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 Atrial Fibrillation

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PostSubject: Atrial Fibrillation    Atrial Fibrillation  Icon_minitimeWed Jun 08, 2011 1:08 pm

Atrial Fibrillation

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Classification of
atrial fibrillation (AF) begins with distinguishing a first detectable
episode, irrespective of whether it is symptomatic or self-limited.
Published guidelines from an American College of Cardiology
(ACC)/American Heart Association (AHA)/European Society of Cardiology
(ESC) committee of experts on the treatment of patients with atrial
fibrillation recommend classification of AF into the following 3
patterns (also see the image below)

  • Paroxysmal AF – Episodes of AF that terminate spontaneously within 7 days (most episodes last less than 24 hours)
  • Persistent
    AF - Episodes of AF that last more than 7 days and may require either
    pharmacologic or electrical intervention to terminate
  • Permanent
    AF - AF that has persisted for more than 1 year, either because
    cardioversion has failed or because cardioversion has not been attemptedAtrial Fibrillation  150072-1332317-151066-1447186tnClassification scheme for patients with atrial fibrillation.
classification schema pertains to cases that are not related to a
reversible cause of AF (eg, thyrotoxicosis, electrolyte abnormalities,
acute ethanol intoxication). Atrial fibrillation secondary to acute
myocardial infarction, cardiac surgery, pericarditis, pulmonary
embolism, or acute pulmonary disease is considered separately because,
in these situations, AF is less likely to recur once the precipitating
condition has been treated adequately and has resolved. Paroxysmal AF

fibrillation is considered to be recurrent when a patient has 2 or more
episodes. If recurrent AF terminates spontaneously, it is designated as
paroxysmal. Some patients with paroxysmal AF, typically younger
patients, have been found to have distinct electrically active foci
within their pulmonary veins. These patients generally have many atrial
premature beats noted on Holter monitoring. Isolation or elimination of
these foci can lead to elimination of the trigger for paroxysms of AF. Paroxysmal
AF may progress to permanent AF, and aggressive attempts to restore and
maintain sinus rhythm may prevent comorbidities associated with AF.
Persistent AF
recurrent AF is sustained, it is considered persistent, irrespective of
whether the arrhythmia is terminated by either pharmacologic therapy or
electrical cardioversion.Persistent AF may be either the first
presentation of AF or the result of recurrent episodes of paroxysmal AF.
Patients with persistent AF also include those with longstanding AF in
whom cardioversion has not been indicated or attempted, often leading to
permanent AF. Patients can also have AF as an arrhythmia
secondary to cardiac disease that affects the atria (eg, congestive
heart failure, hypertensive heart disease, rheumatic heart disease,
coronary artery disease). These patients tend to be older, and AF is
more likely to be persistent.Persistent AF with an uncontrolled,
rapid ventricular heart rate response can cause a dilated cardiomyopathy
and can lead to electrical remodeling in the atria (atrial
cardiomyopathy). Therapy, such as drugs or atrioventricular nodal
ablation and permanent pacemaker implantation, to control the
ventricular rate can improve left ventricular function and improve
quality-of-life scores.
Permanent AF

Permanent AF is
recognized as the accepted rhythm, and the main treatment goals are rate
control and anticoagulation. While it is possible to reverse the
progression from paroxysmal to persistent and to permanent, this task
can be challenging.
Lone atrial fibrillation

In addition
to the above schema, the term "lone atrial fibrillation" has been used
to identify AF in younger patients without structural heart disease, who
are at a lower risk for thromboembolism. The definition of lone AF
remains controversial, but it generally refers to paroxysmal,
persistent, or permanent AF in younger patients (< 60 y) who have
normal echocardiographic findings.

fibrillation (AF) shares strong associations with other cardiovascular
diseases, such as heart failure, coronary artery disease (CAD), valvular
heart disease, diabetes mellitus, and hypertension.[3] These
factors have been termed upstream risk factors, but the relationship
between comorbid cardiovascular disease and AF is incompletely
understood and more complex than this terminology implies. The exact
mechanisms by which cardiovascular risk factors predispose to AF are not
understood fully but are under intense investigation. Catecholamine
excess, hemodynamic stress, atrial ischemia, atrial inflammation,
metabolic stress, and neurohumoral cascade activation are all purported
to promote AF. Although the precise mechanisms that cause atrial
fibrillation are incompletely understood, AF appears to require both an
initiating event and a permissive atrial substrate. Significant recent
discoveries have highlighted the importance of focal pulmonary vein
triggers, but alternative and nonmutually exclusive mechanisms have also
been evaluated. These mechanisms include multiple wavelets, mother
waves, fixed or moving rotors, and macro-reentrant circuits. In a given
patient, multiple mechanisms may coexist at any given time. The
automatic focus theory and the multiple wavelet hypothesis appear to
have the best supporting data.
Automatic focus

A focal
origin of AF is supported by several experimental models showing that AF
persists only in isolated regions of atrial myocardium. This theory has
garnered considerable attention, as studies have demonstrated that a
focal source of AF can be identified in humans and that isolation of
this source can eliminate AF. The pulmonary veins appear to be
the most frequent source of these automatic foci, but other foci have
been demonstrated in several areas throughout the atria. Cardiac muscle
in the pulmonary veins appears to have active electrical properties that
are similar, but not identical, to those of atrial myocytes.
Heterogeneity of electrical conduction around the pulmonary veins is
theorized to promote reentry and sustained AF. Thus, pulmonary vein
automatic triggers may provide the initiating event, and heterogeneity
of conduction may provide the sustaining conditions in many patients
with AF.
Multiple wavelet

The multiple wavelet hypothesis
proposes that fractionation of wave fronts propagating through the
atria results in self-perpetuating "daughter wavelets." In this model,
the number of wavelets is determined by the refractory period,
conduction velocity, and mass of atrial tissue. Increased atrial mass,
shortened atrial refractory period, and delayed intra-atrial conduction
increase the number of wavelets and promote sustained AF. This model is
supported by data from patients with paroxysmal AF demonstrating that
widespread distribution of abnormal atrial electrograms predicts
progression to persistent AF.[4] Intra-atrial conduction prolongation has also been shown to predict recurrence of AF.[5] Together,
these data highlight the importance of atrial structural and electrical
remodeling in the maintenance of AF—hence the phrase "atrial
fibrillation begets atrial fibrillation.

Atrial fibrillation (AF) is strongly associated with the following risk factors:

  • Hemodynamic stress
  • Atrial ischemia
  • Inflammation
  • Noncardiovascular respiratory causes
  • Alcohol and drug use
  • Endocrine disorders
  • Neurologic disorders
  • Genetic factors
  • Advancing age
Hemodynamic stress

intra-atrial pressure results in atrial electrical and structural
remodeling and predisposes to AF. The most common causes of increased
atrial pressure are mitral or tricuspid valve disease and left
ventricular dysfunction. Systemic or pulmonary hypertension also
commonly predisposes to atrial pressure overload, and intracardiac
tumors or thrombi are rare causes.
Atrial ischemia

artery disease infrequently leads directly to atrial ischemia and AF.
More commonly, severe ventricular ischemia leads to increased
intra-atrial pressure and AF.

and pericarditis may be idiopathic or may occur in association with
collagen vascular diseases; viral or bacterial infections; or cardiac,
esophageal, or thoracic surgery.
Noncardiovascular respiratory causes

Pulmonary embolism, pneumonia, lung cancer, and hypothermia have been associated with AF
.Drug and alcohol use

alcohol, and cocaine can trigger AF. Acute or chronic alcohol use (ie,
holiday or Saturday night heart, also known as alcohol-related
cardiomyopathy) and illicit drug use (ie, stimulants, methamphetamines,
cocaine) have been specifically found to be related to AF. Endocrine disorders

Hyperthyroidism, diabetes, and pheochromocytoma have been associated with AF.
Neurologic disorders

Intracranial processes such as subarachnoid hemorrhage or stroke can precipitate AF
.Familial AF

history of parental AF appears to confer increased likelihood of AF
(and occasional family pedigrees of AF are associated with defined ion
channel abnormalities, especially sodium channels).[6] One
cohort study suggests that familial AF is associated with an increased
risk of AF. This increase was not lessened by adjustment for genetic
variants and other AF risk factors.[7]
Advancing age

AF is strongly age-dependent, affecting 4% of individuals older than 60 years and 8% of persons older than 80 years.

fibrillation affects more than 2.2 million persons in the United States.
AF is strongly age-dependent, affecting 4% of individuals older than 60
years and 8% of persons older than 80 years. Approximately 25% of
individuals aged 40 years and older will develop AF during their
lifetime.[8] The
prevalence of AF is 0.1% in persons younger than 55 years, 3.8% in
persons 60 years or older, and 10% in persons 80 years or older. With
the projected increase in the elderly population in the United States,
the prevalence of AF is expected to more than double by the year 2050.
AF is uncommon in childhood except after cardiac surgery.[9] The
incidence of AF is significantly higher in men than in women in all age
groups. AF appears to be more common in whites than in blacks, with
blacks have less than half the age-adjusted risk of developing AF. In
10-15% of cases of AF, the disease occurs in the absence of
comorbidities (lone atrial fibrillation). However, AF is often
associated with other cardiovascular diseases, including hypertension;
heart failure; diabetes-related heart disease; ischemic heart disease;
and valvular, dilated, hypertrophic, restrictive, and congenital
cardiomyopathies.[8] The rate of ischemic stroke
in patients with nonrheumatic AF averages 5% a year, which is somewhere
between 2 and 7 times the rate of stroke in patients without AF. The
risk of stroke is not due solely to AF; it increases substantially in
the presence of other cardiovascular diseases.[10] The
prevalence of stroke in patients younger than 60 years is less than
0.5%; however, in those older than 70 years, the prevalence doubles with
each decade.[11] The
attributable risk of stroke from AF is estimated to be 1.5% for those
aged 50-59 years, and it approaches 30% for those aged 80-89 years.

AF is associated
with a 1.5- to 1.9-fold higher risk of death, which is in part due to
the strong association between AF and thromboembolic events, according
to data from the Framingham heart study.[12] Medical
therapies aimed at rhythm control offered no survival advantage over
rate control and anticoagulation, according to the Atrial Fibrillation
Follow-up Investigation of Rhythm Management (AFFIRM) trial. The study
addressed whether rate control and anticoagulation are sufficient goals
for asymptomatic, elderly patients.[13] Atrial
fibrillation (AF) is associated with increased morbidity and mortality,
in part due to the risk of thromboembolic disease, particularly stroke,
in AF and in part due to its associated risk factors. Studies have
shown that individuals in sinus rhythm live longer than individuals with
AF. Disruption of normal atrial electromechanical function in AF leads
to blood stasis. This, in turn, can lead to development of thrombus,
most commonly in the left atrial appendage. Dislodgement or
fragmentation of a clot can then lead to embolic phenomena, including
stroke. Development of AF predicts heart failure and is
associated with a worse New York Heart Association Heart Failure
classification. AF may also worsen heart failure in individuals who are
dependent on the atrial component of the cardiac output. Those with
hypertensive heart disease and those with valvular heart disease are
particularly at high risk for developing heart failure when AF occurs.
In addition, AF may cause tachycardia-mediated cardiomyopathy if
adequate rate control is not established.
Atrial fibrillation in association with acute myocardial infarction

is a common finding in patients presenting with an acute myocardial
infarction. A meta-analysis pooled data from 43 studies and more than
278,800 patients.[14] The
study found that AF in the setting of acute myocardial infarction was
associated with 40% increase in mortality compared to patients in sinus
rhythm with acute myocardial infarction. The causes of death were
unclear, but may be related to triple anticoagulation therapy with
aspirin, clopidogrel, and warfarin, or may be related to hemodynamic
consequences associated with the loss of atrial contraction. Whether AF
is a complication of myocardial infarction or a marker for myocardial
infarction severity is unclear.

Atrial Fibrillation Clinical Presentation


Clinical presentation spans the entire spectrum from asymptomatic atrial fibrillation (AF) with rapid ventricular response to cardiogenic shock or devastating cerebrovascular accident (CVA). Initial
evaluation of the patient with new-onset atrial fibrillation should
focus on the patient's hemodynamic stability. Care of hemodynamically
unstable patients is guided by Advanced Cardiac Life Support (ACLS)
protocols, including immediate direct current (DC) cardioversion.[15] Symptomatic
patients may benefit from intravenous (IV) rate-controlling agents,
either calcium-channel blockers or beta-adrenergic blockers. While up to 90% of AF episodes may not cause symptoms,[16] many
patients experience a wide variety of symptoms, including palpitations,
dyspnea, fatigue, dizziness, angina, and decompensated heart failure.
In addition, AF can be associated with hemodynamic dysfunction,
tachycardia-induced cardiomyopathy, and systemic thromboembolism. Unstable patients requiring immediate DC cardioversion include the following:

  • Patients with decompensated congestive heart failure (CHF)
  • Patients with hypotension
  • Patients with uncontrolled angina/ischemia
Less severe symptoms and patient complaints include the following:

  • Palpitations
  • Fatigue or poor exercise tolerance
  • Presyncope or syncope
  • Generalized weakness, dizziness, fatigue
addition to eliciting the symptoms above, history taking of any patient
presenting with suspected AF should include questions relevant to
temporality, precipitating factors (including hydration status, recent
infections, alcohol use), history of pharmacologic or electric
interventions and responses, and presence of heart disease. An effort
should also be made to evaluate for potential comorbid diseases that
contribute to initiation or maintenance of AF. Occasionally, a patient
may have a clear and strong belief about the onset of symptoms that may
be helpful in determining a course of action. Initial history includes the following:Documentation of clinical type of AF (paroxysmal, persistent, or permanent) (See Diagnostic Considerations.)

  • Assessment of type, duration, and frequency of symptoms
  • Assessment of precipitating factors (eg, exertion, sleep, caffeine, alcohol use)
  • Assessment of modes of termination (eg, vagal maneuvers)
  • Documentation of prior use of antiarrhythmics and rate-controlling agents
  • Assessment of presence of underlying heart disease
Documentation of any previous surgical or percutaneous AF ablation procedures
Next Section: Physical Examination

Physical Examination

examination always begins with airway, breathing, and circulation
(ABCs) and vital signs, as these guide the pace of the intervention. The
physical examination also provides information on underlying causes and
sequelae of atrial fibrillation. Vital signs

Heart rate,
blood pressure, respiratory rate, and oxygen saturation are
particularly important in evaluating hemodynamic stability and adequacy
of rate control in AF. Patients will have an irregularly
irregular pulse and will commonly be tachycardic, with heart rates
typically in the 110- to 140-range, but rarely over 160-170. Patients
who are hypothermic or who have cardiac drug toxicity may present with
bradycardic atrial fibrillation. Head and neck

of the head and neck may reveal exophthalmos, thyromegaly, elevated
jugular venous pressures, or cyanosis. Carotid artery bruits suggest
peripheral arterial disease and increase the likelihood of comorbid
coronary artery disease. Pulmonary

The pulmonary
examination may reveal evidence of heart failure (eg, rales, pleural
effusion). Wheezes or diminished breath sounds are suggestive of
underlying pulmonary disease (eg, chronic obstructive pulmonary disease
[COPD], asthma). Cardiac

The cardiac examination is
central to the physical examination of the patient with AF. Thorough
palpation and auscultation are necessary to evaluate for valvular heart
disease or cardiomyopathy. A displaced point of maximal impulse or S3 suggests ventricular enlargement and elevated left ventricular pressure. A prominent P2 points to the presence of pulmonary hypertension. Abdomen

presence of ascites, hepatomegaly, or hepatic capsular tenderness
suggests right ventricular failure or intrinsic liver disease. Left
upper quadrant pain may suggest splenic infarct from peripheral
embolization. Lower extremities

Examination of the lower
extremities may reveal cyanosis, clubbing, or edema. A cool or cold
pulseless extremity may suggest peripheral embolization, and assessment
of peripheral pulses may lead to the diagnosis of peripheral arterial
disease or diminished cardiac output. Neurologic

Signs of
a transient ischemic attack or cerebrovascular accident may be
discovered. Evidence of prior stroke and increased reflexes is
suggestive of hyperthyroidism.
Atrial Fibrillation Differential Diagnoses

Diagnostic Considerations

The diagnosis of atrial
fibrillation is based on the physical finding of an irregular heart
rhythm and is confirmed with an ECG or rhythm strip. When atrial
fibrillation is suspected during auscultation of the heart with
irregularly irregular beats, obtaining a 12-lead electrocardiography is
the next step. Because atrial fibrillation is due to irregular atrial
activation at the rate of 350-600 bpm with irregular conduction through
the atrioventricular node, it appears on ECG as irregularly irregular
narrow complex tachycardia. The F waves may be seen as fibrillatory
waves or may be absent. Unless the heart is under excess sympathetic or
parasympathetic stimulation, the ventricular rate is usually between 80
and 180 bpm. With an abnormality in the intraventricular
conduction system, the QRS complexes may become wide. It is important to
pay attention to the electrocardiographic signs of associated cardiac
diseases, such as left ventricular hypertrophy and preexcitation.
Atrial Fibrillation Workup

Approach Considerations

atrial fibrillation is suspected during auscultation of the heart with
irregularly irregular beats, obtaining a 12-lead electrocardiogram (ECG)
is the next step. Because AF is due to irregular atrial activation at a
rate of 350-600 bpm with irregular conduction through the
atrioventricular (AV) node, it appears on ECG as irregularly irregular
narrow complex tachycardia.
Fibrillatory (F) waves may be evident or may be absent. Unless the
heart is under excess sympathetic or parasympathetic stimulation, the
ventricular rate is usually between 80 and 180 bpm. With an
abnormality in the intraventricular conduction system, the QRS complexes
may become wide. It is important to pay attention to the
electrocardiographic signs of associated cardiac diseases, such as left
ventricular hypertrophy (LVH) and preexcitation. Various cardiac
diseases, including ischemic heart disease, valvular diseases, and
cardiomyopathy, are associated with AF. Therefore, after the diagnosis
of AF is confirmed with ECG, an evaluation of serum cardiac biomarkers
and B-type natriuretic peptide (BNP) is usually required to investigate
for underlying heart disease. More invasive cardiac tests (eg, cardiac
catheterization) may be required depending on signs and symptoms and
findings on initial tests. The ECG is also necessary to monitor the QT
and QRS intervals of patients receiving anti-arrhythmic medications for
AF. In addition, many noncardiac diseases, such as pulmonary diseases (eg, COPD), pulmonary embolism, hyperthyroidism,
and many infections and inflammatory diseases, have been associated
with AF. Accordingly, chest radiography, thyroid function tests,
complete blood count (CBC), and serum chemistry may be helpful, and
other tests should be considered, depending on the patient’s
presentation. If a reversible cause of AF (eg, hyperthyroidism) is
found, it should be treated and the patient should be reassessed
Next Section: Electrocardiography


ECG findings usually confirm the diagnosis of atrial fibrillation and include the following:

  • The ventricular rate is typically irregular
  • Discrete
    P waves are absent, replaced by irregular, chaotic F waves, in the
    setting of irregular QRS complexes, as shown in the image below
  • Look also for aberrantly conducted beats after long-short R-R cycles (ie, Ashman phenomenon)
  • Heart rate (typically in the 110-140 range, but rarely over 160-170)
  • Preexcitation
  • Left ventricular hypertrophy
  • Bundle-branch block
  • Acute or prior MI
Note the image below.
Atrial Fibrillation  150072-1332317-151066-151181tn

Ventricular rate varies from 130-168 beats per minute. Rhythm is irregularly irregular. P waves are not discernible.
Next Section: Electrocardiography

Lab Studies

studies are aimed at uncovering underlying disorders, which may be
particularly important to address when ventricular rate is difficult to
control. One study suggests that minor elevations in troponin I levels
upon hospital admission is associated with higher mortality and cardiac
events, which may be useful for risk stratification.[17] Laboratory studies indicated include the following:

  • CBC count (looking for anemia, infection)
  • Serum electrolytes and BUN/creatinine (looking for electrolyte disturbances or renal failure)
  • Cardiac enzymes - CK and/or troponin level (to investigate myocardial infarction as a primary or secondary event)
  • BNP (to evaluate for CHF)
  • D-dimer (if the patient has risk factors to merit a pulmonary embolism workup)
  • Thyroid function studies (looking for thyrotoxicosis, a rare, but not-to-be-missed, precipitant)
  • Digoxin
    level (may be obtained when appropriate for subtherapeutic levels
    and/or toxicity; generally considered safe to give digoxin to patient
    with AF on digoxin for rate control without waiting for lab values if
    patient presents with AF with rapid ventricular response [RVR])
  • Toxicology testing or ethanol level

Next Section: Electrocardiography


may be used to evaluate for valvular heart disease, left and right
atrial size, left ventricular (LV) size and function, left ventricular
hypertrophy (LVH), and pericardial disease. Transthoracic
echocardiography has low sensitivity in detecting left atrial (LA)
thrombus, and transesophageal echocardiography is the modality of choice
for this purpose.[18] Transthoracic echocardiography (TTE) is helpful for making the following determinations:

  • Evaluate for valvular heart disease
  • Evaluate atrial and ventricular chamber and wall dimensions
  • Estimate ventricular function and evaluate for ventricular thrombi
  • Estimate pulmonary systolic pressure (pulmonary hypertension)
  • Evaluate for pericardial disease
Transesophageal echocardiography (TEE) is helpful for making the following determinations:

  • Evaluate for LA thrombus (particularly in the LA appendage)
  • To guide cardioversion (if thrombus is seen, cardioversion should be delayed)
  • When TEE is planned, the concurrent use of TTE may increase cost without providing significant additional information.

Next Section: Electrocardiography

CT and MRI

In patients with a positive D-dimer result, chest CT angiography may be necessary to rule out pulmonary embolus. Three-dimensional
imaging technologies (CT scan or MRI) are often helpful to evaluate
atrial anatomy if AF ablation is planned. Imaging data can be processed
to create anatomic maps of the left atrium and pulmonary veins.
Next Section: Electrocardiography

Chest radiography

radiographic findings are usually normal. However, chest radiography
may provide evidence of CHF as well as signs of lung or vascular
pathology (eg, pulmonary embolism, pneumonia).
Next Section: Electrocardiography

Six-Minute Walk Test or Exercise Test

walk or exercise testing can help assess the adequacy of rate control
(eg, target heart rate of 110 bpm or less during a 6-minute walk).[13] Exercise
testing can exclude ischemia prior to treatment of patients with class
Ic antiarrhythmic drugs and can be used to reproduce exercise-induced
Next Section: Electrocardiography

Holter Monitoring or Event Recording

monitoring and event recording may be helpful to establish a diagnosis
(eg, in cases of paroxysmal AF not evident upon presentation) and
evaluate rate control (eg, target average rate of 100 bpm or less).
Next Section: Electrocardiography

Electrophysiology Study

studies may help identify the mechanism of a wide-QRS tachycardia, a
predisposing arrhythmia, or sites for curative ablation or AV node

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PostSubject: Re: Atrial Fibrillation    Atrial Fibrillation  Icon_minitimeWed Jun 08, 2011 2:00 pm

Atrial Fibrillation Treatment & Management

Approach Considerations

The cornerstones of atrial fibrillation management are rate control and anticoagulation.[19] The
clinical decision to use a rhythm-control or rate-control strategy
requires an integrated consideration of several factors, including
degree of symptoms, likelihood of successful cardioversion, and presence
of comorbidities. Restoration of sinus rhythm with
regularization of the heart's rhythm improves cardiac hemodynamics and
exercise tolerance. By maintaining the atrial contribution to cardiac
output, symptoms of heart failure and overall quality of life can
improve. As AF contributes to pathologic atrial and ventricular
remodeling, restoration of sinus rhythm can slow or, in some cases,
reverse atrial dilatation and left ventricular dysfunction. For these
reasons, most clinicians focus initially on restoration and maintenance
of sinus rhythm in patients with new-onset AF and opt for a rate-control
strategy only when rhythm control fails. However, several
randomized controlled trials have demonstrated that a strategy aimed at
restoring and maintaining sinus rhythm neither improves survival nor
reduces the risk of stroke in patients with AF. In the AFFIRM
study (Atrial Fibrillation Follow-up Investigation of Rhythm
Management), an insignificant trend toward increased mortality was noted
in the rate control group, and importantly, no evidence suggested that
the rhythm-control strategy protected patients from stroke. In the
study, 4060 subjects aged 65 years or older whose AF was likely to be
recurrent and who were at risk for stroke were randomized to a strategy
of rhythm control (cardioversion to sinus rhythm plus drugs to maintain
sinus rhythm) versus a strategy of rate control (in which no attempt was
made to restore or maintain normal sinus rhythm).[13] Clinically
silent recurrences of AF in the rhythm-control group are theorized to
be responsible for the increased rates of thromboembolic events and
mortality noted in this cohort. This underscores the importance of
anticoagulation in both rhythm-control and rate-control patients. New
developments aimed at curing AF are being explored actively. By
reducing the critical mass required to sustain AF through either
surgical or catheter-based compartmentalization of the atria (ie, maze
procedure), fibrillatory wavelets collide with fixed anatomic obstacles,
such as suture lines or complete lines of ablation, thus eliminating or
reducing the development of permanent AF. Some patients with focal
origins of their AF also may be candidates for catheter ablation. Still,
much remains to be accomplished before these procedures may be
considered appropriate for primary treatment. Go to Catheter Ablation for complete information on this topic.
Next Section: Risk-Management Decisions

Risk-Management Decisions

One of the major management decisions in AF (and atrial flutter)
is determining the risk of stroke and appropriate anticoagulation
regimen for low-, intermediate-, and high-risk patients. For each
anticoagulant, the benefit in terms of stroke reduction must be weighed
against the risk of serious bleeding. Overall, approximately
15-25% of all strokes in the United States (75,000/y) can be attributed
to AF. Known risk factors for stroke in patients with AF include male
sex, valvular heart disease (rheumatic valvular disease), heart failure,
hypertension, and diabetes. Additional risk factors, such as advanced
age and prior history of stroke, diabetes, and hypertension, place
patients with preexisting AF at even higher risk for further
comorbidities such as stroke (see Table 1 below).[20] Table 1. Risk Factors for Stroke in Patients with Nonvalvular Atrial Fibrillation (Open Table in a new window)
Risk FactorsRelative Risk
Prior stroke or TIA2.5
History of hypertension1.6
Heart failure and/or reduced left ventricular function1.4
Advanced age1.4
Coronary artery disease1.5
with rheumatic heart disease and AF have an even higher risk for stroke
(17-fold). At least 4 large clinical trials have clearly demonstrated
that anticoagulation with warfarin decreases the risk of stroke by
50-80%. Most clinicians agree that the risk-benefit ratio of
warfarin therapy in low-risk patients with AF is not advantageous.
Warfarin therapy has, however, been shown to be beneficial in
higher-risk patients with AF. A target international normalized ratio
(INR) of 2-3 is traditionally used in this cohort, as this limits the
risk of hemorrhage while providing protection against thrombus
formation. The appropriate treatment regimen for patients with AF
at intermediate risk is controversial. In this population, the
clinician should assess risk factors for thromboembolic disease, patient
preference, risk of bleeding, risk of falls or trauma, and likelihood
of medication adherence. Warfarin is also superior to clopidogrel or a
combination of clopidogrel and aspirin in the prevention of embolic
events in higher-risk patients. Several risk factor assessment
algorithms have been developed to aid the clinician on decisions on
anticoagulation for patients with AF. The CHADS2 index (Cardiac failure, Diabetes, Stroke [or S2 = transient ischemic attack]) is the most widely used of these algorithms.[21] The CHADS2
index uses a point system to determine yearly thromboembolic risk. Two
points are assigned for a history of stroke or transient ischemic attack
(TIA), and one point is given for age older than 75 years or a history
of hypertension, diabetes, or heart failure. The predictive value of
this scoring system was evaluated in 1733 elderly patients with
nonvalvular AF aged 65-95 years who were not given warfarin at hospital
discharge. Although high scores were associated with an increased rate
of stroke, few patients had a score greater than 5 or a score of 0 (see
Table 2 below). However, the
at low risk for thromboembolism.[22] Table 2. Adjusted Stroke Rate in Patients with Nonvalvular Atrial Fibrillation not Treated with Anticoagulation (Open Table in a new window)
CHADS2 ScoreAdjusted Stroke Rate (%/y)
on anticoagulation for patients with nonvalvular AF are based on the
2006 American College of Cardiology (ACC)/American Heart Association
(AHA)/European Society of Cardiology (ESC) task force guidelines on the
management of patients with atrial fibrillation (see Table 3 below).[20] Table 3. Recommendations for Antithrombotic Therapy in Patients with Nonvalvular Atrial Fibrillation (Open Table in a new window)
Risk CategoryRecommended Therapy
No risk factorsAspirin 81-325 mg daily
One moderate-risk factorAspirin 81-325 mg daily or warfarin (INR 2-3)
Any high-risk factor or more than 1 moderate-risk factorWarfarin (INR 2-3)
factors include prior stroke, TIA, and systemic thromboembolism.
Moderate-risk factors include age older than 75 years, hypertension,
heart failure, left ventricular function less than 35%, and diabetes
mellitus. Risk factors of unknown significance include female sex, age
65-74 years, coronary artery disease, and thyrotoxicosis.
Next Section: Risk-Management Decisions

Management of New-Onset AF

The AFFIRM study and similar findings from the smaller Rate Control Versus Electrical Cardioversion (RACE) trial[23] have
led to the development of consensus guidelines that recommend an
initial rate-control strategy for many asymptomatic patients with atrial
fibrillation. The ACC/AHA/ESC 2006 guidelines state that an
initial rate-control strategy is "reasonable" for asymptomatic or
minimally symptomatic older patients with hypertension and comorbid
cardiovascular disease.[20] These
same guidelines state that for younger individuals, especially those
without significant comorbid cardiovascular disease, an initial
rhythm-control strategy may be a better approach. Rate control

of the long-term management strategy chosen, control of ventricular
rate is a critical component of management of new-onset AF. The main
determinants of the ventricular rate during AF are those intrinsic and
extrinsic factors that influence atrioventricular (AV) conduction.
Foremost among these are the intrinsic AV nodal conduction properties.
Underlying sympathetic and parasympathetic tone also influences AV nodal
conduction. Rate-controlling agents act primarily by increasing AV
nodal refractoriness. Beta-blockers and calcium channel blockers
are first-line agents for rate control in AF. These drugs can be
administered either intravenously or orally. They are effective at rest
and with exertion. Intravenous diltiazem or metoprolol are commonly used
for AF with a rapid ventricular response. Caution should be exercised
in patients with reactive airway disease who are given beta-blockers. Digoxin
can be used in the acute setting but does little to control the
ventricular rate in active patients. As such, it is rarely used as
monotherapy. Caution should be exercised in elderly patients and those
with renal failure receiving digoxin. Digoxin is indicated in patients
with heart failure and reduced LV function. Amiodarone has a
class IIa recommendation from the ACC/AHA/ESC for use as a
rate-controlling agent for patients who are intolerant of or
unresponsive to other agents, such as patients with CHF who may
otherwise not tolerate diltiazem or metoprolol. Caution should be
exercised in those who are not receiving anticoagulation, as amiodarone
can promote cardioversion. Extreme care must be taken in patients
with preexcitation syndrome and AF. Blocking the AV node in some of
these patients may lead to AF impulses that are transmitted exclusively
down the accessory pathway, and this can result in ventricular
fibrillation. (If this happens, the patient will require immediate
defibrillation.) Calcium channel blockers and digoxin are
contraindicated in these patients; flecainide or amiodarone can be used
instead.[24] Anticoagulation

of the most important considerations in the acute management of atrial
fibrillation is the need for anticoagulation (see the image below).
Acute cardioversion for AF carries a risk of thromboembolism unless
anticoagulation therapy is initiated prior to the procedure and
continued post procedure. Risk of thromboembolism is similar in patients
undergoing either pharmacologic or electrical cardioversion. The risk
of thromboembolic events is greatest when AF has been present for longer
than 48 hours. Effective anticoagulation in patients with AF reduces
the risk of stroke 3-fold.Atrial Fibrillation  150072-1332317-151066-1445716tn

management for newly diagnosed atrial fibrillation. Subtherapeutic INR:
INR < 2 for 3 consecutive weeks. Warfarin: INR target 2-3.
TEE/cardioversion: low molecular weight heparin 1 mg/kg bid as a bridge
with initiation of warfarin INR 2-3. Patients
with newly diagnosed AF and patients awaiting electrical cardioversion
can be started on intravenous heparin (activated partial thromboplastin
time [aPTT] of 45-60 seconds) or low-molecular-weight heparin (1 mg/kg
bid). Patients can be started concomitantly on warfarin in an
inpatient setting while awaiting a therapeutic INR value (2-3). Many
practices have developed specialized anticoagulation clinics to monitor
INR values closely. Oral direct thrombin inhibitors may present an
alternative to warfarin in a higher-risk population with nonvalvular AF.
In the highest-risk population (eg, AF with valvular heart
disease or prior embolic cerebrovascular accident), bridging
anticoagulation with heparins may be required in the periprocedural
period. Cardioversion

Cardioversion may be performed
electively or emergently to restore sinus rhythm in patients with
new-onset atrial fibrillation. Cardioversion is most successful when
initiated within 7 days after onset of AF. The need for cardioversion
may be acute when AF is responsible for hypotension, heart failure, or
angina. Pharmacologic agents or direct current energy can be used
to cardiovert patients with AF. Pharmacologic cardioversion has the
advantage of not requiring sedation or anesthesia, but the major
disadvantage is the risk of ventricular tachycardia and other serious
Next Section: Risk-Management Decisions

Long-Term Management

management of atrial fibrillation is focused on reducing the likelihood
of AF recurrence, reducing AF-related symptoms, control of ventricular
rate, and reducing stroke risk. As discussed previously, AF is often the
result of established cardiovascular risk factors. Appropriate
management of these risk factors will reduce the likelihood of future
episodes of AF and AF-related morbidity and mortality. Anticoagulation
with either aspirin or warfarin should be initiated for all individuals
with AF, except those with lone AF or contraindications. Selection of
the appropriate antithrombotic regimen for a given patient should be
balanced between the risk of stroke and the risk of bleeding.
Antiarrhythmic therapy can aid in maintenance of sinus rhythm in certain
patients but requires close monitoring. Optimal long-term
strategies for AF management should be based on a thoroughly integrated
consideration of patient-specific factors and likelihood of success. As a
rule, younger patients with more severe symptoms and fewer
comorbidities tend to derive greater benefit from a long-term focus on
rhythm control. Older patients with structural heart disease (eg, left
ventricular hypertrophy, prior MI, depressed ejection fraction, atrial
dilation) are less likely to remain in sinus rhythm and are more likely
to have serious side effects from antiarrhythmic drugs. In this cohort,
most clinicians focus on long-term rate control. Because of the
electrophysiologic and structural remodeling caused by AF, many patients
with paroxysmal AF will progress to persistent and permanent AF. The
degree to which this reflects the continuing influence of underlying
cardiovascular risk factors as opposed to a direct effect of AF is
unknown. Regardless, clinicians need to reevaluate their management
strategies frequently, as AF burden and comorbidities increase with
time. Anticoagulation

The goal of long-term
anticoagulation in atrial fibrillation is to reduce the risk of
thromboembolism. Patients in AF have a risk of stroke or peripheral
embolism that is approximately 5 times that of individuals in sinus
rhythm. Recommendations for anticoagulation for patients with
nonvalvular AF are based on guidelines from a 2006 ACC/AHA/ESC task
force on the management of patients with atrial fibrillation.[2] Anticoagulation
therapy with warfarin is significantly more effective than antiplatelet
therapy (relative risk of 40%) if the INR is adjusted. The INR goal in
AF is usually between 2 and 3, except in patients who are at a
significant risk for stroke (eg, patients with artificial valves, those
with rheumatic heart disease, and those at a high risk for AF with
recurrent prior strokes), in whom the INR should be maintained between
2.5 and 3.5. A lower INR goal (1.8-2) may be considered in elderly
patients who are at high risk for a fall. Anticoagulation clinics
have shown more success and a lower complication rate than primary care
physicians in controlling patients’ INR. In addition, one study
reported that patients who used an Internet-based program for patient
self-management of oral anticoagulant therapy achieved a higher mean
time in the therapeutic range than patients whose INR was controlled by
an established anticoagulation clinic.[25] Similar
programs alone or in combination with regular care provided by
anticoagulation clinics may improve the mean time that patients are in
the therapeutic range and may further reduce the risk of stroke. As
patients with AF age, the relative efficacy of oral anticoagulation
appears not to decrease, whereas the efficacy of antiplatelet therapy
does appear to decrease, according to a study by van Walraven.[26] The
major adverse effect of anticoagulation therapy with warfarin is
bleeding. Factors that increase this risk include the following:

  • History of bleeding (the strongest predictive risk factor)
  • Age older than 75 years
  • Liver or renal disease
  • Malignancy
  • Thrombocytopenia or aspirin use
  • Hypertension
  • Diabetes mellitus
  • Anemia
  • Prior stroke
  • Fall risk
  • Genetic predisposition
  • Supratherapeutic INR
Several risk models have been introduced. The risk model called HEMORR2HAGES assigns points to risk factors, as follows[27] :

  • History of bleeding (2 points)
  • Hepatic or renal disease (1 point)
  • Alcohol abuse (1 point)
  • Malignancy (1 point)
  • Older age (>75 y) (1 point)
  • Reduced platelet count or function, including aspirin therapy (1 point)
  • Hypertension (1 point)
  • Anemia (1 point)
  • Genetic predisposition (1 point)
  • Excessive fall risk (1 point)
  • Stroke (1 point)
Using this scoring, the risks of a major bleeding event per 100 patient-years of warfarin therapy are as follows:

  • 0 points - 1.9%
  • 1 point - 2.5%
  • 2 points - 5.3%
  • 3 points - 8.4%
  • 4 points - 10.4%
  • 5 or more points - 12.3%
the bleeding risk outweighs the benefit, avoidance of anticoagulation
therapy in AF should be considered. In addition, because of its
teratogenic effects, anticoagulation with warfarin is contraindicated in
pregnant women, especially in the first trimester. According to
the 2011 update to ACCF/AHA/HRS guidelines on atrial fibrillation, if
warfarin will not be used, adding clopidogrel to aspirin may be
considered.[28] The
RE-LY study evaluated the efficacy and safety of 2 different doses of
dabigatran relative to warfarin in more than 18,000 patients with atrial
fibrillation. Patients were randomized to 1 of 3 arms: (1) adjusted
dose warfarin, (2) dabigatran 110 mg bid, or (3) dabigatran 150 mg bid.
Dabigatran 110 mg was noninferior to warfarin for the primary efficacy
endpoint of stroke or systemic embolization, while dabigatran 150 mg was
significantly more effective than warfarin or dabigatran 110 mg. Major
bleeding occurred significantly less often with dabigatran 110 mg than
warfarin; dabigatran 150 mg had similar bleeding to warfarin.[29, 30] Guidelines
from the American College of Cardiology Foundation (ACCF)/American
Heart Association (AHA)/Heart Rhythm Society (HRS) on atrial
fibrillation have been updated to include the use of oral direct
thrombin inhibitors (ie, dabigatran).[31] The
guidelines include a class Ib recommendation (ie, treatment is
useful/effective based on a single randomized trial) for dabigatran. The
guidelines recommend dabigatran may be used as an alternative to
warfarin for the prevention of stroke and systemic thromboembolism in
patients with paroxysmal-to-permanent atrial fibrillation and risk
factors for stroke or systemic embolization. Patients with atrial
fibrillation who are not candidates include those with prosthetic heart
valves or hemodynamically significant valve disease, severe renal
failure (creatinine clearance ≤15 mL/min), or advanced liver disease.Anticoagulation
prior to and during an elective surgery may be continued or stopped
depending on the patient’s risk of bleeding and risk of thromboembolism.
If the risk of thromboembolism is high (stratified by the CHADS2
score) and the risk of bleeding is low, anticoagulation should be
continued with the INR in the low therapeutic range. However, a high
risk of bleeding during the procedure should prompt discontinuation of
warfarin for 3-5 days prior to surgery. These patients should then be
treated with heparin prior to and following the operation to allow
discontinuation of anticoagulation if bleeding occurs. In
general, patients who develop AF only postoperatively do not need
anticoagulation. Administration of preoperative and postoperative
beta-blockers is usually sufficient, as postoperative AF is usually
paroxysmal and tends to terminate spontaneously. A mutation in
coagulation factor IX may cause spontaneous bleeding even with INR in
the therapeutic range. Adverse effects of warfarin therapy are not
limited to bleeding, however; other important side effects include skin
necrosis within the first few days of therapy and cholesterol
embolization to the skin or visceral organs in the first few weeks of
therapy.A large cohort study in Denmark compared bleeding risk of
anticoagulants prescribed upon hospital discharge for atrial
fibrillation. During mean follow-up (3.3 y), 11.4% of patients
experienced a nonfatal or fatal bleeding episode. The highest incidence
for bleeding was observed for dual therapy with warfarin and clopidogrel
and for triple therapy with warfarin, aspirin, and clopidogrel (3-fold
higher risk) compared with single agent use.[32] Omega-3 fatty acids

small trials have suggested that treatment for paroxysmal AF with
prescription omega-3 fatty acids may provide a safe and effective
treatment option. However, no benefit has been found to date.[33] Angiotensin converting enzyme (ACE) inhibitors and ACE receptor blockers (ARB)

examining the incidence of AF in patients with heart failure who are
treated with ACE inhibitors or ARBs have demonstrated a potential
beneficial effect on AF recurrence. This recurrence is thought to be
mediated by blocking the rennin-angiotensin-aldosterone system and the
downstream effects on atrial mechanical and electrical remodeling.[34, 35, 36] A
study by Yusuf et al examined the effects of irbesartan in patients
with permanent AF or at least 2 episodes of paroxysmal AF in the
previous 6 months.[37] Irbesartan
did not demonstrate a benefit in patients with AF who were already
receiving an ACE inhibitor or patients in sinus rhythm. No reduction in
cardiovascular death, stroke, or myocardial infarction was noted in the
patient population studied. Rate control

As discussed
previously, several trials have validated the noninferiority of an
initial rate-control strategy. Many clinicians believe, however, that an
attempt at a rhythm-control strategy should be made in most patients.
Older patients with comorbid cardiovascular disease have a lower
likelihood of successful long-term rhythm control, and thus, these
patients are often managed using a rate-control strategy. Some patients
managed initially with a rhythm-control strategy will progress to
recurrent or persistent AF. Clinicians often switch to a rate-control
strategy as the AF burden increases. Effectiveness of rate
control should be assessed both at rest and with exertion, especially in
patients who experience primarily exertional AF-related symptoms.
Twenty-four hour Holter monitoring or exercise-treadmill testing can be
helpful in evaluating heart rate variability. Adequate rate
control was previously defined as a heart rate of 60-80 bpm at rest and
90-115 bpm with moderate exercise. However, ACCF/AHA/HRS guidelines on
management of atrial fibrillation were updated in 2011 to state that
there was no benefit in achieving strict heart rate control (< 80 bpm
at rest, < 110 bpm after a 6-minute walk) relative to more lenient
rate control (< 110 bpm at rest). Strict rate control in patients
with stable ventricular function is no longer recommended.[28] AV
nodal blocking medications are the cornerstone of rate control in
long-standing AF. In the absence of an accessory pathway, oral
beta-blockers, nondihydropyridine calcium channel blockers, and digoxin
are effective. Generally, coadministration of beta-blockers and calcium
channel blockers is reserved for patients in whom adequate rate control
cannot be achieved with a single agent. Digoxin can be effective
in sedentary patients (especially in those with heart failure) but
requires close monitoring of drug levels and renal function.
Combinations of rate-control medications (eg, beta-blocker and digoxin)
may be superior to individual agents in some patients. Amiodarone
may contribute to ventricular rate control. On the other hand,
antiarrhythmic agents may organize AF to a potentially life-threatening
atrial flutter with 1:1 AV conduction. Particularly with class IC
agents, maintenance of effective AV nodal rate control is essential in
most patients. Therefore, administration of a beta-blocker or calcium
channel blocker is recommended before class IC drugs are initiated. In
the presence of tachycardia-mediated cardiomyopathy or inadequate
ventricular rate control despite drug therapy, AV nodal ablation and
pacemaker implantation may be considered. Rhythm control

of sinus rhythm requires treatment of cardiovascular risk factors and
any underlying disorder (ie, hyperthyroidism) that may have triggered
AF. As mentioned previously, several antiarrhythmic drugs (flecainide,
propafenone, dofetilide, amiodarone) have established efficacy in the
pharmacologic conversion of AF to sinus rhythm. The noncardiac adverse
effects and contraindications of each drug should be checked prior to
administration. Amiodarone, as a part of a strategy to achieve
sinus rhythm, appears to be safe and effective in patients with
persistent AF, according to Doyle and Ho. However, in their study,
intolerable adverse effects were more common with amiodarone than with
placebo or rate-control drugs.[38] Nevertheless,
in patients with cardiac disease such as coronary artery disease or
systolic or diastolic heart failure, amiodarone becomes the drug of
choice because of its decreased proarrhythmic effects compared with
other antiarrhythmic drugs.[24] Amiodarone
was also found to be more effective at maintaining sinus rhythm than
other drugs in the Canadian Trial of Atrial Fibrillation (CTAF) and the
Sotalol Amiodarone Atrial Fibrillation Efficacy Trial (SAFE-T).[39, 40] The
2011 update to the ACCF/AHA/HRS AF guideline adds that it is reasonable
to use dronedarone to reduce the probability that hospitalization will
be required for patients with paroxysmal AF or after conversion of
persistent AF. Class IV heart failure or a recent episode of
decompensated heart failure are contraindications.[28] Several
distinct agents, most notably sotalol, are used for the long-term
maintenance of sinus rhythm. Sotalol is efficacious, but as with other
class III drugs, it requires close monitoring of the QT interval and
serum electrolytes. Sotalol is associated with the risk of QT interval
prolongation and torsade de pointes.
The proarrhythmic effect of sotalol is increased in patients with CHF
(unlike dofetilide and amiodarone), so it is generally contraindicated
in such patients or in those with a prolonged QT interval. Hypokalemia
should be corrected and monitored prior to administration of sotalol
because it may also prolong the QT interval. Sotalol can be used in
patients with coronary artery disease.[24] Class
III agents (sotalol, amiodarone) also have some beta-blocking effect
and should be used with caution in patients with a history of
bradycardia. Class Ic drugs increased the mortality risk in
patients with coronary artery disease during the Cardiac Arrhythmia
Suppression Trial (CAST) and therefore should not be used in these
patients.[41] Class
Ic drugs increased the mortality risk in patients with coronary artery
disease during the Cardiac Arrhythmia Suppression Trial (CAST) and
therefore should not be used in these patients.[39] Catheter
ablation performed in experienced centers is recommended in the 2011
update to the ACCF/AHA/HRS AF guidelines for several indications:{Ref55}

  • It is recommended as an alternative
    to pharmacologic therapy to prevent recurrent paroxysmal AF in
    significantly symptomatic patients with little or no structural heart
    disease[40] or severe pulmonary disease (Class I, evidence level A).
  • It is reasonable as a treatment for symptomatic persistent AF.
  • Catheter ablation may be reasonable as a treatment for symptomatic paroxysmal AF in patients with some structural heart disease.
ablation of AF is also an option for patients with AF undergoing other
cardiac surgery and for those patients in whom pharmacologic and
catheter-based procedures are ineffective or contraindicated. Atrial
fibrillation ablation may be superior to AV nodal ablation and
biventricular pacing in heart failure patients but is technically
difficult and demanding, and the widespread applicability of ablation in
this population of patients is uncertain. Go to Catheter Ablation for complete information on this topic.New
medical and device-based rhythm-control therapies are being explored
actively. Experimental and clinical data suggest that renin-angiotensin
system (RAS) antagonists and HMG-CoA-reductase inhibitors (statins) may
decrease the incidence of AF and increase the likelihood of successful
cardioversion.[42, 43, 44, 45] Device-based therapies under investigation include single- and dual-site atrial pacemakers
to prevent AF, as well as atrial defibrillators to rapidly restore
sinus rhythm. Invasive (surgical and catheter-based) therapies to
compartmentalize the atria and localize focal triggers (in the pulmonary
veins) are being evaluated and refined. (See Surgical Care.) Electrical cardioversion

who are hemodynamically unstable, who have severe dyspnea or chest pain
with atrial fibrillation, or who have preexcited atrial fibrillation
should undergo urgent cardioversion.[24] In
stable patients with symptomatic new-onset AF, the rate-control
strategy may be considered first to control the ventricular rate. If
rate-control treatment does not elicit a response or if echocardiography
does not reveal any valvular or functional abnormality of the heart,
cardioversion is indicated. DC cardioversion is the delivery of
electrical current that is synchronized to the QRS complexes; it can be
delivered in monophasic or biphasic waveforms. The required energy for
cardioversion is usually 100-200 J (sometimes higher energy is required)
for monophasic waveforms and less for biphasic waveforms. The patient
should be sedated. In patients with AF of relatively short duration in
whom the left atrium is not significantly large, the success rate of
cardioversion exceeds 75% (ie, the size of the left atrium and the
duration of AF inversely correlate with the success rate of
cardioversion). Embolization is the most important complication
of cardioversion. Accordingly, thrombus in the heart should be ruled out
with transesophageal echocardiography, or warfarin should be given for
anticoagulation for 4 weeks before cardioversion is performed. Stunning
of the atria and stasis can occur after cardioversion, and this can lead
to thrombus formation even though the patient is in sinus rhythm.
Therefore, the patient should receive anticoagulants for at least 4
weeks following the procedure. Other complications of electrical
cardioversion may include pulmonary edema, hypotension, myocardial
dysfunction, and skin burns, which may be avoided with the use of
steroid cream and proper technique. Electrical cardioversion is also
associated with some ST- and T-wave changes on ECG and may elevate
levels of serum cardiac biomarkers. Synchronization prevents serious
ventricular arrhythmias. Placement of pads or paddle positions
include anterior-lateral (ventricular apex and right infraclavicular)
and anterior-posterior (sternum and left scapular), with at least one
study suggesting increased efficacy with the anterior-posterior (AP)
method. Biphasic waveforms are proved to convert AF at lower
energies and higher rates than monophasic waveforms. Strategies include
dose escalation (70, 120, 150, 170J for biphasic or 100, 200, 300, 360J
for monophasic) versus beginning with single high energy/highest success
rate for single shock delivered. Patients who are stable and/or awake
and can tolerate sedation should be pretreated, with typical regimens
involving midazolam, fentanyl, and propofol. Cardioversion of
patients with implanted pacemakers and defibrillator devices is safe
when appropriate precautions are taken. Keeping the cardioversion pads
in an AP orientation ensures that the shocks are not directly over the
generator. Alteration in pacer-programmed data has been reported, as
well as heart block and elevated enzymes if the current is conducted
through a pacer lead. Pharmacologic cardioversion

pharmacologic cardioversion may be used as the first-line strategy, it
is used mainly if DC cardioversion fails or, in some cases, as a
precardioversion strategy. Out-of-hospital self-administration of
either flecainide 300 mg or propafenone 600 mg (weight-based dosages if
>70 kg) was determined to be successful in terminating AF in 94% of
episodes (mean time to symptom resolution of 133 minutes) by Alboni et
al. The investigators studied outpatient treatment of atrial
fibrillation with a “pill-in-the-pocket” approach in 268 patients with
little or no structural heart disease presenting to the emergency
department with symptomatic AF.[46] Pretreatment
with amiodarone, flecainide, ibutilide, propafenone, or sotalol has
been shown to increase the success rate of DC cardioversion and is
recommended by the American College of Cardiology.[2] This strategy is also recommended when DC cardioversion fails and prior to repeat DC cardioversion.[2] Intravenous
amiodarone is typically given as a 150-mg bolus over 10-15 minutes,
followed by a continuous infusion of 1 mg/min for 6 hours and then 0.5
mg/min. Hemodynamically unstable patients (eg, those with
hypotension) may not tolerate antiarrhythmic drugs, and the adverse
effects and contraindications of each antiarrhythmic drug should be
considered carefully before administration. Because of possible
proarrhythmic adverse effects of antiarrhythmic drugs, these patients
should be monitored for at least 24 hours, requiring hospitalization in
most cases. The ACC/AHA/ESC guidelines provide the following recommendations regarding pharmacologic conversion of atrial fibrillation[47] :

  • For
    conversion of AF of 7 days or less, agents with proven efficacy include
    dofetilide, flecainide, ibutilide, propafenone, and, to a lesser
    degree, amiodarone and quinidine; less effective or incompletely studied
    agents include procainamide, digoxin, and sotalol.
  • For
    conversion of AF lasting 7-90 days, agents with proven efficacy include
    dofetilide, amiodarone, ibutilide, flecainide, propafenone, and
    quinidine; less effective or incompletely studied agents include
    procainamide, sotalol, and digoxin.
  • For
    conversion of AF lasting more than 90 days, oral propafenone,
    amiodarone, and dofetilide have been shown to be effective at converting
    persistent AF to normal sinus rhythm (NSR).
The US
Food and Drug Administration (FDA) mandates inpatient monitoring for
dofetilide initiation. Patients who start sotalol usually require
inpatient monitoring (for torsade de pointes), although patients with no
heart disease, with a QT interval less than 450 msec, and with normal
electrolytes should be started on outpatient medications.In 2010,
the American Heart Association-American Stroke Association (AHA-ASA)
issued its guidelines for the primary prevention of stroke, which
included the note that screening patients over 65 years of age for AF in
the primary care settings using pulse taking followed by an ECG may be
useful. Adjusted-dose warfarin should be used for all patients with
nonvalvular AF (target INR 2-3). Aspirin is recommended for low and
moderate-risk patients with AF and for high-risk patients unsuitable for
anticoagulation; a combination of clopidogrel and aspirin may
protection against stroke than aspirin alone.[48] Special considerations

AF is common, and perioperative beta blockers are recommended in all
patients undergoing cardiac surgery unless contraindicated.[49] Preoperative
administration of amiodarone and sotalol may reduce the incidence of AF
in patients undergoing cardiac surgery. As such, these agents may be
used as prophylactic therapy in those at high risk for postoperative AF.
Retrospective data suggest that atrial-based pacing (AAI, DDD
modes) reduces the risk of developing AF and increases the interval
between episodes in patients with sick sinus syndrome.[50]
Next Section: Risk-Management Decisions

Overview of Surgical and Catheter Ablation

goal of catheter ablation and surgical treatment of atrial fibrillation
is to disconnect triggers and/or to modify the substrate for AF.
Mapping and radiofrequency (RF) ablation of AF is one of the most
complex ablation procedures. Numerous approaches are used depending on
the expertise of the cardiac electrophysiologist and characteristics of
the AF. Paroxysmal AF is usually caused by triggered and ectopic
activity in pulmonary veins, and ablation around the veins terminates
the arrhythmia. In persistent AF, triggering foci and reentry circuits
may coexist in the atrial tissue, requiring more extensive mapping and
ablation to terminate the AF; this yields a lower success rate than
ablation used to treat paroxysmal AF.Aniarrhythimic drug (AAD)
treatment for 6 weeks after ablation of paroxysmal AF was shown to be
well tolerated, to reduce the incidence of clinically significant atrial
arrhythmias, and to reduce the need for cardioversion or hospital
admission during that period, according to Roux et al. Class IC drugs
were used as the first line of therapy, and sotalol was the most
commonly used drug in cases of LV dysfunction or CAD. Measured outcomes
included atrial arrhythmias lasting more than 24 hours; atrial
arrhythmias associated with severe symptoms that required
hospitalization, cardioversion, or initiation/change of antiarrhythmic
drug therapy; and intolerance to antiarrhythmic agent requiring drug
Next Section: Risk-Management Decisions

Compartmentalization of the Atria

approaches to compartmentalization of the atria are surgical, by which
multiple cuts are made to the atria, and radiofrequency ablation. Surgical compartmentalization of the atria (maze procedure)

its inception, surgical compartmentalization of the atria, or the
“maze” procedure, has evolved as an exciting approach with the potential
to cure atrial fibrillation. The procedure involves making a series of
small endocardial incisions in the right and left atria to isolate the
pulmonary veins and interrupt potential reentrant pathways required for
AF maintenance. Early experience showed that atrial transport is
restored postoperatively and that long-term anticoagulation is not
required. The downside remains the need for an open chest
procedure; however, thoracoscopic procedures may reduce hospitalization
and recovery times in the future. The maze procedure remains an
attractive procedure for patients with AF who are undergoing concomitant
mitral valve procedures. Its role as a primary therapy for AF is
doubtful. The role of lesion sets on outcome after maze procedure was
studied; the addition of right-sided ablation was found to improve
clinical and electrophysiologic results after maze procedure.[52] Compartmentalization of the atria with continuous ablation lines of blockage

a parallel to the maze procedure, electrophysiologists are attempting
to mimic surgical suture lines with radiofrequency lesions. The
procedures tend to last many hours, and success rates are somewhat
disappointing (50-60%), with the occurrence of left atrial reentrant
tachycardias and left atrial flutters (requiring further ablation
procedures).[53] Researchers
are unsure which areas of the atria are necessary to sustain AF. Purely
right-sided lesions are not sufficient to eliminate AF, making left
atrial procedures necessary. In addition, gaps in linear lesions can be
difficult to find. Research currently focuses on catheter design
to deliver linear continuous lesions. Additionally, alternative energy
sources (eg, cryotherapy, laser, ultrasound) may improve the ability to
deliver transmural lesions in the left atrium.
Next Section: Risk-Management Decisions

Catheter Ablation of Focal Triggers of AF

In some patients, AF appears to be triggered by electrically active pulmonary vein foci.[54] These
patients typically have an abundance of ectopic atrial beats noted on
24-hour Holter monitoring. Electrical isolation of individual pulmonary
veins, and thus the ectopic foci, is performed successfully at many
centers, and patient selection is key to success. A combined
procedure including individual pulmonary vein isolation, as well as left
atrial ablation (ie, encircling pulmonary vein pairs, connecting right
and left pairs along the left atrial roof, and connection to the mitral
valve annulus), is often necessary. Chest CT or MRI can be used to
recreate 3-dimensional anatomy in the left atrium, thus aiding in
mapping and creating contiguous lines in the left atrium, as displayed
in the video below.The
image on the right is a reconstructed 3-dimensional image of the left
atrium in a patient undergoing atrial fibrillation ablation. The figure
on the left was created with a mapping catheter using Endocardial
Solutions mapping technology. It represents the endocardial shell of the
left atrium and is used as the template during left atrial ablation
procedures. Patients with paroxysmal AF
in whom antiarrhythmic drug therapy does not elicit a response are
potential candidates for RF ablation of AF. The threshold for catheter
ablation has fallen over the years and is likely to continue to fall.
Ablation of persistent AF is more complex and yields lower success
rates. Therefore, RF ablation is an option only if antiarrhythmic drugs
fail in patients with persistent AF who remain severely symptomatic
despite adequate ventricular rate control.[55] The
success rate of RF ablation in the treatment of AF varies depending on
the type and duration of AF (ie, paroxysmal vs persistent), structural
remodeling of the heart, and the technique and expertise of the cardiac
electrophysiologist, but it usually ranges from 60-80% over 1-2 years of
follow-up. Complications associated with RF ablation of AF
include cardiac perforation, pericardial effusion, cardiac tamponade,
vascular access complications, pulmonary vein stenosis, thromboembolism,
atrioesophageal fistula, and left atrial flutter. Pulmonary vein
stenosis develops in about 6% of patients and may cause dyspnea, chest
pain, cough, and hemoptysis.[2] If
pulmonary vein stenosis is suspected following RF ablation, further
diagnostic workup with TEE, spiral CT scanning, or MRI is recommended.
MRI is the most accurate test in diagnosing this complication. Patients
with pulmonary vein stenosis should undergo percutaneous angioplasty,
which can significantly improve pulmonary blood flow and the patient's
symptoms. Go to Catheter Ablation for complete information on this topic.
Next Section: Risk-Management Decisions

AV Node Ablation and Permanent Pacemakers

node ablation may be an alternative in patients with persistent AF and
an uncontrolled ventricular response despite aggressive medical therapy.
Catheter ablation of the AV junction permanently interrupts conduction
from the atria to the ventricles. Because the result is permanent
AV block, a permanent ventricular pacemaker is required. AF may still
be present, but the pacemaker governs the ventricular response. The risk
of thromboembolism is unchanged, and patients still require
anticoagulation; however, most patients are relieved of their symptoms.
During the first 1-3 months, the pacing rate must be programmed in the
80- to 90-beat range to prevent torsade de pointes, which presumably
occurs because of slow ventricular rates and early
after-depolarizations. In patients with significant ventricular
dysfunction and permanent ventricular pacing, a biventricular device may
be appropriate.[56] Improvements in LV size and function, functional class, and quality-of-life scores have been demonstrated.[57]
Next Section: Risk-Management Decisions

Left Atrial Appendage Percutaneous Closure

stroke in patients with nonvalvular AF is thought to be associated with
left atrial appendage (LAA) thrombi. LAA closure may be a suitable
alternative to chronic warfarin therapy for stroke prophylaxis in
patients with nonvalvular AF, according to Holmes and colleagues. The
investigators compared the efficacy and safety of LAA percutaneous
closure with warfarin therapy in patients with AF, and follow-up at the
point of 1065 patient-years showed the intervention group (LAA closure
without warfarin treatment) event rate was 3 per 100 patient-years
compared with the control group (patients given warfarin) event rate of
4.9 per 100 patient-years.[58]
Next Section: Risk-Management Decisions


with a cardiac electrophysiologist or knowledgeable clinician is
recommended prior to antiarrhythmic drug initiation.A
cardiologist may be consulted emergently if complicating factors are
present or if the patient is experiencing ongoing cardiac ischemia or
infarction not treatable with DC cardioversion, rate-reduction measures,
and standard chest pain protocols.[59] A
patient with acute myocardial infarction (AMI) and new-onset AF who is
stable may benefit from simple rate-control measures (eg, intravenous
beta-blockers) while being prepared for the catheterization laboratory
and while intravenous nitrates, heparin, and aspirin are begun. In the
patient with an ST elevation MI, the main emphasis, however, is to
minimize door-to-open-artery time. A patient's cardiologist plays
a vital role in determining the most appropriate long-term strategy for
a patient with AF and provides crucial follow-up care.
Next Section: Risk-Management Decisions

Long Term Monitoring

RF ablation of atrial fibrillation

who undergo RF ablation of atrial fibrillation should be monitored for
the signs and symptoms of potential complications, such as the

  • Cardiac perforation
  • Pericardial effusion
  • Cardiac tamponade
  • Vascular access complications
  • Pulmonary vein stenosis
  • Thromboembolism
  • Atrioesophageal fistula
  • Left atrial flutter
addition, AF can recur and most episodes are asymptomatic. Therefore,
it is important to monitor for signs and symptoms of recurrent AF in
follow-up visits and to administer appropriate diagnostic tests if
recurrence is suspected. Further outpatient care

and reassessment of thromboembolic risk is necessary, and periodic ECG
monitoring (especially when taking antiarrhythmics) and Holter
monitoring are often necessary to assess for paroxysmal AF and/or rate
control. Deterrence/preventionExperimental and clinical
data suggest that renin-angiotensin system (RAS) antagonists and HMG-CoA
reductase inhibitors (statins) may decrease the incidence of AF and
increase the likelihood of successful cardioversion.[42, 43, 44, 45] In
addition, treatment of underlying cardiovascular risk factors such as
hypertension, CAD, valvular heart disease, obesity, sleep apnea,
diabetes, and heart failure is likely to decrease the incidence of AF.
Fish oil preparations have also been shown to reduce ventricular
arrhythmias in at-risk populations (CAD) and may also protect against
Atrial Fibrillation Medication

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Medication Summary

goals of medical therapy for patients with atrial fibrillation are to
maintain sinus rhythm, avoid the risk of complications (eg, stroke), and
minimize symptoms. Warfarin represents the cornerstone of anticoagulant
therapy for patients at moderate to high risk of thromboembolic events.
Some patients may not be able to take anticoagulants because of
contraindications or comorbidities. In patients unable to take warfarin,
the addition of clopidogrel to aspirin was shown to reduce the risk of
major vascular events, especially stroke, when compared with placebo and
aspirin in the ACTIVE (Atrial Fibrillation Clopidogrel Trial with
Irbesartan for Prevention of Vascular Events) trial; however, increased
risk for major hemorrhage was more prevalent in the clopidogrel plus
aspirin group than the placebo and aspirin group. The ACTIVE trial
studied 7554 patients with AF with the intent to determine whether
adding clopidogrel to aspirin therapy would reduce the risk for acute
vascular events (ie, stroke, MI, non-CNS systemic embolism, or death
from vascular event).[60] Clopidogrel
has been suggested to be less effective in reducing the rate of
cardiovascular events in individuals who carry the loss-of-function
CYP2C19 alleles. However, a 2010 study concluded that patients with
acute coronary syndromes or AF respond well to clopidogrel, regardless
of CYP2C19 loss-of-function carrier status.[61] The
goal of antiarrhythmic drug therapy is to reduce the duration and
frequency of atrial fibrillation episodes, thus improving patient
quality of life and symptoms. If successful, rhythm control can
eliminate or delay the need for long-term anticoagulation with warfarin
in some patients. Several antiarrhythmic drugs are commonly used
to prevent atrial fibrillation recurrence, such as quinidine,
flecainide, propafenone, sotalol, and dofetilide. Other antiarrhythmic
agents, such as amiodarone, are used in an off-label fashion with great
clinical efficacy. Use of antiarrhythmic drugs requires caution because
they are proarrhythmic. These agents can exacerbate preexisting
arrhythmias and generate arrhythmia de novo. Tachyarrhythmias and
bradyarrhythmias generated by these agents can be of ventricular or
atrial origin. Drug-drug interactions and extracardiac side effects are
common. Consultation with a cardiac electrophysiologist or knowledgeable
clinician is recommended prior to antiarrhythmic drug initiation. If
maintenance of sinus rhythm is the goal, the ACA/AHA/ECC have jointly
developed guidelines for the long-term antiarrhythmic treatment in the
maintenance of sinus rhythm.[20] These guidelines are intended to help clinicians tailor antiarrhythmic therapy on an individual basis for their patients. The following algorithm incorporates clinical trial data on the safety and efficacy of antiarrhythmic agents:Atrial Fibrillation  150072-1332317-151066-1446010tn

Antiarrhythmic drug algorithm for the medical management of sinus rhythm in patients with atrial fibrillation. For
patients with no evidence of structural heart disease, flecainide,
propafenone and sotalol should be considered first-line agents, and
amiodarone and dofetilide can be considered as alternative agents.
Amiodarone is considered a reasonable first-line agent for patients with
substantial LVH. Dofetilide and sotalol are first-line therapy for
patients with CAD, and amiodarone is considered a second-line agent in
this population. For patients with heart failure, amiodarone and
dofetilide are first-line agents.The Atrial arrhythmia Conversion
Trial (ACT) I and the open-label ACT IV trials suggest that intravenous
vernakalant hydrochloride can quickly convert recent-onset AF to sinus
rhythm. This is potentially an important therapeutic option for the
treatment of patients with AF seen in the emergency department, as the
treatment was well tolerated.[62] Current
practice constraints mandate that clinicians carefully consider patient
populations at low and acceptable risks for outpatient antiarrhythmic
drug initiation. Proarrhythmia is the most common adverse effect of
antiarrhythmics during the loading phase. While the proarrhythmic effect
of these drugs extends into the maintenance phase, a monitored
inpatient setting is generally recommended for drug initiation,
especially for those patients with structural heart disease or
substantial comorbidities. Nevertheless, certain antiarrhythmic drugs
have established and acceptable safety profiles when used in outpatients
without structural heart disease or other risk factors.

Calcium Channel blockers

Class Summary

channel blockers are more effective than digoxin when given orally for
long-term rate control and should be the initial drug of choice. They
reduce the rate of AV nodal conduction and control ventricular response.
Intravenous formulations control severe symptoms related to rapid
ventricular rates in emergent situations. View full drug information
Diltiazem (Cardizem)

is the drug of choice for rate control in many cases. During
depolarization, it inhibits calcium ions from entering the slow channels
or voltage-sensitive areas of vascular smooth muscle and myocardium. View full drug information
Verapamil (Calan, Isoptin, Verelan)

can diminish PVCs associated with perfusion therapy and can decrease
the risk of ventricular fibrillation and ventricular tachycardia. During
depolarization, verapamil inhibits calcium ions from entering the slow
channels or voltage-sensitive areas of vascular smooth muscle and

Beta-adrenergic Receptor Blockers

Class Summary

agents slow the sinus rate and decrease AV nodal conduction.
Beta-blockers now have more of a secondary role in AF rate control.
Carefully monitor blood pressure. View full drug information
Esmolol (Brevibloc)

is an ultra–short-acting beta-adrenergic receptor blocker. It
selectively blocks beta-1 receptors, with little or no effect on beta-2
receptor types. It is particularly useful in patients with elevated
arterial pressure, especially if surgery is planned. It has been shown
to reduce episodes of chest pain and clinical cardiac events compared
with placebo. It can be discontinued abruptly if necessary. It is useful
in patients at risk for experiencing complications from beta-blockade,
particularly those with reactive airway disease, mild-to-moderate LV
dysfunction, and/or peripheral vascular disease. A short half-life of 8
min allows for titration to the desired effect and quick discontinuation
if needed. View full drug information
Propranolol (Inderal)

is a nonselective beta-adrenergic receptor blocker as well as a class
II antiarrhythmic, with membrane-stabilizing activity that decreases the
automaticity of contractions. View full drug information
Atenolol (Tenormin)

selectively blocks beta-1 receptors, with little or no effect on beta-2
types. Atenolol is excellent for use in patients at risk for
experiencing complications from beta-blockade, particularly those with
reactive airway disease, mild-to-moderate LV dysfunction, and/or
peripheral vascular disease. View full drug information
Metoprolol (Lopressor)

is a selective beta-1 adrenergic receptor blocker that decreases the
automaticity of contractions. During intravenous administration,
carefully monitor blood pressure, heart rate, and ECG.

Cardiac glycosides

Class Summary

These drugs slow AV nodal conduction primarily by increasing vagal tone. They are used primarily in the setting of AF with CHF. View full drug information
Digoxin (Lanoxin)

slows the sinus node and AV node via vagomimetic effects and is not
very effective if sympathetic tone is increased. It is generally not
recommended unless depressed LV function is present. Digoxin can be
effective in sedentary patients (especially in those with heart failure)
but requires close monitoring of drug levels and renal function.
Combinations of rate-control medications (eg, a beta-blocker and
digoxin) may be superior to individual agents in some patients.

Antiarrhythmics, class IA

Class Summary

procainamide, and disopyramide are class IA antiarrhythmic agents used
to maintain sinus rhythm. Generally, start administration in the
hospital because of the high risk of adverse effects. All patients
treated with class IA agents should be treated concomitantly with AV
nodal blocking agents. Some patients demonstrate a slowing in the atrial
rate and an increase in AV conduction, with rapid ventricular rates,
when treated with class IA agents alone. They are fading as first-line
drugs for AF. View full drug information
Quinidine (Cardioquin, Quinalan, Quinidex, Quinaglute)

Vaughn-Williams class IA agents, only quinidine is FDA approved for
atrial fibrillation. As with all class IA agents, QRS and QTc
prolongation are the main ECG manifestations. It should not be used in
patients with a prolonged QTc baseline (>460 milliseconds). Quinidine
has generally fallen out of favor as a first- or second-line agent for
the treatment of atrial fibrillation. View full drug information
Procainamide (Procanbid, Pronestyl)

is not FDA approved for the treatment of atrial fibrillation; however,
many use this agent for acute cardioversion (eg, postoperatively) and
because it can be administered intravenously. Intravenous administration
is useful for acute conversion, and it can subsequently be converted to
an oral dose. It is a negative inotropic agent and vasodilator, and
care must be taken when administering to patients with reduced LV
function. It is generally considered a second-line agent. View full drug information
Disopyramide (Norpace)

is not commonly used to treat atrial fibrillation because it has
adverse anticholinergic effects and because it is a strongly negative
inotropic agent, which may precipitate CHF and cardiogenic shock in
patients with reduced LV function. It may be useful in vagally mediated

Antiarrhythmics, class IC

Class Summary

agents are indicated for patients with AF and supraventricular
tachycardia without structural heart disease. Given the results of the
CAST I and II trials (increased mortality), class IC agents are
generally not used in patients with concomitant LV dysfunction and/or
CAD. The applicability of the CAST results to other populations (eg,
patients without recent MI) is uncertain. Many specialists initiate
class IC antiarrhythmic agents in an outpatient setting for patients
with paroxysmal AF and no associated structural heart disease.
Regardless, close patient follow-up is mandated, with frequent ECG
monitoring or via transtelephonic monitoring for potential signs of
proarrhythmia. View full drug information
Propafenone (Rythmol)

is indicated for documented life-threatening ventricular arrhythmias,
such as sustained ventricular tachycardia. It appears to be effective in
the treatment of supraventricular tachycardias, including atrial
fibrillation and flutter. It is not recommended in patients with less
severe ventricular arrhythmias, even if symptomatic. Use it in
conjunction with AV nodal blocking agents when administered to patients
in atrial fibrillation, because conversion to AFL with 1:1 conduction
(producing fast ventricular rates) has been noted. View full drug information
Flecainide (Tambocor)

is indicated for the treatment of paroxysmal atrial
fibrillation/flutter associated with disabling symptoms and paroxysmal
supraventricular tachycardias, including AV nodal reentrant tachycardia,
AV reentrant tachycardia, and other supraventricular tachycardias of
unspecified mechanism associated with disabling symptoms in patients
without structural heart disease. It is also indicated for the
prevention of documented life-threatening ventricular arrhythmias (eg,
sustained ventricular tachycardia). It is not recommended in less severe
ventricular arrhythmias even if patients are symptomatic. Use
flecainide in conjunction with AV nodal blocking agents when given to
patients in atrial fibrillation, because conversion to AFL with 1:1
conduction (producing fast ventricular rates) can occur.

Antiarrhythmics, class III

Class Summary

the class III antiarrhythmic agents sotalol and dofetilide are FDA
approved for use in treating atrial arrhythmias; however, amiodarone is
also used widely for maintenance of sinus rhythm in patients with AF.
Dofetilide must be initiated in an inpatient setting. Sotalol is also
initiated in an inpatient setting. View full drug information
Amiodarone (Cordarone)

has antiarrhythmic effects that overlap all 4 Vaughn-Williams
antiarrhythmic classes. It has a low risk of proarrhythmia, and any
proarrhythmic reactions generally are delayed. It is used in patients
with structural heart disease. Most clinicians are comfortable with
inpatient or outpatient loading with 400 mg PO tid for 1 wk because of
low proarrhythmic effect, followed by weekly reductions, with a goal of
the lowest dose with desired therapeutic benefit (usual maintenance dose
for atrial fibrillation is 200 mg/d). During loading, patients must be
monitored for bradyarrhythmias. View full drug information
Sotalol (Betapace atrial fibrillation)

is a class III agent with beta-blocking effects. It is effective in the
maintenance of sinus rhythm, even in patients with underlying
structural heart disease. Inpatient loading is FDA mandated. View full drug information
Dofetilide (Tikosyn)

is approved by the FDA for maintenance of sinus rhythm, as well as for
the conversion of atrial fibrillation to sinus rhythm (approximately
50%) in patients with persistent atrial fibrillation. It has no effect
on cardiac output, cardiac index, stroke volume index, or systemic
vascular resistance in patients with ventricular tachycardia, mild to
moderate CHF, angina, and either normal or reduced LVEF. It has not
shown evidence of any negative inotropic effects. View full drug information
Ibutilide (Corvert)

is indicated for conversion of recent-onset atrial fibrillation or
atrial flutter (3 h to 90 d). It prolongs repolarization by increasing
the slow inward sodium current and by blocking the delayed rectifier
current with rapid onset.

Antiarrhythmic Agent, Miscellaneous

Class Summary

Dronedarone is an antiarrhythmic agent with properties belonging to all 4 Vaughn-Williams antiarrhythmic classes.View full drug information
Dronedarone (Multaq)

is indicated to reduce the risk for cardiovascular hospitalization in
patients with paroxysmal or persistent atrial fibrillation (AF) or
atrial flutter (AFL), with a recent episode of AF/AFL and associated
cardiovascular risk factors (ie, age >70 y, hypertension, diabetes,
history of CVA, LAD >50 mm or LVEF < 40%) who are in sinus rhythm
or who will be cardioverted.


Class Summary

Anticoagulants are used to prevent thromboembolic complications.View full drug information

augments the activity of antithrombin III and prevents the conversion
of fibrinogen to fibrin. It does not actively lyse but is able to
inhibit further thrombogenesis. It prevents reaccumulation of clot after
spontaneous fibrinolysis. View full drug information
Enoxaparin Sodium (Lovenox)

is a low molecular weight heparin. It augments the activity of
antithrombin III and prevents the conversion of fibrinogen to fibrin. It
does not actively lyse but is able to inhibit further thrombogenesis.
It prevents reaccumulation of clot after spontaneous fibrinolysis. View full drug information
Warfarin (Coumadin)

interferes with the hepatic synthesis of vitamin K–dependent
coagulation factors. It is used for the prophylaxis and treatment of
venous thrombosis, pulmonary embolism, and thromboembolic disorders.
Tailor the dose to maintain an INR of 2-3. View full drug information
Dabigatran (Pradaxa)

direct thrombin inhibitor. Thrombin enables fibrinogen conversion to
fibrin during the coagulation cascade, thereby preventing thrombus
development. Inhibits both free and clot-bound thrombin and
thrombin-induced platelet aggregation. Indicated for prevention of
stroke and thromboembolism associated with nonvalvular atrial

Antiplatelet Agents

Class Summary

patients may not be able to take anticoagulants such as warfarin
because of contraindications or comorbidities. In patients unable to
take warfarin, the addition of clopidogrel to aspirin has been shown to
reduce the risk of major vascular events. Apixaban, a novel factor Xa
inhibitor, reduces the risk of or systemic embolism without
significantly increasing the risk of major bleeding or intracranial
hemorrhage in patients unable or unwilling to receive vitamin K
antagonist therapy.[63] View full drug information
Clopidogrel (Plavix)

selectively inhibits adenosine diphosphate (ADP) binding to the
platelet receptor and subsequent ADP-mediated activation of the
glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet
aggregation. It is indicated for reduction of atherothrombotic events
following recent stroke. View full drug information
Aspirin (Bayer Aspirin, Ecotrin)

irreversibly inhibits platelet aggregation by inhibiting platelet
cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid
to PGI2 (potent vasodilator and inhibitor of platelet activation) and
thromboxane A2 (potent vasoconstrictor and platelet aggregate).
Platelet-inhibition lasts for the life of the cell (approximately 10 d).
It may be used at a low dose to inhibit platelet aggregation and
improve complications of venous stases and thrombosis. It reduces the
likelihood of myocardial infarction. It is also very effective in
reducing the risk of stroke. Anticoagulation with either aspirin or
warfarin should be initiated for all individuals with AF, except those
with lone AF or contraindications.

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