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Prevention of embolization prior to and after restoration of

sinus rhythm in atrial fibrillation
Authors: Robert Phang, MD, FACC, FHRS, Warren J Manning, MD
Section Editors: Bradley P Knight, MD, FACC, Brian Olshansky, MD, N A Mark Estes, III, MD
Deputy Editor: Gordon M Saperia, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2019. | This topic last updated: May 29, 2019.

INTRODUCTION

Spontaneous or intended conversion of atrial fibrillation (AF) to sinus rhythm is associated with a
short-term increase from the baseline risk of clinical thromboembolism. This topic will discuss
management strategies that attempt to decrease this risk for patients who are not receiving long-
term anticoagulant therapy. Many of these patients will have newly diagnosed AF (see "New onset
atrial fibrillation") or will have had prior episodes of AF but had a prior decision to not receive long-
term oral anticoagulation due to either a low CHA2DS2-VASc score (table 1) or a very high bleeding
risk.

The modalities used to perform cardioversion, long-term anticoagulation in patients with AF, and
an overview of the management of AF are presented separately. (See "Atrial fibrillation:
Cardioversion to sinus rhythm" and "Atrial fibrillation: Anticoagulant therapy to prevent
thromboembolism" and "Overview of atrial fibrillation".)

EXTREMELY HIGH-RISK PATIENTS

Patients with atrial fibrillation and valvular heart disease, especially rheumatic heart disease/mitral
stenosis and prosthetic heart valves, are at extremely high risk of thromboembolization at all
times, not just at the time of cardioversion. The approach to anticoagulation in such patients is
discussed in other UpToDate topics. (See "Antithrombotic therapy for surgical prosthetic heart
valves and surgical valve repair: Indications" and "Overview of the management of mitral stenosis",
section on 'Prevention of thromboembolism'.)
RATIONALE FOR ANTICOAGULATION

All patients with atrial fibrillation (AF), whether it be paroxysmal, persistent, or permanent, have an
increased risk of embolization compared with those without AF. (See "Atrial fibrillation: Risk of
embolization", section on 'Epidemiology'.)

At the time of reversion to sinus rhythm (SR), whether pharmaceutical, electrical, or spontaneous,
there is an incremental increase from the baseline risk. Most embolic events occur within 10 days
of reversion to SR [1-5]. Patients undergoing cardioversion of AF of more than 48 hours duration
represent a particularly high-risk group (compared with AF of less than 48 hours duration), with an
embolic risk from as low as 1 to as high as 5 percent in the first month after reversion to SR in the
absence of anticoagulation [2-4,6-8]. This rate is substantially higher than the rate that would be
calculated for the general population of patients with AF, in whom the yearly rate is between 1.3
and 5.1 (or higher) percent, depending on age and additional comorbidities. (See "Atrial fibrillation:
Risk of embolization", section on 'Epidemiology'.)

The most common source of stroke associated with cardioversion in these patients is embolism
of a thrombus from the left atrial appendage during or in the first two weeks after the procedure.
Possible causes include embolism at the time of conversion of a left atrial thrombus that was
already present, embolism of a thrombus that formed after conversion due to post-conversion
worsening of left atrial mechanical function, and thrombus formation from subsequent episodes
of AF:

● Pre-cardioversion left atrial thrombus. Embolization after return of synchronous atrial

contraction is due to the dislodgement of left atrial thrombi present at the time of
cardioversion.

The rate of left atrial thrombus in patients studied with transesophageal echocardiography
(TEE) has been between 12 and 14 percent with AF duration of less than 72 hours [9,10].
These values, which did not differ in those with AF of ≤2 days and two to three days duration,
are similar to the 12 to 13 percent incidence noted above in TEE studies of patients with new
onset AF of more than two days duration [11,12].

The prevalence is increased in high-risk patients with severe left ventricular systolic
dysfunction, left atrial enlargement, depressed left atrial appendage ejection velocity, or left
atrial appendage spontaneous echo contrast (a marker of stasis).

● Post-cardioversion left atrial appendage contractile dysfunction/stunning that has been

described with spontaneous, pharmacologic, and electrical conversion. This post-
cardioversion mechanical dysfunction creates a milieu that promotes new thrombus
formation. The transient atrial contractile dysfunction after cardioversion is referred to as
atrial "stunning" and can occur whether SR is restored spontaneously, by external or internal
 direct current cardioversion, or by antiarrhythmic medications. The duration of the left atrial
contractile dysfunction appears to be related in part to the duration of AF prior to
cardioversion. Recovery of atrial mechanical function may be delayed for several weeks [13],
especially for those who have been in AF for a few months prior to cardioversion. In
comparison, for those with AF for only a few days, recovery is within a day. (See
"Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm", section
on 'Atrial stunning'.)

There have been case reports and series of patients developing de novo left atrial thrombi
(primarily in the setting of no anticoagulation) immediately following cardioversion, when the
screening TEE showed no pre-cardioversion left atrial thrombi [9,14-16]. (See "Role of
echocardiography in atrial fibrillation", section on 'Spontaneous echo contrast' and "Mechanisms
of thrombogenesis in atrial fibrillation".)

● Recurrent AF is common during the first month after conversion [17]. Up to 90 percent of
these episodes are asymptomatic [18], and asymptomatic episodes lasting more than 48
hours are not uncommon, occurring in 17 percent of patients in a report using continuous
monitoring [17]. Anticoagulation during the four weeks post-cardioversion thereby provides
prophylaxis against new thrombus formation and facilitates early cardioversion without a
screening transesophageal echocardiogram.

The rationale and indications for chronic anticoagulation after the period of post-conversion
anticoagulation are similar to those for the broad population of patients with AF and are discussed
separately. (See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism", section on
'Summary and recommendations'.)

Patients with spontaneous conversion — Some patients with AF have spontaneous conversion

prior to planned cardioversion. There is no evidence that they are at lower risk of subsequent
embolization in the first few weeks after conversion compared with patients who undergo
electrical or chemical cardioversion. In all these circumstances, the risk is relatively low, but the
risk during this time is likely higher than the ambient rate of thromboembolic events associated
with AF. The risk is extremely low in an individual with a CHA2DS2-VASc scores of 0 or 1 (table 1),
but the risk is not zero.  

In a study of 1041 patients who were anticoagulated prior to and after cardioversion, 16 percent
experienced spontaneous conversion (prior to planned electrical cardioversion). The rate of
thromboembolism was similar between patients with and without spontaneous conversion [19].

We believe that spontaneous cardioversion should not alter the anticoagulant strategy, and that
continuation of long-term anticoagulation should be guided by the CHA2DS2-VASc score, as well
as consideration of the individual's long-term bleeding risk [20].
URGENT CARDIOVERSION

Patients with new onset atrial fibrillation (AF) in whom the ventricular rate is rapid may require
urgent (or emergent) cardioversion to prevent adverse clinical consequences such as
hemodynamic decompensation. (See "Overview of atrial fibrillation", section on 'Treatment
issues'.)

The indications for urgent cardioversion of AF are uncommon, but in the setting of hemodynamic
instability due to rapid AF that is refractory to pharmacologic support, such as in patients with
Wolff-Parkinson-White syndrome, the need for restoration of sinus rhythm may take precedence
over the need for protection from thromboembolism. When possible, the patient should receive
pre-cardioversion anticoagulation as soon as possible, and it should be continued for at least four
weeks post-cardioversion, unless it is contraindicated [20]. (See 'AF of less than 48 hours duration'
below.)

AF OF MORE THAN 48 HOURS DURATION

Patients with atrial fibrillation (AF) of more than 48 hours duration should receive at least three
weeks of therapeutic oral antithrombotic therapy prior to an attempt at cardioversion. In these
patients, the risk of thromboembolism after cardioversion can be diminished to less than 1
percent (during the four weeks after cardioversion) by the use of three weeks of therapeutic
antithrombotic therapy prior to (and extending for four weeks after) cardioversion [2-4,6,7,21-23].
Some experts extend anticoagulation for four weeks pre-cardioversion.

For patients in whom there is a reason to not wait three weeks, an option for management is pre-
cardioversion anticoagulation of shorter (less than one month) duration in conjunction with a
screening transesophageal echocardiogram (TEE) to guide early cardioversion. This strategy can
be used for patients in whom cardioversion needs to be performed either urgently or before four
weeks of therapeutic anticoagulation have been completed (but when the patient is fully
anticoagulated) [12]. While the TEE approach shortens the pre-cardioversion duration of
anticoagulation, it does not change our recommendation for four weeks of anticoagulation after
cardioversion or the need to be therapeutically anticoagulated at the time of the cardioversion.
(See 'Transesophageal echocardiography-based approach' below.)

Prospective studies have shown that the risk of clinical stroke or systemic embolism ranges from
0 to 0.9 percent if preceded by at least three weeks of anticoagulation with warfarin or one of the
non-vitamin K oral anticoagulants (NOACs; also referred to as direct oral anticoagulants [DOAC])
[2-4,12], or the TEE-guided approach discussed directly above. Retrospective data demonstrated
that the risk is 4 to 7 percent in non-anticoagulated patients [7,8,24].  
Anticoagulant approach — Since many patients will require long-term anticoagulation, we prefer
the NOACs to warfarin before and after cardioversion (see "Atrial fibrillation: Anticoagulant therapy
to prevent thromboembolism", section on 'Choice of agent'). While the use of warfarin prior to
cardioversion has been studied to a longer extent than the NOACs, we believe there is sufficient
evidence to believe that they are as effective and as safe as warfarin in this setting.

Advantages of the NOAC include convenience (no international normalized ratio [INR] testing
required) and the possibility of a shorter duration of pre-cardioversion anticoagulation in very
compliant patients since it often takes five to six weeks for the patient to have at least four weeks
of effective anticoagulation with warfarin.

The following data are available for the NOACs:

● Dabigatran – In a post-hoc analysis of the RE-LY trial, which compared dabigatran with
warfarin, in which there were 1983 cardioversions in 1270 participants, there was no
significant difference in the rate of thromboembolism and stroke within 30 days between
those who received at least three weeks of dabigatran 110 or 150 mg twice daily or warfarin
(0.8, 0.3, and 0.6 percent, respectively) [2].

● Apixaban – In a post-hoc analysis of the ARISTOTLE trial, which compared apixaban with
warfarin, 743 cardioversions were performed in 540 patients. No strokes or systemic
embolism occurred during the 30-day follow-up period of both warfarin and apixaban groups
[3]. (See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism", section on
'Select an anticoagulant'.)

● Rivaroxaban – In the X-VeRT study, 1504 patients with AF of unknown or longer than 48 hours
duration were randomly assigned in a 2:1 manner to cardioversion after at least three weeks
of rivaroxaban or a vitamin K antagonist. There was no statistically significant difference in
the rate of the primary efficacy outcome (a composite of stroke, transient ischemic attack,
peripheral embolism, myocardial infarction, and cardiovascular death) or the safety outcome
of major bleeding (0.51 versus 1.02 percent and 0.6 percent versus 0.8 percent, respectively)
[4].

Similarly, in a post-hoc analysis of the ROCKET-AF trial, which compared rivaroxaban with
warfarin, 143 patients underwent 181 electric cardioversions, 142 patients underwent 194
pharmacologic cardioversions, and 79 patients underwent 85 catheter ablations. There was
no significant difference in the long-term rate of stroke or systemic embolism (hazard ratio
1.38; 95% CI 0.61-3.11) [25]. (See "Atrial fibrillation: Anticoagulant therapy to prevent
thromboembolism", section on 'Select an anticoagulant'.)

● Edoxaban – In the ENSURE-AF trial, 2199 patients were randomly assigned to receive
edoxaban or enoxaparin and warfarin with discontinuation of enoxaparin when the INR was
>2.0 [5]. There was no significant difference in the primary efficacy end point (0.5 percent in
 the edoxaban group versus 1 percent in the enoxaparin–warfarin group; odds ratio [OR] 0.46,
95% CI 0.12–1.43). The primary safety end point occurred in 1.6 percent of the edoxaban
group versus 1.1 percent in the enoxaparin–warfarin group (OR 1.48, 95% CI 0.64–3.55). The
results were independent of the TEE-guided strategy and anticoagulation status.

In patients in whom compliance with a NOAC is questionable/missed doses leading up to the

cardioversion, we often obtain pre-cardioversion TEE to exclude an atrial (appendage) thrombus.
Routine pre-cardioversion TEE is not recommended for patients who have been therapeutically
anticoagulated (INR 2.0 or greater) with warfarin for three weeks or who have been compliant with
their daily NOAC. (See 'Transesophageal echocardiography-based approach' below.)

Compliance with warfarin can be ascertained with INR monitoring. For patients started on
warfarin, the target INR should be 2.5 (range 2.0 to 3.0), and cardioversion should not take place
until an INR of 2.0 or greater has been documented for at least four consecutive weeks (figure 1
and figure 2) [26,27].

Therapeutic anticoagulation prior to cardioversion appears to be effective largely due to thrombus

resolution, rather than organization and adherence of left atrial thrombi [28,29]. (See 'Rationale for
anticoagulation' above.)

Transesophageal echocardiography-based approach — We suggest a TEE-based approach (table

2A-B) for symptomatic patients and for patients for whom there is a concern about a three-week
(or more) delay to cardioversion. Such a concern might arise from a preference to not have
ongoing symptoms or a possible lower likelihood of successful cardioversion with a longer period
of AF. Other individuals for whom this strategy may be reasonable include those at high bleeding
risk, as the TEE-guided approach shortens the total pre-cardioversion anticoagulation time for
those without thrombus; and those at highest risk for a cardioversion-related thromboembolic
event, including prior thromboembolism and elderly women with diabetes and heart failure.
Patients who require hospitalization are also candidates for this approach [30,31]. This
recommendation for a limited use of the TEE-based approach is based on our concerns about
cost, the small potential for complications, and the possibility of worse outcomes.  

In a TEE-based approach, the imaging study is performed after therapeutic anticoagulation (of
short duration) and prior to anticipated cardioversion. Patients without evidence of left and right
atrial (specifically the left atrial appendage, which is the site for the vast majority of thrombi)
thrombus proceed to cardioversion. If thrombus is found (or cannot be confidently excluded) on
TEE, cardioversion should not be performed, and therapeutic anticoagulation should be continued
for at least four weeks after which time we recommend that a TEE be repeated (to screen for
residual thrombus, which would be a contraindication to cardioversion) if cardioversion is desired.

Observational studies have suggested that patients with AF of more than 48 hours duration can be
acutely anticoagulated with heparin/oral anticoagulant and proceed directly to cardioversion
without prolonged anticoagulation if no atrial thrombus is seen on pre-cardioversion TEE (table 2A-
B) [11,32-34]. The ACUTE trial compared a TEE-guided strategy with a conventional strategy
(including therapeutic warfarin [INR 2.0 to 3.0] anticoagulation for at least three weeks prior to
electrical cardioversion) in 1222 patients with AF of more than two days duration (median duration
13 days) who were undergoing electrical cardioversion [12,35]. Patients assigned to the TEE-
guided strategy were anticoagulated with heparin before TEE if they were inpatients or with oral
warfarin for five days (target INR 2.0 to 3.0) before TEE if they were outpatients. TEE was then
followed by cardioversion if no atrial thrombi were identified. With both approaches, warfarin
therapy was continued for four weeks after cardioversion. If the initial TEE demonstrated
thrombus (which was present in 12 percent), cardioversion was postponed and patients received
therapeutic (INR 2.0 to 3.0) anticoagulation for three weeks, at which time a repeat TEE was
performed. Patients assigned to conventional strategy received three weeks of therapeutic
anticoagulation before cardioversion.

The following findings were noted:

● Within the eight weeks after study enrollment, there was no significant difference between the
TEE and conventional groups in the incidence of ischemic stroke (0.6 versus 0.3 percent,
respectively; relative risk [RR] 1.95, 95% CI 0.36-10.60) or all embolic events, including stroke,
transient ischemic attack, and peripheral embolism (0.8 versus 0.5 percent, respectively; RR
1.62, 95% CI 0.39-6.76). One important difference is that the majority of thromboembolic
events in the TEE arm occurred in patients who had reverted back to AF and/or had a
subtherapeutic INR at the time of the event, while the thromboembolic events in the warfarin
arm occurred in patients with SR with a therapeutic INR.

● There were significantly fewer hemorrhagic events with the TEE strategy (2.9 versus 5.5
percent), but no significant difference in the incidence of major bleeding (0.8 versus 1.5
percent) [12,36]; in addition, there was no significant difference in all-cause mortality (2.4
versus 1 percent) or cardiac deaths (1.3 versus 0.7).

● The TEE strategy led to a shorter mean time to cardioversion (3 versus 31 days) and a greater
incidence of successful restoration of SR (71 versus 65 percent).

Thromboembolism has been reported after a negative pre-cardioversion TEE in some patients who
were not therapeutically anticoagulated at the time of TEE and for one month after cardioversion
[9,14,15]. These adverse events may be related to the limited sensitivity of TEE for small thrombi,
or to new thrombus formation that has been reported during the period between TEE and
cardioversion or after cardioversion [9,14,15]. Thus, we recommend therapeutic anticoagulation
with warfarin or NOAC or, if necessary, heparin for all patients undergoing a TEE-based approach
before cardioversion.
The development of impaired left atrial mechanical function and of new thrombi after
cardioversion provides the rationale for four weeks of therapeutic anticoagulation after
cardioversion (INR 2.0 to 3.0), even when the pre-cardioversion TEE shows no thrombus [15,16].
There is suggestive evidence that such an approach reduces the incidence of embolic events [16].
(See 'Rationale for anticoagulation' above.)

Although the results of the ACUTE study discussed above raise concerns about possible worse
outcomes in patients treated with this strategy [30], some experts have suggested that the TEE
strategy is a reasonable alternative to a conventional approach in some patients, such as those
with a strong preference for early cardioversion, those with AF of less than three to four weeks
duration who would benefit most from left atrial mechanical recovery, and those at increased risk
of hemorrhagic complications (as the duration of pre-cardioversion anticoagulation may be
shortened). Another potential reason to consider this strategy is that a shorter period of AF may
increase the likelihood of successful cardioversion and long-term maintenance of SR. (See "Atrial
fibrillation: Cardioversion to sinus rhythm", section on 'Electrical cardioversion'.)

The TEE approach should include the following sequential steps before cardioversion:

● For inpatients, the options include using heparin plus warfarin or using an NOAC. With the
former, we administer either low molecular weight or unfractionated heparin (bolus and
continuous drip with a goal partial thromboplastin time 1.5 to 2 times control) and
simultaneously initiate oral warfarin (target INR 2.0 to 3.0). With the latter, we give at least two
doses of a NOAC. As the pharmacokinetics of the NOACs are different than warfarin, the
combination of a heparin plus NOAC may lead to supratherapeutic anticoagulation. We do not
recommend overlap of or combined use of heparin and a NOAC.

● For most outpatients, we prefer NOAC to warfarin. There are multiple factors that determine
whether a NOAC or warfarin would be used, including cost and patient preference, but NOACs
have the advantage of faster onset of action and ease of dosing. A strategy of at least two
days of NOAC prior to TEE-guided cardioversion can be used. As an alternative, oral warfarin
can be started five days before TEE with the target INR 2.0 to 3.0 [12]. A minimal pre-
cardioversion INR of 2.0 is acceptable, though 2.5 may be preferred.

● Obtain a TEE to assess for the presence of atrial thrombi. The use of an endocardial border
definition echo contrast agent may help in cases where there is uncertainty about the
presence or absence of thrombus [37].

If no thrombus is seen, proceed with cardioversion. Continue therapeutic anticoagulation from

the time of TEE through cardioversion and extend for another four weeks.

If a thrombus is seen on TEE, the patient should receive a minimum of four weeks of
therapeutic anticoagulation and a repeat TEE to document thrombus resolution if
cardioversion is desired [28]. If no cardioversion is desired, a follow-up TEE is not needed, as
 the patient should receive lifelong antithrombotic therapy. If thrombus is absent on repeat
TEE, cardioversion may be performed. If thrombus is still evident, the rhythm control strategy
may be changed to a rate control strategy, especially when AF-related symptoms are
controlled, since there is a high risk of thromboembolism if cardioversion is performed.
However, the evidence supporting this latter recommendation of avoidance of cardioversion
with a residual thrombus is minimal.

It is best to be conservative with at least three weeks of pre-cardioversion oral anticoagulant if

an atrial thrombus cannot be confidently excluded on TEE.

● Continuous oral anticoagulation (warfarin INR 2.0 to 3.0 or full-dose NOAC) for at least four
weeks after cardioversion in all eligible patients, regardless of the cardioversion method,
CHA2DS2-VASc score, or apparent maintenance of SR. In patients who have not achieved
therapeutic anticoagulation with warfarin at the time of cardioversion, unfractionated or low
molecular weight heparin should be continued until the INR is therapeutic.

Recommendations of others — Our recommendations our broadly in agreement with those from

the American Heart Association/American College of Cardiology/Heart Rhythm Society, the
European Society of Cardiology, and the European Heart Rhythm Association [20,38-40].

AF OF LESS THAN 48 HOURS DURATION

The overall embolic risk appears to be very low if cardioversion (either intended or spontaneous)
occurs within 48 hours of the onset of atrial fibrillation (AF) [41-43]. However, we believe that
many, and perhaps most, patients cannot accurately define the onset of AF. As a result, we label a
patient as having AF of less than 48 hours duration only if we have a high level of confidence in the
patient’s history. Otherwise, we approach the patient as if AF has been present for more than 48
hours.

The choice of 48 hours for the cut-off is arbitrary and based on limited evidence. For example, the
prevalence of left atrial thrombus on transesophageal echocardiography (TEE) is substantially
lower when the duration of AF is less than 48 hours (1.4 percent) [44]. Some of our experts are
comfortable recommending early cardioversion only if the duration is less than 24 hours. This
shorter duration is based on limited evidence suggesting the risk of embolic events is significantly
greater after 24 hours compared with 6 to 24 hours [45].

However, an attempt at cardioversion does not apply to extremely high-risk patients (eg,
rheumatic/valvular disease; severe left ventricular dysfunction; prosthetic valves; or prior
thromboembolism, heart failure, or diabetes). In these patients, we anticoagulate for four weeks
prior to an attempt at cardioversion based on the rationale presented above.
Anticoagulation with heparin or a newer oral anticoagulant (NOAC) with TEE is an alternative
approach for these high-risk patients prior to cardioversion.

Even with a history of AF of less than 48 hours in duration, there is likely a range of risk based on
CHA2DS2-VASc score (table 1). A retrospective study of 3143 patients with AF of less than 48
hours duration demonstrated that patients with heart failure and diabetes were at high risk for
clinical thromboembolism (up to 10 percent if both risk factors were present). The absence of
both risk factors and age <60 years conveyed a very low risk of 0.2 percent [43]. (See 'AF of more
than 48 hours duration' above and 'Rationale for anticoagulation' above.)

There are two central clinical questions with regard to the use of anticoagulant therapy in patients
where the duration of the episode is definitely less than 48 hours and early cardioversion is being
considered:

● Should an anticoagulant be used prior to restoration of sinus rhythm (and if so, which one)?

● Should an oral anticoagulant be given for four weeks after restoration of sinus rhythm?

Anticoagulation prior to cardioversion — For patients in whom cardioversion will take place in less
than 48 hours, we start a NOAC in all patients with a CHA2DS2-VASc score ≥1 rather than no
anticoagulant. Intravenous heparin is a reasonable alternative for hospitalized patients (see
below). If cardioversion needs to take place within six hours, whether for patient instability or
convenience, we start intravenous heparin or a low molecular weight heparin; we do not give
NOAC and heparin together. (See 'Urgent cardioversion' above.)

For patients at very high bleeding risk, some of our experts suggest cardioversion without
anticoagulation if normal sinus rhythm can be restored within 48 hours of documented onset.
Other experts recommend anticoagulation prior to cardioversion even in these high-bleeding-risk
patients.

We generally wait to cardiovert until six hours after the first dose of a NOAC. When a NOAC is
used, the specific choice of NOAC should be individualized for each patient. We generally choose
the agent that will be given at the time of discharge. (See 'Anticoagulation after reversion to sinus
rhythm' below.)  

For the rare patient in whom heparin anticoagulation is chosen rather than NOAC, we administer
either low molecular weight heparin (1 mg/kg subcutaneously every 12 hours) or unfractionated
heparin (bolus and continuous drip goal partial thromboplastin time 1.5 to 2.0 times control). If a
heparin is used, warfarin is started simultaneously and the heparin is continued until the
international normalized ratio exceeds 2.0.

With regard to the question as to whether to anticoagulate these patients or not, there are no
studies comparing heparin with no heparin in patients with AF of less than 48 hours duration.
However, data regarding the rate of clinical thromboembolization after cardioversion in patients
with AF of less than 48 hours duration have raised a concern about the safety of cardioversion
without anticoagulation in this population. In an observational study of 2481 such individuals
(5116 successful cardioversions) who were not treated with peri- or post-procedural anticoagulant,
definite thromboembolic events occurred in 38 (0.7 percent) within in 30 days (median of two
days); of these, 31 were strokes [43]. Four additional patients suffered a transient ischemic attack.
Age greater than 60 years, female sex, heart failure, and diabetes were the strongest predictors of
embolization, with nearly 10 percent of those with both heart failure and diabetes experiencing a
stroke. The risk of stroke in those without heart failure and age less than 60 years was 0.2 percent.
An observational study of 16,274 patients undergoing direct current cardioversion with and
without oral anticoagulant therapy also demonstrated that the absence of post-cardioversion
anticoagulation was associated with a high risk of thromboembolism, regardless of CHA2DS2-
VASc scores [46]. There was a greater-than-twofold increased risk of thromboembolism in those
not treated with post-cardioversion anticoagulation (hazard ratio 2.21; 95% CI 0.79-6.77 and 2.40;
95% CI 1.46-3.95 with CHA2DS2-VASc score 0 to 1 and CHA2DS2-VASc score 2 or more,
respectively). The rationale for lack of post-cardioversion anticoagulation could not be exactly
discerned in this trial but was deemed to be multifactorial, including presumed short-duration AF,
perceived low thromboembolic risk, and lack of guideline adherence.  

With regard to the question of which anticoagulant to use, there are no studies comparing differing
forms of heparin in patients with AF of short duration nor are there studies comparing a NOAC
with heparin. Indirect evidence comparing the two heparins comes from a trial of 496 patients with
AF of more than 48 hours duration who were randomly assigned to either low molecular weight
heparin or unfractionated heparin followed by oral anticoagulation [47]. Patients were cardioverted
after either 21 days of anticoagulation or after a TEE that was negative for thrombus;
anticoagulation continued for 28 days after cardioversion. Low molecular weight heparin was
noninferior to unfractionated heparin followed by oral anticoagulation in terms of the combined
primary end point of ischemic neurologic events, major hemorrhage, or death by the end of study
treatment (2.8 versus 4.8 percent). Low molecular weight heparin also has a safety and efficacy
profile similar to unfractionated heparin when used as a bridge to oral anticoagulation in patients
undergoing TEE-based therapy [48].

Anticoagulation after reversion to sinus rhythm — Though unproven in efficacy, some of our

contributors recommend anticoagulation for four weeks after reversion to sinus rhythm (either
spontaneous or intended) for patients with AF of less than 48 hours duration, even for those with a
low CHA2DS2-VASc score. The rationale for this approach is a concern regarding the high
likelihood of AF recurrence in the first month after reversion to sinus rhythm, as well as transient
post-cardioversion atrial stunning in the immediate pericardioversion period. This decision may be
modified in patients at very high bleeding risk.

Some of our contributors are comfortable not anticoagulating after restoration of sinus rhythm if
AF was less than 48 hours duration and the CHA2DS2-VASc score is 0 in men and 1 in women
[43,49]. Similarly, careful decision-making needs to occur in patients at very high bleeding risk.
(See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism", section on 'Estimating
bleeding risk'.)

We recommend that continuation of long-term anticoagulation should be guided by the CHA2DS2-

VASc score, as well as consideration of the individual's long-term bleeding risk. (See "Atrial
fibrillation: Anticoagulant therapy to prevent thromboembolism", section on 'Our approach to
anticoagulation'.)

Recommendations of others — Our recommendations are broadly in agreement with those from

the American Heart Association/American College of Cardiology/Heart Rhythm Society, the
European Society of Cardiology, and the European Heart Rhythm Association [20,38-40].

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and
"Society guideline links: Arrhythmias in adults".)

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The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on “patient info” and the keyword(s) of interest.)

● Beyond the Basics topic (see "Patient education: Atrial fibrillation (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Conversion of atrial fibrillation (AF) to sinus rhythm (SR), either spontaneously or intended, is
associated with a clinically important transient increase in the risk of thromboembolism,
 particularly stroke. This risk increases significantly after 48 hours of AF and can be lowered by
therapeutic anticoagulation before cardioversion. (See 'Rationale for anticoagulation' above.)

● The following recommendations apply to patients with AF of less than 48 hours duration (see
'AF of less than 48 hours duration' above):

• For patients with prior thromboembolism, heart failure, or diabetes, we suggest deferral
of cardioversion to allow for three weeks of effective pre-cardioversion anticoagulation
rather than early cardioversion (Grade 2C).

Anticoagulation with heparin or a non-vitamin K oral anticoagulant (NOAC; also referred

to as direct oral anticoagulants [DOAC]) before, during, and after cardioversion with
transesophageal echocardiography (TEE) is an alternative approach for these high-risk
patients prior to cardioversion.

• For patients not at high risk of thromboembolism (listed in the above bulleted
recommendation), we anticoagulate all patients with a CHA2DS2-VASc score ≥1 (Grade
2C). We start either NOAC or a combination of heparin and warfarin prior to
cardioversion.

For patients with low risk of thromboembolism (CHA2DS2-VASc score 0 in men, 1 in

women), our experts have differing approaches regarding post-cardioversion
anticoagulation, with some using four weeks of post-cardioversion warfarin or NOAC
anticoagulation and others not.

● The following recommendations apply to patients with AF of more than 48 hours duration or
when the duration is unknown (see 'AF of more than 48 hours duration' above):

• We recommend a minimum of three consecutive weeks of therapeutic anticoagulation

(warfarin with an international normalized ratio [INR] greater than 2.0 or NOAC) prior to
cardioversion, rather than proceeding directly to cardioversion (Grade 1B).  

• We recommend a NOAC prior to elective cardioversion rather than warfarin irrespective of

whether the anticoagulant will be given long term (Grade 1B). (See 'Anticoagulant
approach' above.)

• For symptomatic patients in whom there is a strong preference to not delay

cardioversion, or in whom there is a concern about bleeding with prolonged oral
anticoagulation, or who are not likely to tolerate AF despite adequate rate slowing, a TEE
strategy is a reasonable approach using therapeutic anticoagulation with
heparin/warfarin or NOAC throughout the pericardioversion period. (See
'Transesophageal echocardiography-based approach' above.)
 • We recommend therapeutic oral anticoagulation (warfarin with INR 2.0 to 3.0 or a NOAC)
for four weeks after cardioversion in all patients, rather than discontinuing
anticoagulation after cardioversion (Grade 1B).

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30. Silverman DI, Manning WJ. Strategies for cardioversion of atrial fibrillation--time for a
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31. Seto TB, Taira DA, Tsevat J, Manning WJ. Cost-effectiveness of transesophageal
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32. Klein AL, Murray RD, Grimm RA. Role of transesophageal echocardiography-guided
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34. Manning WJ, Silverman DI, Keighley CS, et al. Transesophageal echocardiographically
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36. Klein AL, Murray RD, Grimm RA, et al. Bleeding complications in patients with atrial fibrillation
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37. Jung PH, Mueller M, Schuhmann C, et al. Contrast enhanced transesophageal

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40. Heidbuchel H, Verhamme P, Alings M, et al. Updated European Heart Rhythm Association
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valvular atrial fibrillation: Executive summary. Eur Heart J 2016.

41. Gallagher MM, Hennessy BJ, Edvardsson N, et al. Embolic complications of direct current
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42. Weigner MJ, Caulfield TA, Danias PG, et al. Risk for clinical thromboembolism associated
with conversion to sinus rhythm in patients with atrial fibrillation lasting less than 48 hours.
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43. Airaksinen KE, Grönberg T, Nuotio I, et al. Thromboembolic complications after cardioversion
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44. Kleemann T, Becker T, Strauss M, et al. Prevalence of left atrial thrombus and dense
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48. Klein AL, Jasper SE, Katz WE, et al. The use of enoxaparin compared with unfractionated
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Clin Electrophysiol 2016; 2:487.

Topic 906 Version 56.0

GRAPHICS
Clinical risk factors for stroke, transient ischemic attack, and systemic embolism
in the CHA 2 DS 2 -VASc score

(A) The risk factor-based approach expressed as a point based scoring system, with
the acronym CHA 2 DS 2 -VASc
(NOTE: maximum score is 9 since age may contribute 0, 1, or 2 points)
CHA 2 DS 2 -VASc risk factor Points

Congestive heart failure +1

Signs/symptoms of heart failure or objective evidence of reduced
left ventricular ejection fraction

Hypertension +1
Resting blood pressure >140/90 mmHg on at least two occasions or
current antihypertensive treatment

Age 75 years or older +2

Diabetes mellitus +1
Fasting glucose >125 mg/dL (7 mmol/L) or treatment with oral
hypoglycemic agent and/or insulin

Previous stroke, transient ischamic attack, or thromboembolism +2

Vascular disease +1
Previous myocardial infarction, peripheral artery disease, or aortic
plaque

Age 65-74 years +1

Sex category (female) +1

(B) Adjusted stroke rate according to CHA 2 DS 2 -VASc score

CHA 2 DS 2 -VASc score Patients Stroke and thromboembolism
(n = 73,538) event rate at one-year follow-up
(%)

0 6369 0.78

1 8203 2.01

2 12,771 3.71

3 17,371 5.92

4 13,887 9.27

5 8942 15.26

6 4244 19.74

7 1420 21.50

8 285 22.38

9 46 23.64

CHA 2 DS 2 -VASc: Congestive heart failure, Hypertension, Age (≥75) (doubled), Diabetes, Stroke (doubled), Vascular
disease, Age (65-74), Sex.

Part A from: Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC Guidelines for the management of atrial fibrillation
developed in collaboration with EACTS. Europace 2016; 18(11):1609-1678. By permission of Oxford University Press on
behalf of the European Society of Cardiology. Copyright © 2016 Oxford University Press. Available at: www.escardio.org/.

Graphic 83272 Version 21.0

Optimal INR which minimizes both bleeding and
thromboembolism in patients with atrial fibrillation

(A) Odds ratios (ORs) for thromboembolism (TE, 396 cases, 1581 controls) and intracranial
hemorrhage (ICH, 164 cases, 656 controls) by INR level in adults with nonvalvular atrial
fibrillation, with 8 INR categories using INR 2.0 to 2.5 as the referent. Vertical bars
indicate 95 percent confidence intervals (CIs). The numbers of cases and controls for each
INR category are given below the figure.
(B) ORs for TE (396 cases, 1581 controls) and ICH (164 cases, 656 controls) by INR level
in adults with nonvalvular AF, with 6 INR categories using INR 2.0 to 2.5 as the referent.
Vertical bars indicate 95 percent CIs. The numbers of cases and controls for each INR
category are given below the figure.

Reproduced with permission from: Singer DE, Chang Y, Fang MC, et al. Should patient
characteristics influence target anticoagulation intensity for stroke prevention in nonvalvular
atrial fibrillation? The ATRIA study. Circ Cardiovasc Qual Outcomes 2009; 2:297. Copyright ©
2009 Lippincott Williams & Wilkins.

Graphic 65373 Version 12.0

Odds ratios for ischemic stroke and intracranial bleeding in
relation to intensity of anticoagulation

Adjusted odds ratios for ischemic stroke and intracranial bleeding in relation to
intensity of anticoagulation.

Reproduced with permission from: Fuster V, Ryden LE, Cannom DS, et al. 2011
ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 Guidelines for
the management of patients with atrial fibrillation: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines
developed in partnership with the European Society of Cardiology and in collaboration with
the European Heart Rhythm Association and the Heart Rhythm Society. Circulation 2011;
123:e269. Copyright © 2011 Lippincott Williams & Wilkins.

Graphic 87025 Version 4.0

Advantages and disadvantages of the conventional approach to cardioversion
(one month of pretreatment with warfarin) in patients with atrial fibrillation

Advantages Disadvantages
Use of warfarin for one month before cardioversion Delaying cardioversion to normal sinus rhythm for one month
may lower the stroke rate from 5.6 percent to a potentially decreases functional capacity.
very low stroke rate of <2 percent.

Relatively easy to administer with regular Prolonging treatment for seven to eight weeks one month
monitoring of INRs. prior to and one month after cardioversion increases the risk
of bleeding complications.

Suitable for community hospitals. Not followed by routine clinical practice, especially in the
elderly.

The conventional approach has withstood the "test Patients who are at the highest risk for developing systemic
of time" since the 1960s. embolization who should receive more prolonged or intensive
anticoagulation are not routinely identified.

Reprinted with permission from the American College of Cardiology. J Am Coll Cardiol 2001; 37:691.
https://www.journals.elsevier.com/journal-of-the-american-college-of-cardiology.

Graphic 72971 Version 6.0

Advantages and disadvantages of the transesophageal echocardiography-guided
approach to cardioversion of patients with atrial fibrillation undergoing
cardioversion

Advantages Disadvantages
Transesophageal echocardiography (TEE) should be able TEE is performed without any definitive guidelines about
to detect left atrial appendage thrombi, which increase who should receive the procedure (high versus low risk)
the risk of embolic stroke after electrical cardioversion,
thus sparing patients with thrombi from undergoing
cardioversion

In the majority of patients without left atrial appendage Residual thrombus on repeat TEE may diminish the cost-
thrombi, earlier cardioversion may shorten the period of effectiveness of the TEE-guided approach
anticoagulation and lower the corresponding risk of
bleeding complications

A TEE-guided approach may prove more cost-effective Transesophageal echocardiography requires a level III-
owing to the reduction in laboratory monitoring costs trained physician and availability of expensive
and the reduction in bleeding complications echocardiographic machines

Earlier cardioversion is believed to increase the Transesophageal echocardiography may miss thrombi
likelihood of a successful return to and maintenance of that may embolize after cardioversion. In contrast, TEE
sinus rhythm may render false positive results by erroneously
identifying spontaneous echocardiographic contrast,
sludge, multilobed appendages or pectinate muscles as
thrombus.

Reprinted with permission from: The American College of Cardiology. J Am Coll of Cardiol 2001; 37:691-704.
https://www.journals.elsevier.com/journal-of-the-american-college-of-cardiology.

Graphic 54077 Version 6.0

Contributor Disclosures
Robert Phang, MD, FACC, FHRS Speaker's Bureau: Bristol-Myers Squibb; Pfizer [Stroke prevention in
NVAF (Apixaban)]. Warren J Manning, MD Patent Holder: Samsung Electronics [MRI]. Equity
Ownership/Stock Options: Pfizer [Anticoagulants]. Equity Ownership/Stock Options (Spouse): General
Electric [Cardiac imaging]. Bradley P Knight, MD, FACC Grant/Research/Clinical Trial Support: BSCI; MDT;
Abbott; Biotronik; Biosense Webster [EP (implantable devices and ablation tools)]. Speaker's Bureau:
BSCI; MDT; Abbott; Biotronik; Biosense Webster [EP (implantable devices and ablation tools)]; Baylis
Medical. Consultant/Advisory Boards: BSCI; MDT; Abbott; Biotronik; Biosense Webster; Apama Medical
[EP (implantable devices and ablation tools)]. Brian Olshansky, MD Speaker’s Bureau: Lundbeck
[Orthostatic hypotension (Droxidopa)]. Consultant/Advisory Boards: Lundbeck [Orthostatic hypotension
(Droxidopa)]; Sanofi Aventis; Respircardia. Other Financial Interest: Amarin [Hypertriglyceridemia (EPA;
Chair, Data and Safety Monitoring Board)]; Boehringer Ingelheim [Atrial fibrillation (GLORIA AF trial)]. N A
Mark Estes, III, MD Consultant/Advisory Boards: Medtronic [Arrhythmias (Pacemakers and ICDs)]; St Jude
Medical [Arrhythmias (Pacemakers and ICDs)]; Abbott [Arrhythmias (Pacemakers and ICDs)]; Boston
Scientific [Arrhythmias (Pacemakers and ICDs)]. Gordon M Saperia, MD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
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