Download Evaluation and Management of New

Atrial fibrillation
Evaluation and Management of New-Onset Atrial
Fibrillation
Ryan G. Aleong, MD, and Paul D. Varosy, MD
Abstract
• Objective: To review the evaluation and management
of new-onset atrial fibrillation (AF).
• Methods: Review of relevant scientific literature and
clinical/professional society guidelines addressing AF.
• Results: AF is growing in prevalence with the aging of
the population and the increasing prevalence of heart
failure. The initial evaluation of patients with newonset AF should include investigation of reversible
causes and assessment of the patient’s underlying
cardiac function. Key areas in the management of
new-onset AF include reducing the risk of systemic
thromboembolism, control of ventricular rates, and
rhythm control. Maintenance of sinus rhythm with
antiarrhythmic medications or ablation represents a
treatment goal in patients who remain symptomatic after stroke risk reduction has been addressed and
attempts at adequate rate control have been made.
• Conclusion: AF is common and poses challenges for
clinicians, but modern treatment strategies can successfully address stroke risk and effectively manage
symptoms.
A
trial fibrillation is the most common arrhythmia
encountered in clinical practice, affecting as
many as 6 million people in the United States
today [1]. It is a major risk factor for embolic stroke and
is associated with increased risk of hospitalization and
mortality [1]. The initial evaluation of the patient should
be individualized and involves minimizing the risk of
systemic thromboembolism, controlling ventricular rates,
and rhythm control. In this review, we highlight evidence from clinical trials, observational data, and clinical
guidelines to describe our approach to the management
of new-onset atrial fibrillation.
Pathophysiology and Classification
Atrial fibrillation is characterized by disorganized atrial
activation that leads to a deterioration of atrial mechani162 JCOM April 2013 Vol. 20, No. 4
cal function. This chaotic atrial activation, generally at
atrial rates of 350 to 450 beats per minute, can lead to
rapid conduction over the atrioventricular (AV) node,
resulting in a fast ventricular response [2]. Disorganized
and rapid atrial activity coupled with refractoriness of the
AV node leads to irregularly irregular ventricular conduction. The lack of atrial systole may also result in thrombus
formation with subsequent increased risk of stroke and
systemic thromboembolism, particularly in patients with
risk factors, such as advanced age, underlying structural
heart abnormalities (eg, valvular disease or cardiomyopathy), concomitant hypertension, diabetes, or prior history
of cerebrovascular events [2].
The initiation and propagation of atrial fibrillation
may result from several processes. Focal atrial tachycardia
triggers for atrial fibrillation initiation are most commonly found in the pulmonary veins but occur at other
structures, such as the superior vena cava, ligament of
Marshall, and posterior left atrial wall [3,4]. Similarly,
atrial fibrillation can be initiated by atrial flutter, AV
nodal reentry tachycardia, or AV reentry tachycardia and
atrial tachycardias [5,6]. Regarding the maintenance of
atrial fibrillation, Moe and colleagues initially proposed
the multiple wavelet model in which wavelets of activation result in daughter wavelets [7,8]. Maintaining atrial
fibrillation generally requires changes either in the underlying atrial structural substrate, or changes in atrial action
potential duration and conduction, or both [9].
Atrial fibrosis represents the predominant pathological finding in patients with atrial fibrillation [10]. This
fibrosis may be diffuse throughout the atria and involve
the sinoatrial and AV nodes [11]. In addition, interstitial
fibrosis replaces atrial myocytes and may lead to atrial dilation. The degree of fibrosis increases with the duration
From the VA Eastern Colorado Health Care System, the University of Colorado Denver, and the Colorado Cardiovascular
Outcomes Research (CCOR) Group, Denver, CO.
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Clinical Review
of atrial fibrillation, and ongoing progression of structural changes leads to a greater burden of atrial fibrillation.
Heart failure and atrial fibrillation often coexist and
each may promote the development and/or the worsening of the other. One of the mechanisms by which atrial
fibrillation can cause or worsen heart failure is through
tachycardia-mediated cardiomyopathy, which has been
shown to be reversible in canine models [12,13]. Atrial
fibrillation may also lead to adverse outcomes in heart
failure by increasing the risk of cerebrovascular accidents
or through the associated side effects from medications or
procedures used for rate or rhythm control of atrial fibrillation [14]. In the SOLVD and DIAMOND trials, atrial
fibrillation was associated with increased mortality, and in
the CHARM study atrial fibrillation was associated with
increased mortality in patients with less severe heart failure
[15,16]. However, in patients with mild to moderate heart
failure in the V-HeFT I and V-HeFT II trials, cumulative
mortality and heart failure hospitalization rates were not
increased in patients with atrial fibrillation [17].
The classification of atrial fibrillation can help guide
evaluation and treatment strategies [18]. Atrial fibrillation that is recurrent and self-terminating is defined as
paroxysmal; when sustained for greater than 7 days, it
is defined as persistent. Long-standing atrial fibrillation
is defined as permanent atrial fibrillation. First detected
atrial fibrillation may be paroxysmal, persistent, or permanent in pattern. “Lone” atrial fibrillation is said to
occur in patients without other cause, whereas secondary
atrial fibrillation occurs in patients with other known
precipitating causes such as pericarditis or hyperthyroidism. Clearly, the current classification system is imperfect
and there is significant overlap between different atrial
fibrillation subtypes [19].
Prevalence and Risk Factors
The prevalence of atrial fibrillation is 0.4% to 1.0% in the
general population and increases with age, with a prevalence of approximately 8% in patients 80 years of age.
Overall median age for patients with atrial fibrillation is
75 years [20]. The incidence of atrial fibrillation increases
with age from 0.1% per year in patients under 40 years
of age to as high as 1.5% in women and 2.0% per year in
men greater than 80 years of age [21]. Atrial fibrillation
will likely continue to represent a major cause of hospitalization as the population continues to age.
Multiple risk factors that contribute to the development of new-onset atrial fibrillation have been identified.
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In the Framingham cohort, identified risk factors included increasing age, structural heart disease (such as the
presence of a murmur or heart failure), body mass index,
hypertension, and prolonged PR interval on electrocardiogram [22]. Patients who had a greater number of risk
factors had an increasing risk of developing atrial fibrillation. In the Etude en Activité Libérale sur la Fibrillation Auriculaire Study (ALFA), a total of 756 patients
were followed for an average of 8.6 years. Characteristics
that were more common among patients who developed
atrial fibrillation included the presence of structural heart
disease, including heart failure, hypertrophic cardiomyopathy, valvular heart disease, and coronary artery disease
[23]. Hypertension is also an important risk factor for the
development of atrial fibrillation.
Presentation
The symptoms associated with atrial fibrillation vary
widely from acute, highly symptomatic episodes to
asymptomatic episodes. Patients may present with a
variety of symptoms including palpitations, chest pain,
fatigue, and shortness of breath. Syncope is an uncommon presentation but may represent sinus node pauses
after conversion out of atrial fibrillation, rapid ventricular
rates, or the presentation of other associated conditions
including aortic stenosis and hypertrophic cardiomyopathy. Asymptomatic atrial fibrillation may present as
heart failure, presumably related to untreated high ventricular rates. Ambulatory monitoring has shown that
patients often have symptomatic and asymptomatic episodes [24], and as atrial fibrillation becomes more persistent the severity of symptoms often decreases. Finally,
thromboembolism resulting in cerebrovascular accident
or systemic embolism may occur and has been shown
to be common in patients with asymptomatic or short
episodes of atrial fibrillation [25].
Initial Evaluation
The initial evaluation of new-onset atrial fibrillation
should include a search for acute reversible causes, such
as acute alcohol consumption, pericarditis, and highcatecholamine states such as those associated with surgery, hyperthyroidism, and pulmonary embolus. Treatment of hypertension may also decrease the frequency of
atrial fibrillation. Atrial fibrillation may also be associated
with other cardiac arrhythmias, such as atrial flutter,
Wolff-Parkinson-White syndrome, and AV nodal reentry
tachycardia, and treatment of the primary arrhythmia
Vol. 20, No. 4 April 2013 JCOM 163
Atrial fibrillation
Initial evaluation of atrial fibrillation: Complete history and physical, ECG, transthoracic echocardiogram, serum electrolytes, creatinine, thyroid function tests, hepatic function tests
Look for reversible or "easily" treatable etiologies: Substance abuse (alcohol), abnormal thyroid function, underlying SVT including pre-excitation on ECG
Further tests to consider: Prolonged ambulatory monitor, transesophageal echocardiogram, electrophysiology study, ischemia evaluation (stress test)
Figure 1. Initial evaluation for atrial fibrillation. ECG = electrocardiogram.
may prevent further atrial fibrillation. An overview of
the initial evaluation for atrial fibrillation is included in
Figure 1.
The initial evaluation should include a thorough history and physical to evaluate for the common etiologies
previously discussed. It is important to look for underlying heart disease, such as hypertension, heart failure,
valvular disease, and atherosclerosis, as well as underlying
pulmonary disease. Although less common, potential
thyroid disease or underlying supraventricular tachycardias should also be investigated. Presence of symptoms
should be determined. Physical examination should try
to document an irregularly irregular rhythm, signs of
associated cardiac disease, or other associated systemic
diseases. Finally, characterization of whether atrial fibrillation is occurring in a paroxysmal, persistent or permanent pattern will help to guide treatment.
The cornerstone of diagnosis is electrocardiographic
documentation of atrial fibrillation, which is characterized by the replacement of consistent P waves by rapid
oscillations or fibrillatory waves, which results in an
irregularly irregular rhythm when AV conduction is intact (Figure 2a). The QT interval can also be assessed,
which may affect choice of antiarrhythmic treatment. In
164 JCOM April 2013 Vol. 20, No. 4
patients with an accessory pathway and associated WolffParkinson-White Syndrome, AV conduction results in
an irregularly irregular ventricular rhythm and QRS
morphology due to varying degrees of conduction via the
AV nodal and the accessory pathway (Figure 2b). Other
associated cardiac arrhythmias may include atrial flutter
(Figure 2c) or supraventricular tachycardias.
If atrial fibrillation occurs frequently, it may be recorded either through electrocardiogram or an ambulatory
monitor. An electrocardiogram can also document other
associated cardiac pathology including left ventricular
hypertrophy, pulmonary hypertension, pre-excitation,
prior myocardial infarction and evidence of AV conduction disease. Longer-duration ambulatory monitors
may be necessary if atrial fibrillation is infrequent or
asymptomatic [26]. These monitors may be shorter-term
continuous Holter monitors (1–2 days) where the patient
records a diary of symptoms, or alternatively, longer-term
event monitors where the patient triggers the monitor for
symptoms or a loop monitor which continuously records
and documents the rhythm shortly before and after the
patient recorded symptom. Auto-triggered loop monitors
trigger ECG storage during symptomatic and asymptomatic episodes and have been shown to have a higher yield
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Clinical Review
2A
2B
2C
Figure 2. A: Atrial fibrillation. Note that there is no organized atrial activity and irregularly irregular ventricular rhythm.
B: Pre-excited atrial fibrillation. Note that there is an irregularly irregular QRS duration and ventricular response. C: Atrial flutter.
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Vol. 20, No. 4 April 2013 JCOM 165
Atrial fibrillation
than Holter and 30-day loop monitors [27]. Finally, implantable loop monitors can record patient-initiated and
auto-triggered events for 1 to 2 years [28]. With regard
to atrial fibrillation, these monitors have a role in the diagnosis of unexplained symptoms (palpitations, dyspnea)
and cryptogenic stroke, and in following the efficacy of
various treatments.
Several other tests should be used to characterize the
cardiac pathology. A 2-dimensional Doppler echocardiogram should be performed as part of the initial evaluation
in all patients with atrial fibrillation. An echocardiogram
will document associated left ventricular hypertrophy,
valve disease, and other ventricular systolic or diastolic dysfunction. A transesophageal echocardiogram is not needed
as part of the initial evaluation but is a more sensitive test
to document intracardiac thrombus formation [29,30].
A chest x-ray is mostly useful to document associated
pulmonary pathology and may give some insight into the
overall cardiac dimension. Blood tests to investigate renal,
hepatic, and thyroid function are useful. A stress test may
be useful if underlying coronary atheroscelorotic disease is
suspected. In selected patients, an electrophysiology study
may help to detect underlying atrial flutter or supraventricular tachycardia that may serve as a trigger for atrial
fibrillation.
Management
The management of atrial fibrillation varies according
to the individual patient’s characteristics. The variables
important to consider are
• Presence of structural heart disease
• Pattern of atrial fibrillation: paroxsymal, persistent
or permanent
• Presence of comorbid conditions: hypertension,
diabetes, previous stroke
• Severity of associated symptoms: asymptomatic to
severe
Treatment of atrial fibrillation can be complex but
revolves around 3 interdependent management considerations: controlling ventricular rates, preventing thromboembolism and rhythm control. It should be remembered
that the primary 2 goals of management of atrial fibrillation are rate control and prevention of thromboembolism, which often supercede the need for rhythm control.
A general outline for the initial management of newly
diagnosed atrial fibrillation is shown in Figure 3.
166 JCOM April 2013 Vol. 20, No. 4
Rate Control
Choice of the appropriate strategy to control ventricular
rates during atrial fibrillation will depend on the acuity of the presentation and the presence of co-existing
conditions such as heart failure and pre-excitation. It
should be noted that ventricular rates in atrial fibrillation depend on sympathetic tone during the acute
and chronic settings (sepsis, exercise). Very high ventricular rates may cause hemodynamic compromise,
particularly in the setting of underlying structural heart
disease.
During the acute setting, control of ventricular rates
depends the degree of hemodynamic compromise. In
patients who are hemodynamically unstable, which may
occur in hypertrophic cardiomyopathy, aortic stenosis
or pre-excited atrial fibrillation, prompt cardioversion
is indicated. In patients without pre-excitation, control
of ventricular rates acutely can be accomplished with
IV beta-blocker (propranolol, esmolol, or metoprolol)
or nondihydropyridine calcium channel antagonist (diltiazem, verapamil). In heart failure patients, amiodarone
and digoxin are indicated for control of ventricular rates.
Low-dose beta-blockers may be used but with careful
attention to avoid worsening hemodynamic compromise.
In patients with pre-excited atrial fibrillation, medications that selectively affect the AV node are contraindicated due to risk of promoting conduction exclusively
over the AV accessory pathway and subsequent risk of
ventricular fibrillation. Therefore, antiarrhythmic medications such as amiodarone, procainamide, or ibutilide
may be used to terminate atrial fibrillation and to inhibit
AV accessory pathway conduction.
In patients who are not acutely hemodynamically
compromised, oral medications to control heart rate
are indicated. In patients without pre-excitation, oral
beta-blockers (propranolol, metprolol) and nondihydropyridine calcium channel antagonists (diltiazem, verapamil) can effectively control the rapid ventricular rate
response to atrial fibrillation. With regard to the degree
of ventricular rate control required, the RAte Control
Efficacy in Permanent Atrial Fibrillation II trial (RATE
II) compared lenient control to strict heart rate control
(< 110 bpm vs < 80 bpm) and found no difference in
patient outcomes between the 2 strategies [31]. Similarly, there was no association between the degree of rate
control and adverse cardiac remodeling as assessed by
echocardiogram in RATE II [32]. It should be noted
that the RATE II trial did include a substantial proporwww.jcomjournal.com
Clinical Review
Newly Discovered AF
Paroxysmal
Persistent
Accept permanent AF
Rate control and anticoagulation as needed
Anticoagulation and rate control as needed
Consider antiarrhythmic
drug therapy
No therapy needed unless significant
symptoms (eg, hypotension, heart failure, angina pectoris)
Anticoagulation as needed
Cardioversion
Long-term antiarrhythmic drug therapy unnecessary
Figure 3. Initial management of newly diagnosed atrial fibrillation (AF). (Modified from 2011 ACC/AHA/ESC Focused Update
on Atrial Fibrillation.)
tion of patients with structural heart disease, including
those with decreased left ventricular function and valvular heart disease. In heart failure patients, low-dose
beta-blockers, digoxin, and amiodarone are indicated for
ventricular rate control. In patients with pre-excitation,
ablation of the accessory pathway should be considered.
The ultimate form of ventricular rate control can be
achieved with AV node ablation, which is recommended
for patients with severe symptoms from atrial fibrillation
or tachycardia-mediated cardiomyopathy that cannot be
controlled with antiarrhythmic or rate-controlling medications [33]. Several trials have shown AV node ablation
to be effective and safe in patients with medically refractory atrial fibrillation, but it should be noted that these
trials were performed before ablation directed at atrial
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fibrillation or pulmonary vein isolation was commonly
practiced. The Ablate and Pace Trial was a prospective
study following 156 patients with chronic and paroxysmal atrial fibrillation that was medically refractory [34].
There was a significant improvement in quality of life
measurements and an improvement in left ventricular
function in those with baseline reduced systolic function.
In a smaller trial of patients with chronic atrial fibrillation who had AV node ablation and pacemaker placement, there was an improvement of quality of life that
was associated with a discontinuation of rate controlling
medications [35]. In a recent meta-analysis, there was no
improvement of quality of life indices or LV function in
patients with normal LV function who underwent an ablate and pace strategy [36]. In another meta-analysis that
Vol. 20, No. 4 April 2013 JCOM 167
Atrial fibrillation
comprised 21 studies with 1181 patients between 1989
and 1998, AV node ablation and pacemaker placement
was associated an improved quality of life and improved
LV ejection fraction (4.4 ± 0.01%) [37].
Although AV node ablation is a technically straightforward procedure, it is associated with some serious
complications that deserve mention. Overall, AV node
ablation and pacemaker placement was associated with
a reported overall incidence of sudden death of 2.1%
(range, 0% to 11.3%) that may be associated with a lower
pacing rate post AV node ablation (< 70 bpm) [37,38].
Other notable complications post-procedure include
pacemaker lead failure, complications related to the need
for long-term anticoagulation, and life-long pacemaker
dependency. In general, AV node ablation can be performed from the right heart but does require a left-sided
approach approximately 6.9% of the time [36].
Atrial fibrillation has been shown to worsen outcomes
in heart failure with significant increased mortality
among heart failure patients also diagnosed with atrial
fibrillation in the Framingham cohort [39]. One area
of controversy is whether to offer heart failure patients
with atrial fibrillation biventricular pacing, as they may
not receive the same benefit as those in sinus rhythm.
Patients with atrial fibrillation, in general, have less biventricular pacing given that rapid AV nodal conduction may
decrease the degree of biventricular pacing and increase
the nonresponder rate. Guidelines from the American
College of Cardiology/American Heart Association/
Heart Rhythm Society endorse biventricular pacing for
patients with left ventricular ejection fraction less than
35% and QRS duration greater than 120 ms, but do suggest that AV node ablation may be required to increase
the amount of biventricular pacing [33]. Ganesan et al
reported on 6 trials comprising 768 patients with atrial
fibrillation who had biventricular pacing and reported
significant improvements in all-cause mortality, cardiovascular mortality, and improvement in New York Heart
Association function class in patients who underwent AV
node ablation [40].
Several trials have analyzed the best approach for
either rate or rhythm control in heart failure. The Pulmonary-Vein Isolation for Atrial Fibrillation in Patients
with Heart Failure (PABA-CHF) trial assigned patients
with drug-refractory, symptomatic atrial fibrillation with
an ejection fraction less than 40% to either pulmonary
vein isolation (PVI) (n = 41) or AV node ablation with
placement of a biventricular pacemaker (n = 40) [41].
168 JCOM April 2013 Vol. 20, No. 4
With regard to the primary composite endpoint of ejection fraction, 6-minute walk test, and Minnesota Living
with Heart Failure (MLWHF) score, patients in the PVI
group did better, with significant improvements in all
individual components of the composite endpoint. This
trial was clearly limited by the relatively small number
of patients in each group. In addition, persistent atrial
fibrillation patients only had ablation around the pulmonary veins (PVI), which may not be sufficient ablation
in this group; however, the overall freedom from atrial
fibrillation was 71% without antiarrhythmic medications.
The role of ablation directly targeting atrial fibrillation
in heart failure remains unclear, and the current debate
often focuses on whether AV node ablation is reasonable
and will increase the response to biventricular pacing.
Regarding AV node ablation in patients with normal
LV function, it is reasonable to consider this strategy in
patients who have failed rate-controlling medications.
In heart failure patients, AV node ablation to increase
the degree of biventricular pacing is also reasonable
if patients have failed medical management. In both
groups we assess whether rhythm control, including with
PVI ablation, is a reasonable approach for the patient.
In patients with severe left atrial enlargement, severely
decreased left ventricular function or where the risks of a
more invasive ablation for atrial fibrillation outweigh the
benefits, a less invasive approach of AV node ablation may
be more reasonable. Further trials are needed to validate
this approach, which will be discussed below in the section on ablation for atrial fibrillation.
Anticoagulation Strategies
Embolic events in atrial fibrillation result from a complex
sequence of events. Thrombus formation in atrial fibrillation usually arises from the left atrial appendage. Due to
the posterior position of the left atrium, transesophageal
echocardiography has a higher sensitivity and specificity
for imaging the left atrial appendage (LAA) compared
with transthoracic echocardiography [29]. It is generally
believed that 48 hours of atrial fibrillation is required for
thrombus formation; however, thrombus formation may
occur sooner in the correct milieu (stasis, endothelial
dysfunction and hypercoaguable state). After any type of
cardioversion atrial stunning occurs, the risk of thrombus
formation increases from 3 days to 3 to 4 weeks [42].
Another consideration is that up to 25% of cerebrovascular accidents in atrial fibrillation are due to other
noncardiac causes, such as embolism from aortic plaques
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Clinical Review
Table 1. CHADS2, CHA2DS2-VASc, and HAS-BLED Scoring Systems
CHADS2
CHF
Hypertension
Age ≥ 75 yr
Diabetes mellitus
Previous CVA or
TIA
Points
1
1
1
1
2
CHA2DS2-VASc
CHF
Hypertension
Age ≥ 75 yr
Diabetes mellitus
Stroke/TIA/
thromboemblism
Vascular disease†
Age 65-74 yr
Female gender
Points
1
1
2
1
2
1
1
1
HAS-BLED
Hypertension
Abnormal renal or liver function
Stroke
Bleeding history/
predisposition
Labile INR
Elderly (age > 65 yr)
Drugs or alcohol
Points
1
1*
1
1
1
1
1*
*2 points for both.
†Vascular disease: Prior myocardial infarction, peripheral artery disease, or aortic plaque.
and intrinsic cerebrovascular disease. Patients with atrial
fibrillation associated with valvular heart disease (especially mitral valvular stenosis) are at particularly high risk
for thromboembolic events, and among patients with nonvalvular atrial fibrillation, consistent independent risk factors for stroke in several studies include diabetes, left ventricular systolic dysfunction, increasing age, hypertension,
female gender, and prior stroke or transient ischemic attack
[43–47]. The CHADS2 scoring system, commonly used
to assess the risk of stroke, assigns 1 point for Congestive
heart failure, Hypertension, Age greater than 75 years or
Diabetes mellitus, and 2 points for previous Stroke. Based
on this scoring system, a score of 0 had an annualized
stroke rate of 1.9%, score of 1 had a rate of 2.8%, and score
of 2 a rate of 4.0% [48]. While there are several different
scoring methods, the CHA 2DS2-VASc scoring (Table 1)
was recently refined and introduced gender, vascular
disease, and a younger age (65 to 75 years) into the risk
assessment [49]. Two validation studies comparing the
CHA 2DS2-VASc to the CHADS2 demonstrated that the
CHA 2DS2-VASc scoring system is better able to predict
the risk of stroke and thromboembolism [50,51]. Its main
strength is that it is better able to dentify truly low-risk
patients compared with the CHADS2.
With regard to anticoagulation, there are several different recommendations based on the different risk scoring systems that have emerged. The AHA/ACC 2011
guidelines divide patients into high risk (previous stroke,
mitral stenosis or prosthetic valves), where warfarin is
recommended with goal INR 2.0 to 3.0, and low risk
(female gender, age 65 to 74 years, coronary artery disease and thyrotoxicosis), where aspirin is recommended.
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For intermediate-risk patients (hypertension, age > 75
years, diabetes mellitus, left ventricular ejection fraction
< 35%), either aspirin or warfarin with goal INR 2.0 to
3.0 is recommended based on the patient’s individual risk/
benefit ratio [2]. Similarly, according to the CHADS2
scoring system, patients with a score of 2 should receive
warfarin or similar oral anticoagulation, and those with
a score of 0 should receive aspirin 81 to 325 mg. There
has been debate about intermediate-risk patients or those
with a CHADS2 of 1, since these patients have an annualized adjusted stroke rate of 2.8%. The ACC/AHA 2012
guidelines for atrial fibrillation recommend either aspirin
or warfarin for these patients, while the American College
of Chest Physicians suggest oral anticoagulation rather
than aspirin and furthermore recommends dabigatran
rather than warfarin [2,52]. The latter recommendation
is derived by pooling 11 randomized trials with 6526
patients, which demonstrated a 50% decrease in the risk of
stroke that was thought to outweigh the 50% increase in
the risk of bleeding. The implications of anticoagulation
based on the CHA 2DS2-VASc score suggest that those
with a score of 0 do not need any antithrombotic therapy
while patients with a score of ≥ 2 should be placed on oral
anticoagulation given that this patient group has an annualized thromboembolism rate of 1.6% [49,51,53,54]. The
CHA 2DS2-VASc score may allow for better risk stratification of patients with a CHADS2 score of 1.
There are several other important factors that deserve
mention with regard to anticoagulation for atrial fibrillation. In the Stroke Prevention in Atrial Fibrillation studies,
paroxysmal atrial fibrillation patients receiving aspirin had
a similar risk of stroke compared to persistent atrial fibril-
Vol. 20, No. 4 April 2013 JCOM 169
Atrial fibrillation
lation patients (3.2% vs 3.3%) [43]. This association between intermittent atrial fibrillation and stroke was further
demonstrated in a recent trial of implantable loop monitors
placed in 2580 patients, which demonstrated an association between ischemic stroke and at least 6 minutes of subclinical atrial tachycardia [25]. It also should be noted that
anticoagulation guidelines are the same for patients with
atrial flutter and atrial fibrillation as there appears to be a
similar risk of cardiac thrombus formation [2,55].
Despite more aggressive recommendations for anticoagulation for atrial fibrillation, a minority of appropriate patients are receiving anticoagulation or are able to
achieve a therapeutic INR [56]. An overestimation of
bleeding risk by clinicians is an important reason why
patients are not prescribed anticoagulation. There have
been several recent scoring schemes designed to estimate
a patient’s risk of bleeding [57,58]. The HAS-BLED
score (Table 1) uses the following criteria to estimate a
patient’s risk of bleeding: hypertension, abnormal renal
or liver function, previous stroke, bleeding history of
predisposition, labile INRs, elderly, and current drug
and/or alcohol excess [57]. A HAS-BLED score ≥ 3
indicates a higher risk of bleeding. It should be noted
that the HAS-BLED should not be used to withhold
otherwise appropriate anticoagulation but rather indicates risk factors that can be modified and/or monitored
during anticoagulation. Regarding the net benefit of
anticoagulation compared with the risk of bleeding, a
recent Danish analysis of > 130,000 patients showed a
net clinical benefit in patients with a CHADS2 ≥ 1 and a
CHA 2DS2-VASc score ≥ 2 [59]. In this group at higher
risk of thromboembolism, the clinical benefit was still
present in patients with a HAS-BLED score ≥ 3. Therefore, the risks of anticoagulation need to be individualized and balanced against the benefits of anticoagulation
in appropriate patients.
Several novel anticoagulants have recently been approved for use in nonvalvular atrial fibrillation as alternatives to warfarin. Dabigatran is a direct thrombin
inhibitor that was shown to have similar rates of major
hemorrage and lower rates of stroke and systemic thromboembolism [60]. Rivaroxaban is an oral factor Xa inhibitor that has also been shown to have similar stroke
and systemic embolism rates with slightly lower rates of
major bleeding episodes compared with warfarin [61].
Apixaban, another oral factor Xa inhibitor, has also been
demonstrated to be superior to warfarin in preventing
stroke and systemic embolism as well as caused less hem170 JCOM April 2013 Vol. 20, No. 4
orrhagic stroke [62]. Dabigatran, rivaroxaban, and apixaban are currently all approved by the Food and Drug
Administration (FDA).
There are several nonpharmacological devices that are
either available or will likely become available in the near
future that avoid the need for chronic anticoagulation.
The left atrial appendage (LAA) represents the site of
thrombus formation in approximately 90% of patients
with nonvalvular atrial fibrillation, and decreased blood
flow velocity and stasis are common in atrial fibrillation. Therefore, elimination or closing the entrance of
the LAA may substantially reduce the risk of thrombus
formation. The WATCHMAN device is a nitinol selfexpanding device meant to seal the LAA and is percutaneously delivered. The Watchman Left Atrial Appendage
System for Embolic Protection in Patients with Atrial Fibrillation (PROTECT-AF) was a noninferiority trial that
randomized patients with a CHADS2 ≥ 1 to warfarin or
LAA occlusion with the Watchman device [64]. The trial
demonstrated a 99.9% probability of noninferiority with
a significant decrease in the primary efficacy endpoint of
stroke, cardiovascular death, and systemic embolism in
the Watchman group. There were also a significant number of serious pericardial effusions requiring draining
in the Watchman device group. This device is currently
being evaluated in a second trial, the Evaluation of the
Watchman LAA Closure Device in Patients with Atrial
Fibrillation vs. Long Term Warfarin Therapy (PREVAIL) trial, a randomized trial that will address some
of the safety issues in the PROTECT-AF trial. Another
innovative approach to LAA closure is the LARIAT suture delivery device in which a snare-like pre-tied suture
loop is delivered via a percutaneous epicardial approach
using an endocardial ballon catheter and wire as a marker
[65,66]. There is preliminary data suggesting that this
may be a safe and effective approach and an ongoing
registry is following these patients. The LARIAT device
is being implanted in select centers in the United States
and current eligible patients are those with a CHADS2
≥ 2 and a contraindication to oral anticoagulation. These
nonpharmacological techniques to exclude the LAA will
most likely become more common over time, especially
for those with new-onset atrial fibrillation.
Rhythm Control
Conversion to sinus rhythm represents the third priority
in the management of atrial fibrillation after effective
rate control and prevention of thromboembolism. The
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Clinical Review
primary reasons to pursue rhythm control include hemodynamic compromise and bothersome symptoms associated with atrial fibrillation still present after effective rate
control. For patients with new-onset atrial fibrillation
in particular, at least 1 attempt at restoration of normal
sinus rhythm by either electrical or chemical cardioversion may be reasonable.
Regardless of the means of cardioversion, risk of atrial
thromboembolism should be addressed. Patients with
atrial fibrillation of unknown duration or known to be
greater than 48 hours should receive at least 3 weeks of
anticoagulation with warfarin to a goal INR of 2.0 to 3.0
(or treatment with an alternative anticoagulation agent),
or transesophageal echocardiography prior to cardioversion to exclude left atrial thrombus. For those patients
with atrial fibrillation known to be of less than 48 hours’
duration and believed to be at low risk for thrombosis,
proceeding to cardioversion may be reasonable. A higher
CHADS2 score may be useful to predict the presence of
left atrial and/or left atrial appendage thrombus. Decker et
al found no thrombi in patients with a CHADS2 score of
0 and found that heart failure in particular was associated
with a higher risk of thrombus [67]. This is in contrast
to the findings of the Assessment of Cardioversion Using
Transesophageal Echocardiography (ACUTE) trial, which
detected LAA thrombi in 10% of patients with a CHADS2
score of 0 [68]. Therefore, following the guidelines of either anticoagulation for 3 weeks prior to cardioversion or
pre-procedural TEE is prudent [2]. After cardioversion, all
patients should receive at least 1 month of anticoagulation
due to the increased risk of thrombosis associated with atrial
stunning.
Although there is evidence to suggest that patients
in sinus rhythm have better outcomes compared with
those in atrial fibrillation [69], several large studies demonstrate that strategies to maintain sinus rhythm with
antiarrhythmic medications do not reduce the risk of
mortality or hospitalization. Trials in the past pursuing
rhythm control with antiarrhythmic medications have
demonstrated no significant mortality benefit to rhythm
control [70,71]. The AFFIRM (A Comparison of Rate
Control and Rhythm Control in Patients with Atrial
Fibrillation) and RACE (Rate Control versus Electrical
Cardioversion in Persistent Atrial Fibrillation) trials are
often cited as the key trials comparing a strategy of rate
versus rhythm control with anti-arrhythmic medications in patients with newly diagnosed atrial fibrillation
and persistent atrial fibrillation, respectively [72,73].
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The AFFIRM trial suggested that there may be an increased mortality (although not statistically significant)
in the rhythm control arm and more hospitalizations and
adverse drug reactions in the rhythm control arm. The
RACE trial found that a rate control strategy was not
inferior to a rhythm control for the prevention of death
and other comorbidities. However, it should be noted
that patients recruited were mostly older than 65 years of
age or had other risk factors for stroke, which emphasizes
the need to consider other comorbidities when choosing an antiarrhythmic medication. Anticoagulation was
often stopped once normal sinus rhythm was achieved
likely without adequate monitoring, which was associated with worse outcomes in the rhythm control arms
and emphasizes the need to continue anticoagulation
in these patients. In addition, these patients were not
necessarily symptomatic from their atrial fibrillation,
which represents the primary reason to pursue rhythm
control. Importantly, roughly 12% of subjects in the rate
control arm of AFFIRM crossed over to rhythm control,
primarily due to a failure of symptom control with rate
control alone in this subset of patients. Similarly, approximately 29% of patients in the rhythm control arm
crossed over to the rate control arm due to side effects
or inability to maintain normal rhythm. Therefore, the
results of the AFFIRM trial emphasize that rhythm control should be reserved for symptomatic patients given
the many side effects that accompany antiarrhythmic
medications.
Electrical Cardioversion
Electrical cardioversion synchronized to the R wave represents a safe method of cardioversion. The primary indications for electrical cardioversion include hemodynamically
unstable atrial fibrillation with or without pre-excitation
or as a method to restore sinus rhythm due to intolerable
patient symptoms. It should be noted that frequent, repeated electrical cardioversion is not indicated in patients
who convert quickly back to atrial fibrillation and in those
with significant drug or electrolyte abnormalities, such as
digoxin toxicity or hypokalemia. A short-term anesthetic
should be used. There are varying strategies with regarding to picking the appropriate energy for electrical cardioversion with some practitioners starting low and gradually
increasing while others start at a higher initial energy to
minimize the number of shocks. In general, starting with
at least 200 J for either monophasic or biphasic shock
waveforms has proven to be most effective.
Vol. 20, No. 4 April 2013 JCOM 171
Atrial fibrillation
Table 2. Medications Used to Chemically Cardiovert Atrial Fibrillation and Maintain Sinus Rhythm
Dose for Cardioversion
Daily Dose for Maintenance
of Sinus Rhythm
Side Effects and Precautions
Flecainide
200 to 300 mg
200 to 300 mg
Atrial flutter; avoid in structural heart disease
Propafenone
600 mg
400 to 900 mg
Hypotension, atrial flutter; avoid in structural
heart disease
Ibutilide
1 mg
NA
Avoid in heart failure, prolonged QT
Dofetilide
125 mcg to 500 mcg
500 mcg to 1 g
Avoid with prolonged QT; dose adjust for
renal dysfunction
Amiodarone
Oral 1.2 g/day until 10 g total
100 to 400 mg
Bradycardia, hypotension, QT prolongation;
toxicities include: hepatic, thyroid, pulmonary,
skin
Sotalol
NA
160 to 320 mg
Avoid with prolonged QT, reactive airway
disease and heart failure; dose adjust for
renal dysfunction
Dronedarone
NA
800 mg
QT prolongation, GI side effects; avoid in
heart failure, persistent AF
Chemical Cardioversion
Antiarrhythmic medications have been shown to be effective for cardioversion of atrial fibrillation. From a practical standpoint, antiarrhythmic medications are used less
commonly for conversion of atrial fibrillation given that
they are less effective than electrical cardioversion. When
electrical cardioversion has previously been unsuccessful, adjunctive antiarrhythmic medications may improve
the success rate of electrical cardioversion. Chemical
cardioversion with antiarrhythmic drugs also has the
advantages of not requiring sedation and the associated
required period of pre-sedation fasting. Conversion with
antiarrhythmic medications is generally most successful
for recent onset atrial fibrillation (< 24 hours). Before
discussing these individual uses, it is worth considering
each of these medications individually and circumstances
when they should be considered. Table 2 lists the commonly used antiarrhythmic medications by VaughnWilliams classification as well as associated precautions
and initial doses for chemical cardioversion and maintenance of sinus rhythm.
Flecainide and propafenone are class Ic antiarrhythmic medications that are quite effective at chemical
cardioversion [74,75]. These medications are generally
given once for atrial fibrillation that lasts greater than 2
to 4 hours with the goal to decrease the duration of the
arrhythmia. Both of these medications have been studied
to cardiovert infrequent episodes of atrial fibrillation
where the patient may take a higher oral dose at home in
172 JCOM April 2013 Vol. 20, No. 4
order to decrease the duration of the episode and avoid a
visit to the hospital [76]. These class Ic medications may
cause several side effects that are listed in Table 2. Class
Ic medications should not be used in patients with structural heart disease, particularly those with abnormal ventricular function or ischemic heart disease. Conversion
to atrial flutter with 1:1 AV conduction, or “1c Flutter,”
causing a rapid ventricular response may also occur and,
therefore, the patient may need an AV nodal blocking
medication as well.
Ibutilide is used intravenously and is effective for conversion of atrial fibrillation and flutter [77,78]. It can be
used in patients with structural heart disease but should
be avoided in patients with depressed left ventricular
function and/or heart failure. Ibutilide is a class III antiarrhythmic medication that prolongs cellular repolarization and, therefore, is related to an increased QT interval
and risk of torsades de pointes. Pre-treatment with magnesium may decrease the risk of ventricular arrhythmias
and the patient should be monitored for at least 4 hours
after drug infusion.
Dofetilide is modestly effective for cardioversion
of atrial fibrillation or flutter. In the SAFIRE-D trial,
conversion was increasingly successful with higher doses
(125 mcg, 6.1%; 250 mcg, 9.8%; 500 mcg, 29.9%) and
increased with greater duration of treatment (24 hours,
70%; 36 hours, 91%) [79]. In general, dofetilide is used
for chronic, maintenace treatment of atrial fibrillation
as it requires inpatient initiation of the medication.
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Clinical Review
Dofetilide is also a class III anti-arrhythmic and has
the same risks of torsades de pointes associated with
ibutilide.
In general, amiodarone has been associated with
lower efficacy for cardioversion compared to class Ic
and III antiarrhythmic medications [80–82]. However,
amiodarone can be given to patients with structural heart
disease, is effective for ventricular rate control, and is the
most effective antiarrhythmic drug for maintaining sinus
rhythm over longer periods of time. As listed in Table 2,
amiodarone is associated with several long-term toxicities
for which long-term monitoring is required.
Vernakalant is a relatively new antiarrhythmic medication approved in the European Union for chemical
cardioversion of recent-onset atrial fibrillation (duration
of ≤ 7 days for nonsurgical patients and ≤ 3 days for
post–cardiac surgery patients). Vernakalant is thought
to act by blocking potassium channels that control early
repolarization, including the ultra-rapid component of
the delayed rectifier current (IKur). In the Atrial Arrhythmia Conversion Trials (ACT-I and ACT-III), vernakalant
compared with placebo was associated conversion to
sinus rhythm in approximately 51% of patients [83,84].
There were serious adverse events in both trials, including one patient with severe aortic stenosis in ACT-III
who experienced hypotension and ventricular fibrillation
and died. The ACT 5 was a confirmatory Phase 3 trial
that was halted due to a patient who developed cardiogenic shock. This medication is not approved by the FDA
due to these serious adverse effects, especially hypotension in some patients.
Maintenance of Sinus Rhythm
Maintenance of sinus rhythm with antiarrhythmic medications or ablation represents the next treatment goal in
patients who remain symptomatic from atrial fibrillation
even after stroke risk reduction has been addressed and
attempts at adequate rate control have been made. The
reasons to consider rhythm control as a long-term strategy include bothersome symptoms despite adequate rate
control and, potentially, to improve ventricular function
in selected patients with LV dysfunction believed to be
due to atrial fibrillation. While it is intuitive that rhythm
control may reduce cardiovascular mortality or decrease
risk of stroke, it should be remembered that these endpoints have not been shown to improve with rhythm
control. The Pharmacological Intervention in AF (PIAF)
trial demonstrated that rate control was not inferior to
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rhythm control to improve symptoms and quality of
life [71]. The AF Follow-up Investigation of Rhythm
Management (AFFIRM) trial randomized 4060 atrial
fibrillation patients at high risk of stroke and death to
rhythm or rate control and demonstrated no significant
difference in all-cause mortality between the treatment
arms [72]. However in a post-hoc analysis of AFFIRM,
the presence of sinus rhythm was associated with a significant mortality benefit, whereas the use of antiarrhythmic
medications was associated with an increase in mortality
[85]. These trials stress that rhythm control is indicated
to control AF-related symptoms despite adequate rate
control. While antiarrhythmic medications are associated
with drug-related side effects and toxicities, these medications are indicated as first-line therapies for rhythm
control and worth discussing before ablation.
Choice of an initial antiarrhythmic medication is
often dictated by the presence of structural heart disease,
coronary artery disease, or heart failure as outlined in
Figure 4. In addition, the presence of accompanying
renal, hepatic, lung, or other systemic disease also guides
the initial choice of an appropriate antiarrhythmic medication. Importantly, all antiarrhythmic medications have
both potential toxicities and risk of proarrhythmia, and
the risk/benefit ratio of antiarrhythmic drug therapy
should be considered by clinicians and patients prior to
initiation of treatment.
For patients with a structurally normal heart, either flecainide or propafenone is an appropriate initial
medication choice. This includes patients with hypertension but without left ventricular hypertrophy. Several
placebo-controlled trials demonstrated that flecainide
and propafenone delay the recurrence of atrial fibrillation [86–88]. Dofetilide and sotalol also represent
reasonable choices for patients with structurally normal
hearts [79,89]; however, the QT interval and renal
function should be carefully monitored during an inpatient drug initiation. Sotalol should be used with caution in patients with reactive airway disease and heart
failure.
For patients with coronary artery disease, sotalol
has significant beta-blocking activity and represents the
initial choice for maintenance of sinus rhythm [90].
Amiodarone may represent a reasonable alternative but
given the risk of long-term toxicities, it should not be
used initially [91]. Finally, dofetilide has been shown
to be safe in this population but inpatient monitoring
is required [92]. The class Ic agents should not be used
Vol. 20, No. 4 April 2013 JCOM 173
Atrial fibrillation
Maintenance of Sinus Rhythm
No (or minimum) heart disease
Hypertension
Coronary artery
disease
Heart failure
Flecainide Propenone Sotalol
Substantial LVH
Dofetilide
Sotalol
Amiodarone Dofetilide
Yes
No
Amiodarone Dofetilide
Catheter
ablation
Flecainide Propenone Sotalol
Amiodarone Dofetilide
Catheter
ablation
Amiodarone
Amiodarone
Catheter
ablation
Catheter
ablation
Catheter
ablation
Figure 4. Choice of antiarrhythmic medications for maintenance of sinus rhythm based on presence of underlying structural
heart disease. (Modified from 2011 ACC/AHA/ESC Focused Update on Atrial Fibrillation.)
in patients with coronary artery disease given the previously increased mortality risk observed in the CAST trial,
though it should be noted that propafenone was not used
in this trial [93].
In patients with heart failure (LVEF < 35%), dofetilide
and amiodarone should be used to prevent episodes of
atrial fibrillation. In the Congestive Heart Failure Survival
Trial of Antiarrhythmic Therapy trial, amiodarone was
associated with greater likelihood of conversion to sinus
rhythm and improved survival compared to placebo [94].
In the Danish Investigators of Arrhythmias and Mortality
on Dofetilife in Heart Failure trial, patients treated with
dofetilide were more likely to maintain sinus rhythm compared to those receiving placebo. The risk of proarrhythmias (torsades de pointes) occurred in 3.3% of patients
receiving dofetilide and occurred within the first 3 days
of therapy [95]. Class Ic agents, sotalol, and dronedarone
should be avoided in patients with heart failure.
174 JCOM April 2013 Vol. 20, No. 4
Hypertension and associated left ventricular hypertrophy (LVH) are common among patients with atrial
fibrillation. Ventricular ectopy can be common in LVH,
and therefore class III antiarrhythmic medications,
which further prolong repolarization, should not be used
in LVH. In patients without LVH, class Ic agents and
amiodarone are favored. However, in patients with LVH,
only amiodarone and dronedarone have been shown to
be safe, where the QT prolonging activity of these medications does not increase the risk of proarrhythmia.
Although dronedarone has been shown to be safe
and effective in patients with atrial fibrillation, it does
deserve special consideration given that several of the
trials leading to its release and postmarket research have
indicated that this medication may not be appropriate
for all patient groups [96,97]. In the EURIDIS and
ADONIS trials, which tested the efficacy of dronedarone compared with placebo in patients with normal LV
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Clinical Review
function, dronedarone was more effective at maintaining
normal rhythm and controlling ventricular rates when
atrial fibrillation recurred [98]. There was no difference
in the rate of adverse effects in the dronedarone group
with the exception of an increased serum creatinine. In
the Effect of Dronedarone on Cardiovascular Event in
Atrial Fibrillation (ATHENA) trial, dronedarone was associated with a 24% relative risk reduction of the primary
endpoint of all-cause mortality or cardiovascular hospitalization [99]. For the most part, patients in ATHENA
had normal left ventricular function with only 11.9%
having a LVEF < 45%. These trials contrast with those
performed in patients with persistent atrial fibrillation
or heart failure. The PALLAS trial tested the effect of
dronedarone compared to placebo on major vascular and
cardiovascular events in permanent atrial fibrillation and
found that dronedarone was associated with increased
rates of heart failure, stroke and cardiovascular mortality
[96]. Patients included in the PALLAS trial were at least
65 years old and had at least 1 risk factor for a vascular
event and included approximately 20% of patients with a
LVEF ≤ 40%. In patients with severe heart failure (LVEF
≤ 35%), the ANDROMEDA study demonstrated an increased mortality associated with dronedarone compared
to placebo that was mostly associated with worsening
heart failure. The FDA has also reported rare liver failure
associated with dronedarone use. Currently dronedarone
is FDA-approved to reduce the risk of hospitalization in
patients with paroxysmal or persistent atrial fibrillation,
with special warnings in patients with advanced heart
failure and permanent atrial fibrillation.
Ablation for Atrial Fibrillation
Ablation for atrial fibrillation is assuming a more prominent role in the treatment algorithm for maintenance of
normal sinus rhythm. The goal of ablation is to isolate
atrial tachycardias that degenerate into atrial fibrillation
and are for the most part located in the pulmonary veins
(PV) [3,100]. Focal firing from the pulmonary veins
originate from muscular sleeves that extend from the
left atrium into the pulmonary veins [3]. There is also
evidence that action potentials are shorter in the pulmonary veins due to larger delayed-rectifier K+ currents and
smaller inward Ca2+ currents in the PV [101,102]. As
atrial fibrillation progresses from paroxysmal to persistent, ion channel remodeling occurs, which may increase
the activity of triggers to perpetuate the rhythm and
subsequently results in structural changes within the atria
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[103,104]. Ablation around the pulmonary veins, or PVI
or pulmonary vein antral isolation (PVAI), is the common ablation strategy for paroxysmal atrial fibrillation
and part of the ablation strategy for persistent atrial fibrillation. Surgical options for ablation of atrial fibrillation
also exist, including both cut-and-sew approaches and
also ablation-assisted approaches; in the hands of at least
some surgeons, these Cox-Maze III and IV procedures
are associated with greater than 85% freedom from atrial
fibrillation at 2 years among patients with lone paroxysmal atrial fibrillation [105].
There is some data to suggest that an ablation strategy may lead to superior patient outcomes compared
with antiarrhythmic medications. In a nonrandomized
study, Pappone et al compared ablation (PVI) to antiarrhythmic therapy and found that ablation was associated
with decreased all-cause mortality, less stroke and heart
failure, and improved quality of life [106]. Since this was
a nonrandomized, single-center trial, these results should
be considered preliminary. Wazni et al randomized 70
patients to first-line ablation (PVI) or antiarrhythmic
medication and found less atrial fibrillation recurrence
and improved symptoms in the ablation group [107].
Wilber et al found similar decreased atrial fibrillation
recurrence and improved quality of life in the ablation
group among 167 patients randomized to ablation or
antiarrhythmic medication who had previously failed one
treatment [108].
Although these results are encouraging, larger trials
are needed before ablation can be recommended for all
atrial fibrillation patients and to investigate if there are
other benefits besides symptom relief. The CABANA
(Catheter Ablation versus Antiarrhythmic Drug Therapy
for Atrial Fibrillation) trial is an ongoing multicenter trial
funded by the National Heart Lung and Blood Institute
that compares ablation to current antiarrhythmic medications for the treatment of atrial fibrillation. Eligible
patients are over 65 years of age or less than 65 years old
with 1 stroke risk factor. The primary endpoint is total
mortality with a composite secondary endpoint of mortality, stroke, serious bleeding, and cardiac arrest. The
Safety of Atrial Fibrillation Ablation Registry Initiative
(SAFARI) is a national registry effort that, if successfully
implemented, will track the real-world safety and durability of the procedure [109].
The most recent Heart Rhythm Society guidelines
recommend ablation for symptomatic paroxysmal atrial
fibrillation for patients who have failed at least one
Vol. 20, No. 4 April 2013 JCOM 175
Atrial fibrillation
Class 1 or 3 antiarrhythmic medication (recommendation
class I) [110]. Ablation of persistent and long-standing
atrial fibrillation that is symptomatic for patients who
have failed at least 1 antiarrhythmic medication is also
considered reasonable, though with a lower strength of
recommendation (class IIa and IIb, respectively). For
patients undergoing cardiac surgery for another indication, surgical ablation is reasonable, regardless of whether
patients have failed an antiarrhythmic medication (recommendation class: paroxysmal IIa, persistent IIb). Surgical
ablation is also recommended as a stand-alone procedure
for patients who prefer a surgical approach (recommendation class IIb). The guidelines emphasize that the primary
goal of ablation for atrial fibrillation is for symptom relief
in patients who are adequately rate controlled.
Conclusion
Atrial fibrillation is the most common cardiac arrhythmia encountered in clinical practice. It has many
different presentations and may occur in isolation or in
association with other medical conditions. Therefore,
the approach to newly diagnosed atrial fibrillation
needs to be individualized based on the patient’s comorbidities. Treatment options are evolving and focus
on prevention of systemic thromboembolism, rate
control, and rhythm control.
Corresponding author: Paul D. Varosy, MD, VA Eastern
Colorado Health Care System, Cardiology Section (111B),
1055 Clermont St., Denver, CO 80220, [email protected].
Financial disclosures: None.
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