ic focus , o f ten near the pu lmonaryve ins , may cause a t r ia l f ib r i l l a t ion .

required for internaldefibrillation is quite low,

nevertheless, internal shocks are painful and not well tolerated.

Currently, atrial defibrillators are combined with ventricular defibrillators and may prove to bevery helpful for patients with infrequent episodes of atrial fibrillation. "Stand alone" atrial internaldefibrillation has been abandoned.

A number of surgical centers are currently using the maze procedure to try to cure atrial fibrillation.This procedure involves placing transmural lesions over both atria in such a manner that thefibrillatory impulses cannot complete a reentrant circuit. The maze procedure involves all of the risks ofmajor open-heart surgery. This procedure should be considered for patients with atrial fibrillation who

require cardiac surgery for correction of

valvular diseases, coronary artery disease, or congenital heart disease.

The current experience using catheter ablativeprocedures to cure atrial fibrillation has been validated bya number of studies.

It was found that attempts to ablate a specific focus within the pulmonary vein resulted in a long-term success rate of 50–60% but was associated with an unacceptably high incidence of pulmonary vein stenosis (2–8%).

Currently most groups have advocated use of pulmonary vein isolation, which involves placement ofa number of lesions around the ostium of the pulmonary vein in order to isolate discharges frompulmonary venous focus.

Isolation procedures for at least three of the four pulmonary veins are associated with short-term success rates of 70–90% and are associated with a zero incidence of pulmonary veinstenosis.

Pulmonary vein isolation is currently reserved for highly symptomatic patients with atrial fibrillationthat is resistant to multiple drug trials.

. In addition, a number of groups have designedlesions to ablate areas of fractionated potentials. These

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ve ins as we l l a s use o f le s ionsconnect ing the le f t a t r ia l roof andi s thmus

potentials are thought to be derived from the pivot pointsof random reentrant circuits or from activation of vagalganglion, or both.

The ablative procedures have matured, and in the currentACC/AHA/ESC guidelines, these procedures may be used after failureof a single drug therapy.

Intravenous Pharmacologic Agents for Heart Rate Control in Atrial Fibrillation.

Management, Pharmacologic Agents for Rate Control

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Source: American Heart Association/American Collegeof Cardiology/European Society of Cardiology

Drug Loading Dose Onset MaintenanceDose

Major SideEffects

Diltiazem 0.25 mg/kg IV over 2min

2–7min

5–15 mg/hinfusion

Hypotension,heart block, HF

Esmolol 0.5 mg/kg over 1 min 5 min0.05–0.2 mg

kg–1 min–1

Hypotension,heart block,bradycardia, asthma,HF

Metoprolol 2.5–5 mg IV bolusover 2 min; up to 3 doses 5 min NA

Hypotension,heart block,bradycardia, asthma,HF

Hypotension,

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Propranolol 0.15 mg/kg IV 5 min NA heart block,bradycardia, asthma,HF

Verapamil 0.075–0.15 mg/kg IVover 2 min

3–5min NA Hypotension,

heart block, HF

Digoxin 0.25 mg IV each 2 h,up to 1.5 mg 2 h 0.125–0.25 mg

dailyDigitalis toxicity,

heart block,bradycardia

HF, heart failure.

Reprinted, with permission, from Fuster V et al. J Am Coll Cardiol. 2001;38:266i.

Antiarrhythmic Drug Therapy for Atrial Fibrillation

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Antiarrhythmic drug therapy to maintain sinus rhythm in patients with recurrent paroxysmal or persistent atrial fibrillation.Drugs in boxes are listed alphabetically and not in order of suggested use. CAD, coronary artery disease; HF, heart failure; LVH,left ventricular hypertrophy.

Management, Antiarrhythmic Drug Therapy

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Typical Doses of Drugs Used to Maintain Sinus Rhythm in Atrial Fibrillation, ListedAlphabetically.

Drug DailyDosage Potential Adverse Effects

Amiodarone100–

400 mgPhotosensitivity, pulmonary toxicity, polyneuropathy,

GI upset, bradycardia, torsades de pointes (rare), hepatictoxicity, thyroid dysfunction

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Disopyramide400–

750 mgTorsades de pointes, HF, glaucoma, urinary retention,

dry mouth

Dofetilide500–

1000 mcg Torsades de pointes

Flecainide200–

300 mgVentricular tachycardia, congestive HF, enhanced AV

nodal conduction (conversion to atrial flutter)

Procainamide1000–

4000 mgTorsades de pointes, lupus-like syndrome, GI

symptoms

Propafenone450–

900 mgVentricular tachycardia, congestive HF, enhanced AV

nodal conduction (conversion to atrial flutter)

Quinidine600–

1500 mgTorsades de pointes, GI upset, enhanced AV nodal

conduction

Sotalol240–

320 mgTorsades de pointes, congestive HF, bradycardia,

exacerbation of chronic obstructive or bronchospastic lungdisease

AV, atrioventricular; GI, gastrointestinal; HF, heart failure.

Reprinted, with permission, from Fuster V et al. J Am Coll Cardiol. 2001;38:266i.

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The 12-lead electrocardiogram shows a rapid irregular rhythm with broad QRS complex. This ispathognomonic of atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. This arrhythmiarequires urgent treatment. Acceptable therapy includes use of intravenous ibutilide or procainamide ordirect-current shock.

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Atrial Fibrillation. (ECG contributor: R. Jason Thurman, MD.)

R-to-R interval varies in an "irregularly irregular" pattern (double arrows). The baseline "rumble,"representing "F waves," may be very fine or even indiscernible.

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I t i s now wel l es tab l i shed thatpat ients w i th recurrent paroxysmalat r ia l f ib r i l l a t ion are a t s imi la r s t roker i sk as those who are in a t r ia lf ib r i l l a t ion chron ica l l y .

I f no drug works , rad io f requencyAV node ab la t ion and permanent pac ingensure ra te contro l and may fac i l i t a te amore phys io log ic ra te response toact iv i ty , but th i s i s used on ly as a l a s tresor t .

Recurrent Paroxysmal Atrial Fibrillation

Although these episodes may be apparent tothe patient, many are not recognized and may betotally asymptomatic.

Thus, ambulatory ECG monitoring or event recorders areindicated in those in whom paroxysmal atrial fibrillation is suspected.

Antiarrhythmic agents are usually not successful in preventing all paroxysmal atrialfibrillation episodes. However, dofetilide has been shown to be as effective as amiodarone in maintainingsinus rhythm in certain patients and does not have as many untoward long-term effects.

Long-term anticoagulation is indicated except in those who are under 75 years of age and haveno additional stroke risk factors

Refractory Atrial Fibrillation

Because of trial results indicating that important adverse clinical outcomes (death, stroke,hemorrhage, heart failure) are no more common with rate control than rhythm control, atrialfibrillation should generally be considered refractory :

if it causes persistent symptoms or limits activity.

This is much more likely in younger individuals and those who are very active or engage instrenuous exercise. Even in such individuals, two-drug or three-drug combinations of a β-blocker,rate-slowing calcium blocker, and digoxin usually can prevent excessive ventricular rates, thoughin some cases they are associated with excessive bradycardia during sedentary periods.

The current practice for drug-refractory,symptomatic atrial fibrillation is catheter ablation offoci in and around the pulmonary veins that initiateatrial fibrillation, following which sinus rhythm maybe restored or maintained.

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Atrial fibrillation,the most commonsustained clinicalarrhythmia,

The QRS complex is usual lynarrow, but i t may be wide i faberrant conduction or bundlebranch block is present

This therapy has become mainstream and is a reasonable second-line therapy for individuals withsymptomatic atrial fibrillation that is refractory to pharmacologic therapy.

This procedure is routinely performed in the electrophysiology laboratory using a catheter-basedapproach and can also be performed thorascopically, via thoracotomy, or via median sternotomy in theoperating room by experienced surgeons.

General Considerations :

is diagnosed by finding

an irregularly irregular ventricular rhythmwithout discrete P waves

Atrial fibrillation associated with the Wolff-Parkinson-White syndrome may occur with veryrapid ventricular rates and may be life-threatening.

This arrhythmia is diagnosed by

its very rapid irregular rate associated withwide preexcited QRS complexes and

REQUIRES EMERGENCY TREATMENT

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Pearls

1. Most "irregularly irregular" rhythms are due to atrial fibrillation, but other rhythms may producesimilar findings. These include multifocal atrial tachycardia, atrial flutter with variable AV block, and frequentPJCs.

2. Therapy is geared toward keeping the ventricular response at an appropriate rate.3. Synchronized cardioversion may be indicated if a patient is unstable, but the risk of clot

embolization must be carefully considered when planning nonemergent electrical cardioversion of atrialfibrillation.

The 12-lead electrocardiogram shows the typical rapid irregular rhythm seen with atrial fibrillation.

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Risk factors for ischemic stroke and systemic embolism in patients withnonvalvular atrial fibrillation.

Risk Factors (Control Groups) Relative Risk

Previous stroke or TIA 2.5

Diabetes mellitus 1.7

History of hypertension 1.6

Congestive heart failure 1.4

Advanced age (continuous, per decade) 1.4

1Data derived from collaborative analysis of five untreated control groups in primary prevention trials. As agroup, patients with nonvalvular atrial fibrillation have about a sixfold increased risk of thromboembolism comparedwith patients in normal sinus rhythm.

TIA, transient ischemic attack.

Reproduced, with permission, from ACC/AHA/ESC 2006 guidelines for the management of patients with atrialfibrillation. © 2006, American Heart Association, Inc.

Atrial fibrillation associated with AMI most typically occurs in the first 24 h and is usually transient.

It more often occurs in patients with :

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excess catecholamine release,hypokalemia,hypomagnesemia,hypoxia,chronic lung disease, andsinus node or left circumflex ischemia.

Patients with

supraventricular tachycardia,atrial fibrillation, andatrial flutter

who have hemodynamic compromise should receive cardioversion with 100 J, 200 to 300 J, and then 360 J, if lower energiesfail.

Patients without

hemodynamic compromise,clinical left ventricular dysfunction,reactive airway disease, orheart block

can be treated with -adrenergic antagonists, such asatenolol (2.5 to 5 mg over 2 min to a total of 10 mg) ormetoprolol (2.5 to 5 mg every 2 to 5 min to a total of 15 mg). Patients with contraindications to -adrenergic antagonists

can be treated with

digoxin (0.3- to 0.5-mg initial bolus with a repeat in 4 h) ora calcium antagonist such as verapamil or diltiazem.

Digoxin will take longer to work but is still preferred by the ACC/AHA guidelines,because of the potential negative inotropic effects of calcium antagonists,their lack of efficacy in reducing mortality during AMI, andpotentially harmful effects in some subsets of AMI patients.30 The AHA/ACC recommend sotalol as the initial antiarrhythmic agent in the setting of ACS based on its -blocking

activity.This medication is contraindicated in patients with CHF. The alternative antiarrhythmic agent is amiodarone.30 The etiology of the tachydysrhythmia should also be addressed. Heparin should be given, because atrial fibrillation during AMI is associated with a threefold risk in systemic embolization.

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Atrial Fibrillation affectsapproximately 2.3 millionpeople in the United Statesand is the most commonrhythm disorder among U.S.patients hospitalized with aprimary diagnosis of anarrhythmia.

In the United States,hospitalization for AF hasincreased two- to threefold inthe past 15 years and the sizeof the AF population isprojected to triple by 2050.

The median age of AF patients is 75 years;

84% are older than 65 years.

Pooled data from studies of chronic AF in North America, Britain, and Iceland

suggest a prevalence of 0.5% to 1% in the general population.

In two separate studies restricted to patients older than 60 years, theincidence was 5% to 9% after 5 to 15 years of follow-up.

The genesis of this AF "epidemic" is strongly linked to the expanding elderly population. AF has a substantial impact on both morbidity and mortality. It is a strong independent risk factor for stroke, responsible for an estimated 75 000

cerebrovascular accidents annually.

AF is also associated with a more than twofold increase in all-cause mortality.

(For a comprehensive review of AF, see: ACC/AHA/ESC Guidelines for the Management of Patientswith Atrial Fibrillation; http://www.cardiosource.com/guidelines/guidelines/atrial_fib/pdfs/AF_final.pdf.)

Symptoms and Signs :

Irregularly irregular pulse (harder to distinguish with more rapid heart rates)

Often occurs paroxysmally before becoming the established rhythm

Although AF frequently coexistswith other medical conditions,especially cardiovascular andpulmonary disorders, mortality remainshigher after adjusting for these andother conditions.

http://www.google.com/url?q=http%3A%2F%2Fwww.cardiosource.com%2Fguidelines%2Fguidelines%2Fatrial_fib%2Fpdfs%2FAF_final.pdf&sa=D&sntz=1&usg=AFQjCNHf8uql_mvXFsngL6Miag333B_eyQ

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Older or inactive individuals may have relatively few symptoms

However, some patients are made uncomfortable by the irregular rhythm due to palpitations or fatigue

In patients with heart disease, rheumatic disease, and other valvular heart disease,

attacks can be caused by

– Dilated cardiomyopathy– Atrial septal defect– Hypertension– Coronary heart disease– Thyrotoxicosis

In patients with normal hearts, attacks can be caused by

– Pericarditis

– Chest trauma

– Thoracic or cardiac surgery

– Pulmonary disease

– Electrolyte disturbances

– Acute alcohol excess or withdrawal

– Medications, such as theophylline and -adrenergic agonists

Atrial fibrillation itself is rarely life-threatening; however, it can have serious consequences

if the ventricular rate is sufficiently rapid to precipitate

hypotension,myocardial ischemia, ortachycardia-induced myocardial dysfunction.

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Moreover , par t i cu lar ly inpat ients w i th r i sk fac tors , a t r ia lf ib r i l l a t ion i s a major preventab le causeof s t roke.

Although manypatients—particularlyolder or inactiveindividuals—haverelatively fewsymptoms if the rate iscontrolled, somepatients are aware ofthe irregular rhythmand may find it as veryuncomfortable.

Most patients willcomplain of fatiguewhether they experienceother symptoms or not.

The hear t ra te mayrange f rom qu i te s low to ex t reme ly rap id , but i s un i fo rmly i r regu la run less under ly ing comple te hear t b lock and a permanent vent r i cu la rpacemaker i s in p lace .

Atrial fibrillation is the only common arrhythmia in which theventricular rate is rapid and the rhythm very irregular. Because of thevarying stroke volumes resulting from varying periods of diastolic filling,not all ventricular beats produce a palpable peripheral pulse.

The difference between the apical rate and the pulse rate is the " pulse deficit ";

this deficit is greater when the ventricular rate is high.

Laboratory Tests

ECG– Surface ECG typically demonstrates erratic, disorganized atrial activity between discrete QRS

complexes occurring in an irregular pattern– Atrial activity may be very fine and difficult to detect on the ECG, or quite coarse and often

mistaken for atrial flutter

Echocardiography

– Visualization of fibrillating atria with irregular ventricular contractions

– Recommended in patients with newly diagnosed atrial fibrillation to excludeoccult valvular or myocardial disease

Ambulatory ECG monitoring or event recorders are indicated when paroxysmalatrial fibrillation is suspected

Obtain thyroid-stimulating hormone level to exclude thyrotoxicosis as a potentialcause

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When cal led on to managenew - onset atr ial f ibr i l lat ion, i t isimportant to establ ish theprecipitat ing factors because thetype of associated condit iondetermines long- term prognosis.

For example, thisarrhythmia may developin patients withhyperthyroidism or lungdisease, or after eithercardiac or pulmonarysurgery, especially inolder patients.

Atr ial f ibr i l lat ion is alsoseen in pat ients with acutepulmonary embol ism, myocardit is ,or acute myocardial infarct ion,part icular ly when the lastcondit ion is complicated by eitherocclusion of the r ight coronaryartery or heart fai lure.

In some patients, episodes of atrial fibrillation may beinitiated by

caffeine,alcohol, ormarijuana use.

Atrial fibrillation may result from acute intercurrent ailments [= ασθένεια, αδιαθεσία, αρρώστια ]

When atrial fibrillationoccurs in these settings, it almostalways abates [= is reduced ]spontaneously if the patientrecovers from the underlyingproblem.

Hence, management usuallyinvolves

administration of drugs to control the heart rate, andlong-term antiarrhythmic therapy is generally not needed.

Alternatively, atrial fibrillation may occur in association with structural cardiac disease.

Important associated conditions include rheumatic mitral stenosis, hypertension, hypertrophiccardiomyopathy, or chronic heart failure

In contrast to patients with acute intercurrent ailments [= illness, sickness; pain, ache, suffering ],

those with structural heart disease may expect (even with antiarrhythmic therapy)many recurrences and chronic atrial fibrillation may supervene.

Lone fibrillation

is the term used to describe patients with atrial fibrillation not associated with known cardiac conditions or

noncardiac precipitants.

The natural history of the atrial fibrillation for those with lone atrial fibrillation issimilar to that in patients with structural cardiac disease, in that episodes of atrial fibrillation are

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Fur ther tes t ing w i l l depend onvar ious aspects o f the h is tory orphys ica l examinat ion . For example , i fa t r ia l f ib r i l l a t ion is usua l ly p rec ip i ta tedby exerc ise , then an exerc ise t readmi l ltes t i s appropr ia te

likely to recur and, eventually, the arrhythmia may become sustained.

Physical Examination

The initial evaluation of new-onset atrial fibrillation includes

a detailed history focusing on possible precipitating factors as well asthe presence of organic cardiac disease.

As such, the initial evaluation includes, at a minimum,

a careful physical examination,12-lead electrocardiogram,chest radiograph, echocardiogram, andtests of thyroid function.

. In the patient with frequent episodes of paroxysmal atrialfibrillation, A 24-HOUR TO 48-HOUR HOLTERRECORDING MAY DISCERN WHETHER atrial fibrillation wastriggered by another arrhythmia such as

a premature atrial complex alone or whetherthe fibrillation was preceded by an episode of supraventricular

tachycardia.

In addition, patients with vagally mediated fibrillation

will typically have episodes either after heavy meals or during sleep .

These clues may help identify those patients who may respond to specific approaches

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Atrial fibrillation Etiology

● Rheumatic heart disease● Dilated cardiomyopathy● Pulmonary disease, eg, chronic obstructive pulmonary disease, pulmonary embolism● Mitral stenosis● Mitral regurgitation● Mitral valve prolapse● Coronary artery disease● Atrial septal defect● Atrial myxoma● Hypertension● Hypertrophic obstructive cardiomyopathy● Thyrotoxicosis (hyperthyroidism)● Pericarditis● Chest trauma or chest surgery● Medications: theophylline, beta-agonists● Alcohol withdrawal● Sepsis

DDx

● Frequent premature atrial contractions (PACs)● Atrial flutter (especially if variable block)● Multifocal atrial tachycardia (MAT)● Sinus tachycardia● Sinus arrhythmia● Atrial tachycardia● Supraventricular tachycardia (AVNRT, AVRT, WPW)● Ventricular tachycardia

See related DDx

● Tachycardia

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Antiarrhythmic drugs

Agent IntravenousDosage

OralDosage

TherapeuticPlasma Level

RouteofElimination

SideEffects

Class Ia:Action: Sodiumchannel blockers:Depress phase 0depolarization; slowconduction; prolongrepolarization.

Indications:Supraventriculartachycardia,ventriculartachycardia,prevention ofventricular fibrillation,symptomaticventricular prematurebeats.

Quinidine

6–10 mg/kg(intramuscularly orintravenously) over20 min (rarely usedparenterally)

200–400 mg every4–6 h orevery 8 h(long-acting)

2–5 mg/mL Hepatic GI, LVF, Dig

Procainamide

100 mg/1–3min to 500–1000 mg;maintain at 2–6mg/min

50mg/kg/d individeddoses every3–4 h orevery 6 h(long-acting)

4–10 mg/mL;NAPA (activemetabolite), 10–20mcg/mL

Renal SLE,hypersensitivity, LVF

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Disopyramide

100–200 mg every6–8 h

2–8 mg/mL Renal Urinaryretention, drymouth, markedly LVF

Moricizine

200–300 mg every8 h

Note: Activemetabolites

Hepatic Dizziness,nausea, headache,theophylline level, LVF

Class Ib:Action: Shortenrepolarization.

Indications:Ventriculartachycardia,prevention ofventricular fibrillation,symptomaticventricular beats.

Lidocaine

1–2 mg/kg at50 mg/min; maintainat 1–4 mg/min

1–5 mg/mL Hepatic CNS, GI

Mexiletine

100–300 mg every6–12 h;maximum:1200 mg/d

0.5–2 mg/mL Hepatic CNS, GI,leukopenia

Class Ic:Action: Depressphase 0repolarization; slowconduction.

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Propafenone is a weakcalcium channelblocker and -blocker and prolongsaction potential andrefractoriness.

Indications:Life-threateningventriculartachycardia orfibrillation, refractorysupraventriculartachycardia.

Flecainide

100–200 mg twicedaily

0.2–1 mg/mL Hepatic CNS, GI, LVF, incessant VT,sudden death

Propafenone

150–300 mg every8–12 h

Note: Activemetabolites

Hepatic CNS, GI, LVF, Dig

Class II:Action: -blocker,slows AV conduction.Note: Other -blockers may alsohave antiarrhythmiceffects but are notyet approved for thisindication in theUnited States.

Indications:Supraventriculartachycardia; mayprevent ventricularfibrillation.

500 mcg/kgover 1–2 min;

Other -blockers

Notestablished

Hepatic LVF,bronchospasm

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Esmolol

maintain at 25–200mcg/kg/min

may be usedconcomitantly

Propranolol

1–5 mg at 1mg/min

40–320 mg in 1–4 doses daily(dependingonpreparation)

Notestablished

Hepatic LVF,bradycardia, AVblock,bronchospasm

Metoprolol

2.5–5 mg 50–200 mg daily

Notestablished

Hepatic LVF,bradycardia, AVblock

Class III:Action: Prolongaction potential.

Indications:Amiodarone:refractory ventriculartachycardia,supraventriculartachycardia,prevention ofventriculartachycardia, atrialfibrillation, ventricularfibrillation; dofetilide:atrial fibrillation andflutter; sotalol:ventriculartachycardia, atrialfibrillation; bretylium:ventricular fibrillation,ventriculartachycardia; ibutilide:conversion of atrialfibrillation and flutter.

Amiodarone

150–300 mginfused rapidly,followed by 1-mg/mininfusion for 6 h (360mg) and then 0.5mg/min

800–1600 mg/dfor 7–21days;maintain at100–400mg/d (higher

1–5 mg/mL Hepatic Pulmonaryfibrosis,hypothyroidism,hyperthyroidism,corneal and skindeposits, hepatitis, Dig, neurotoxicity,

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doses maybe needed)

GI

Sotalol

80–160 mg every12 h (higherdoses maybe used forlife-threateningarrhythmias)

Renal(dosingintervalshould beextended ifcreatinineclearance is <60 mL/min)

Earlyincidence oftorsades depointes, LVF,bradycardia,fatigue (and otherside effectsassociated with -blockers)

Dofetilide

500mg twicedaily

Renal(dose must bereduced withrenaldysfunction)

Torsades depointes in 3%;interaction withcytochrome P-450inhibitors

Ibutilide

1 mg over 10min, followed by asecond infusion of0.5–1 mg over 10 min

Hepaticand renal

Torsades depointes in up to 5%of patients within 3h afteradministration;patients must bemonitored withdefibrillator nearby

Class IV:Action: Slow calciumchannel blockers.

Indications:Supraventriculartachycardia.

Verapamil

10–20 mg over2–20 min; maintain at5 mg/kg/min

80–120 mg every6–8 h; 240–360 mg oncedaily withsustained-releasepreparation

0.1–0.15mg/mL

Hepatic LVF,constipation, Dig,hypotension

Diltiazem

0.25 mg/kgover 2 min; second0.35-mg/kg bolusafter 15 min ifresponse isinadequate; infusion

180–360 mg dailyin 1–3 dosesdepending onpreparation(oral forms

Hepaticmetabolism,renalexcretion

Hypotension,LVF

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rate, 5–15 mg/h not approvedforarrhythmias)

Miscellaneous:Indications:Supraventriculartachycardia.

Adenosine

6 mg rapidlyfollowed by 12 mgafter 1–2 min ifneeded; use halfthese doses ifadministered viacentral line

Adenosinereceptorstimulation,metabolizedin blood

Transientflushing, dyspnea,chest pain, AVblock, sinusbradycardia; effectby theophylline, bydipyridamole

Digoxin

0.5 mg over 20min followed byincrement of 0.25 or0.125 mg to 1–1.5 mgover 24 h

1–1.5mg over 24–36 h in 3 or 4doses;maintenance,0.125–0.5mg/d

0.7–2 mg/mL Renal AV block,arrhythmias, GI,visual changes

AV, atrioventricular; CNS, central nervous system; Dig, elevation of serum digoxin level; GI, gastrointestinal (nausea,

vomiting, diarrhea); LVF, reduced left ventricular function; NAPA, N-acetylprocainamide; SLE, systemic lupus erythematosus;VT, ventricular tachycardia.

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Fetal Endocardial Cushion DefectUpdates: Williams Obstetrics

Dabigatran: An End to Warfarin?Updates: Hurst's The Heart

ECG-Gated Myocardial Perfusion SPECT: Influence ofArrhythmia

Updates: Hurst's The Heart

Lenient versus Strict Rate Control in Patients with AtrialFibrillation


Pulmonary-Vein Isolation for Atrial Fibrillation in Patientswith Heart Failure


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