For chronic therapy, oral negative dromotropic agents (usually a β-blocker or
nondihydropyridine calcium-channel blocker) are recommended. If higher dose
monotherapy with one of these drugs is needed to control symptoms but is associated
J.K. has signs of mild HF, so digoxin is a reasonable choice, although short-term
IV diltiazem is often used in this type of patient as well. IV verapamil and β-blockers
may worsen the signs and symptoms of HF, and the β-blockers may mask signs of
hypoglycemia in J.K. The goal of rate control should be a resting heart rate between
60 and 80 beats/minute and an exercising heart rate between 90 and 115
7 A recent study has explored the use of a more lenient target resting
heart rate (<110 beats/minute) and reported similar patient outcomes as compared
with a more strict target heart rate (resting heart rate <80 beats/minute).
may suggest that it could be acceptable for a patient’s heart rate to be greater than 80
beats/minute, if there is difficulty in achieving this level of heart rate control and in
asymptomatic patients or those with HF and a preserved EF.
Rate Control versus Rhythm Control
CASE 15-1, QUESTION 7: After loading of digoxin, J.K.’s heart rate is still 120 beats/minute and he
will be successfully converted to normalsinus rhythm?
The use of a rhythm control strategy has become much less common during the last
several years. This change is because of the completion of several studies comparing
the effect of a rate or rhythm control strategy on patient outcomes.
study (Atrial Fibrillation Follow-up Investigation of Rhythm Management), a
randomized, multicenter study, was one of the largest to compare rate control with
rhythm control for management of AF. AFFIRM enrolled 4,060 patients with AF and
27 The primary end point was all-cause mortality. Antiarrhythmic
drugs were chosen at the discretion of the treating physician, but greater than 60% of
the patients received amiodarone or sotalol as the initial antiarrhythmic agent. Rate
control agents included digoxin, β-blockers, and nondihydropyridine calcium-channel
blockers. After a mean follow-up of 3.5 years, there was a trend toward lower
overall mortality (p = 0.08) with significant reductions in hospitalizations (10%
lower; p = 0.001) and TdP (300% lower; p = 0.007) in the rate control group.
Therefore, using rhythm control in patients with AF rather than rate control does not
improve outcomes and increases the risk of hospitalizations and TdP.
The default long-term treatment strategy for most patients should be a rate control
strategy, in which heart rate is controlled and anticoagulation is provided, if
indicated. However, rhythm control is necessary when patients experience symptoms
despite adequate rate control, when heart rate cannot be adequately controlled with
currently available treatments, or if patients cannot tolerate the adverse effects of
rate-controlling medications. J.K.’s heart rate is not adequately controlled with
digoxin and an oral β-blocker. A nondihydropyridine calcium-channel blocker could
be added or the β-blocker dose could be increased in order to better control his heart
rate; however, his BP may not tolerate the increased dose of the β-blocker or the
addition of a nondihydropyridine calcium-channel blocker. Therefore, pursuit of a
rhythm control strategy is warranted.
Likelihood of successful conversion to, and maintenance of, normal sinus rhythm is
determined by the duration of the arrhythmia, underlying disease processes, and left
33 Duration of AF for more than 1 year significantly reduces the chances of
maintaining a normal sinus rhythm.
34 When the atrial size exceeds 5 cm, there is less
than a 10% chance of maintaining normal sinus rhythm at 6 months. J.K.’s chance of
being maintained in normal sinus rhythm is good because the duration of his AF is
short and the echocardiogram revealed only slight enlargement of his left atrium.
Conversion to Normal Sinus Rhythm
determine whether cardioversion can be performed, and why is warfarin therapy being used?
When the onset of AF is less than 48 hours, the likelihood of atrial clot formation
is low. However, if patients are at a high risk for stroke, they should receive an
anticoagulant (unfractionated heparin, low-molecular-weight heparin, factor Xa, or
direct thrombin inhibitor) as soon as possible surrounding the cardioversion,
followed by long-term anticoagulation.
7 When the duration of AF is greater than 48
hours, or if duration is unknown, then an oral anticoagulant agent (warfarin,
dabigatran, factor Xa inhibitor) should be given for 3 weeks before cardioversion at
doses providing an INR between 2 and 3 if using warfarin.
AF showed that those who were anticoagulated with warfarin before cardioversion
had a lower incidence (0.8%) of emboli than those who were not anticoagulated
35 Alternatively, a TEE can be used to determine whether atrial clots have
7,36 Atrial clots form most often in small side pouches on the atria called atrial
37 Because the frequency of right atrial appendage thrombosis is half that
of left atrial appendage thrombosis in AF patients, the risk of stroke is enhanced
much more than the risk of pulmonary embolism.
If no clot is observed on TEE, then there is low risk for stroke with cardioversion
36 However, if an atrial clot is evident on TEE, J.K. would need to be
3 weeks before cardioversion to prevent embolization of the clot and stroke. If
cardioversion is successful, patients should remain on an oral anticoagulant agent for
at least 4 weeks after cardioversion because normal atrial contraction may not return
for up to 3 weeks, and patients may be at risk of late embolization.
provide long-term oral anticoagulation is dependent on the patient’s underlying
stroke and bleeding risk. This will be discussed further below.
Chemical Conversion—Ibutilide, Propafenone, Flecainide
How does ibutilide therapy compare with the other therapeutic choices for chemical cardioversion?
The most effective method of cardioversion is by direct current (DC)
cardioversion (see Electrical Cardioversion section below). However, the use of DC
cardioversion may be undesirable if the patient is a poor candidate for conscious
sedation or if the patient is not willing to undergo DC cardioversion. In these
situations, pharmacologic cardioversion may be attempted. Many class I and III
antiarrhythmic agents have been evaluated for efficacy in placebo-controlled trials
for conversion of AF or atrial flutter to normal sinus rhythm. The available agents
with the most positive data for chemical conversion include IV ibutilide, oral
propafenone, oral flecainide, oral and IV amiodarone, and oral dofetilide. This
section will focus on ibutilide, propafenone, and flecainide.
IV ibutilide, a class III antiarrhythmic agent with potassium-channel blocking and
slow sodium-channel enhancing effects, was the first agent that the US Food and Drug
Administration (FDA) approved for the termination of recent-onset AF and atrial
Ibutilide is administered as a 1-mg infusion for 10 minutes, followed by
another 1-mg infusion for 10 minutes if conversion has not occurred by 10 minutes
after the infusion. The conversion rate for recent-onset AF is 35% to 50%; the
conversion rate is 65% to 80% in atrial flutter. In a retrospective study of hospital
inpatients with either AF or atrial flutter, 50% of patients converted initially (41%
conversion AF, 65% atrial flutter), but only 33% of patients left the hospital in sinus
rhythm. If the duration of AF or atrial flutter before cardioversion was fewer than 15
days, significantly more patients remained in sinus rhythm at discharge compared
with patients who had AF or atrial flutter for more than 15 days before
40 As is the case with most class III antiarrhythmic agents, the main
adverse effect is TdP, which occurred in approximately 4% of patients. Ibutilide
should be avoided in patients with hypokalemia, hypomagnesemia, QT prolongation,
and a low ejection fraction (<30%). Aside from the risk of TdP, therapy is well
Propafenone is a class Ic agent with β-blocking properties. When given in doses of
450 to 750 mg orally (600 mg was the most common dose), the initial conversion rate
in patients with AF ranged from 41% to 57%. In contrast to ibutilide, no patients
experienced ventricular arrhythmias (including TdP), but a risk of hypotension,
bradycardia, and QRS prolongation was noted.
Oral flecainide is another class Ic antiarrhythmic agent. In one study, 300 mg oral
flecainide converted 68% of patients to sinus rhythm within 3 hours and 91% of
patients by 8 hours. The efficacy in atrial flutter has yet to be established. Sinus node
dysfunction, prolongation of intraventricular conduction, dizziness, weakness, and
gastrointestinal (GI) disturbances have been reported.
A β-blocker or nondihydropyridine calcium-channel antagonist should be
administered ≥30 minutes before administering the Vaughan Williams class Ic agent
to prevent a rapid ventricular response due to 1:1 AV conduction during atrial
7 J.K. is not a candidate for these agents due to his structural heart disease.
hours. What is electrical cardioversion? How efficacious and safe is it?
DC cardioversion quickly and effectively restores 85% to 90% of patients with
If DC conversion alone is ineffective, it can be repeated
in combination with antiarrhythmic drugs.
In one study, the success rate of
electrical cardioversion was significantly higher in AF patients (duration of AF
averaged 119 days) with ibutilide pretreatment (1 mg) compared with those without
pretreatment (100% vs. 72%; p = 0.001).
49 This is because ibutilide pretreatment
lowered the energy requirement for atrial defibrillation by 27% (p = 0.001). TdP
occurred in 3% of patients receiving ibutilide, all of whom had an ejection fraction
less than 20%. Flecainide, propafenone, amiodarone, and dofetilide could also be
considered for enhancing DC cardioversion.
DC cardioversion is clearly indicated for patients who are hemodynamically
unstable. A reason one may wish to avoid DC conversion is because anesthesia
(short-acting benzodiazepine, barbiturate, or propofol) is required for the procedure.
CASE 15-1, QUESTION 11: J.K. is discharged after successful DC conversion. However, when he returns
the best option for this patient?
To choose the best antiarrhythmic agent for J.K., the efficacy and adverse effect
profiles for each agent should be reviewed. Class Ia, Ic, and III antiarrhythmic drugs
(see Tables 15-2 and 15-3) prevent the recurrence of AF. Flecainide, sotalol,
dofetilide, and dronedarone are approved by the FDA for maintenance of sinus
rhythm. Propafenone and amiodarone are commonly used as well.
The class Ic agents flecainide and propafenone are effective in suppressing AF.
The efficacy rate may be as high as 61% to 92% for flecainide.
possibly other class Ic agents are proarrhythmic, especially in patients with structural
heart disease, and they should be avoided in such patients. Propafenone, a class Ic
agent with β-blocking properties, is as efficacious as flecainide and is relatively safe
in patients without ischemic heart disease and an ejection fraction greater than 35%;
it may be preferred in patients who require additional AV blockade to control
ventricular response. In a direct comparison with flecainide (200–300 mg/day),
propafenone (450–900 mg/day) was equally safe and effective. Over the course of 12
months, a similar percentage of patients (approximately 12% in each group) did not
have adequate control of their arrhythmia. Adverse events were comparable and
occurred in 10.3% of patients on flecainide and 7.7% of patients on propafenone. Of
all the adverse events noted, only one patient who was receiving propafenone
developed a ventricular arrhythmia. Another 1-year comparative study of
propafenone versus flecainide demonstrated similar efficacy, but this study showed a
trend toward better tolerability in the flecainide group.
antiarrhythmic medications in the hospital?
Class III agents (sotalol, dofetilide, amiodarone, dronedarone) prolong
refractoriness in the atria, ventricles, AV node, and accessory pathway tissue and can
prevent recurrence of AF. All of these agents act by blocking potassium channels;
however, sotalol also has additional β-blocking properties.
dronedarone block sodium channels and calcium channels, and have antiadrenergic
effects in addition to potassium-channel blocking properties.
Sotalol, Amiodarone, Dofetilide, and Dronedarone
62 The median times to recurrence were 27, 106, 229, and
175 days with placebo, sotalol 160 mg/day (divided in two doses), sotalol 240
mg/day (divided in two doses), and sotalol 320 mg/day (divided in two doses),
respectively. Sotalol is contraindicated in patients with a creatinine clearance (CrCl)
of less than 40 mL/minute because of the fact that the drug is largely renally cleared
and can cause TdP in high concentrations. In a comparative study versus
propafenone, sotalol was similarly effective in producing at least a 75% reduction in
AF recurrence (79% of patients on propafenone vs. 76% on sotalol). Bradycardia,
dizziness, and GI disturbances were the most common intolerable side effects.
Sotalol should not be used in patients with systolic heart failure owing to the negative
inotropic effects of the drug. It may be useful as a first-line agent in patients with AF
and concomitant underlying coronary artery disease or in patients with no
Amiodarone is more effective at maintaining sinus rhythm than sotalol and
64 The Canadian Trial of Atrial Fibrillation (CTAF) compared the
ability of low-dose amiodarone (200 mg/day) versus propafenone (450–600 mg/day)
and sotalol (160–320 mg/day) to prevent recurrence of AF.
of 16 months, 35% of the amiodarone-treated patients had a recurrence of AF versus
63% in the combined group with sotalol and propafenone (p = 0.001). In view of its
unusual pharmacokinetics and potential serious adverse effects (see Table 15-3 and
Case 15-7, Question 2), amiodarone is only recommended as a first-line choice for
patients with HF, for which it has specific safety data, or for patients with significant
7 Amiodarone could also be used when other agents such
as sotalol, propafenone, or dofetilide have failed.
Dofetilide has been shown to be an effective pharmacologic agent for conversion
to, and maintenance of, normal sinus rhythm. Two clinical trials, EMERALD
(European and Australian Multicenter Evaluative Research on Atrial Fibrillation
66 and SAFIRE-D (Symptomatic Atrial Fibrillation Investigation and
Randomized Evaluation of Dofetilide),
67 have shown conversion rates of 30% in
patients with AF or atrial flutter receiving higher doses of dofetilide. Patients failing
chemical conversion received electrical conversion. If this conversion succeeded,
they were continued on dofetilide for 1 year. At 1 year, 60% of those converted were
still in sinus rhythm with the 500-mcg dose. Also, dofetilide appears to exert neutral
effects on mortality rates in HF and post-MI patients.
Dofetilide dose is based on the patient’s CrCl; the doses are 500, 250, and 125
mcg twice daily with CrCl greater than 60, 40 to 60, and 20 to 39 mL/minute,
respectively. Drug interactions pose a significant problem with dofetilide.
Cimetidine, ketoconazole, prochlorperazine, megestrol, and trimethoprim (including
in combination with sulfamethoxazole) inhibit active tubular secretion of dofetilide
and can elevate dofetilide plasma concentrations.
60 Because the incidence of TdP is
directly related to dofetilide plasma concentrations, concomitant use with these
70 Concomitant administration of dofetilide with verapamil
or hydrochlorothiazide increases the incidence of TdP by an unclear mechanism and
60 Concurrent use of agents that can prolong the QTc
interval is not recommended with dofetilide.
70 Dofetilide also undergoes metabolism
by the cytochrome P-450 CYP3A4 isoenzyme to a minor extent. Therefore, inhibitors
of this isoenzyme (e.g., azole antifungal agents, protease inhibitors, serotonin
reuptake inhibitors, amiodarone, diltiazem, nefazodone, zafirlukast) should be
coadministered with caution with dofetilide. Other agents that can potentially
increase dofetilide levels (through inhibition of tubular secretion) include metformin,
triamterene, and amiloride. Hence, these agents should be cautiously coadministered
Dofetilide is considered a first-line agent for patients with heart failure or
coronary artery disease, as the impact on mortality in this patient population is
7 Dofetilide can also be considered as a first-line agent for patients without
cardiovascular disease, but should be avoided in patients with severe left ventricular
Dronedarone is structurally and pharmacologically similar to amiodarone;
however, it lacks iodine, and it has a much smaller volume of distribution than
61 Dronedarone has been shown to have modest
efficacy in maintaining sinus rhythm when compared with placebo. The rate of
recurrence of AF at 1 year is approximately 40%, and the number of days to
recurrence is nearly doubled with dronedarone.
71 The major clinical trial evaluating
dronedarone was the ATHENA study. The primary end point of ATHENA was a
composite of death or cardiovascular hospitalization, and patients received either
dronedarone 400 mg twice daily or placebo for at least 1 year.
composite end point was significantly reduced from 39.4% with placebo to 31.9%
with dronedarone. This reduction in the composite was completely attributable to the
reduction in cardiovascular hospitalizations, most of which were related to AF
recurrence. GI events were the most common type of adverse effect with dronedarone
in this study. It should be noted that patients with recent decompensated HF or New
York Heart Association (NYHA) class IV heart failure were excluded from this trial.
The exclusion of patients with severe or unstable heart failure was related to
negative findings that led to the early discontinuation of the ANDROMEDA study.
ANDROMEDA was designed as a safety study, to evaluate the impact of
dronedarone on mortality in patients with HF. Patients admitted with NYHA class III
or IV systolic HF were included in this study. The study was stopped early because
of an approximate doubling in the risk of death with dronedarone as compared with
placebo. Therefore, dronedarone is contraindicated in a patient with severe or
recently decompensated HF. Based on the findings of the PALLAS study,
dronedarone should be avoided in patients with permanent AF as well.
found that the rate of stroke, heart failure, and cardiovascular death was increased
when dronedarone was used in this patient population. Dronedarone has also been
compared directly with amiodarone.
In this study, dronedarone was less effective
than amiodarone, but was less likely than amiodarone to cause thyroid, neurologic,
skin, or ocular adverse effects. GI adverse effects were more common with
75 Dronedarone is appropriate as a first-line agent for patients with AF
and concomitant coronary artery disease, and possibly left ventricular
hypertrophy or in patients with no cardiovascular disease. Dronedarone should not
be used in a patient with severe HF symptoms or a recent hospitalization for HF, but
may be used with mild, well-controlled HF.
In view of J.K.’s HF, sotalol, propafenone, and flecainide would not be indicated.
Although dronedarone may be better tolerated than amiodarone, it would be
contraindicated because J.K. was recently admitted with decompensated HF.
Therefore, the only available options for J.K. would be either dofetilide or
amiodarone, both of which have been proven safe in patients with HF. Selection
between dofetilide and amiodarone could be based on renal function, the presence of
any major drug interactions, or the desire to avoid adverse effects with amiodarone.
Dofetilide was approved with the requirement for in-hospital initiation because of
the relatively high risk of TdP in clinical trials. ECG monitoring is required for
patients being initiated on dofetilide for a minimum of 3 days in a properly equipped
facility. The initial regimen is determined by the patient’s estimated CrCl. The QTc
interval must be measured (using a 12-lead ECG) 2 to 3 hours after the first dose and
each subsequent dose while the patient is hospitalized. If the QTc interval increases
by greater than 15% or if it surpasses 500 ms (>550 ms in patients with ventricular
conduction abnormalities) after the first dose, the dofetilide regimen should be
reduced by 50%. If the QTc interval exceeds the above parameters any time after the
second subsequent dose, dofetilide should be discontinued.
Sotalol may also be arrhythmogenic in high doses, and the risk of inducing TdP has
prompted its manufacturer to mandate a minimum of 3 days of ECG monitoring in a
properly equipped facility during therapy initiation as well.
initiation and titration, QTc intervals should be monitored 2 to 4 hours after each
dose. In fact, most antiarrhythmic agents for AF should probably be initiated in the
inpatient setting, with the exception of amiodarone owing to the low risk of
remain on warfarin therapy? Could any other antithrombotic options be considered?
Patients with nonvalvular and valvular AF have a 5- and 17-fold increased risk for
stroke compared with patients without AF, respectively.
4,5 Stroke can lead to death or
significant neurologic disability in up to 71% of patients, with an annual recurrence
In three large, randomized trials, patients with nonvalvular AF benefited from
In the Stroke Prevention in Atrial Fibrillation (SPAF)
study, both aspirin 325 mg/day and warfarin (titrated to an INR of 2.0–4.5) reduced
the risk of stroke significantly with an acceptable level of hemorrhagic
80 The results of SPAF II, a direct comparison of warfarin and aspirin,
indicated that warfarin was more effective than aspirin in preventing stroke.
results were verified by the Copenhagen AFASAK study, which found warfarin to be
significantly better than aspirin and placebo at preventing cerebral emboli and
overall vascular deaths (cerebral and cardiovascular).
antagonist (dabigatran) and oral factor Xa antagonists (rivaroxaban, apixaban,
edoxaban) are now available. These newer anticoagulant agents have been shown to
have similar or better efficacy and safety compared to warfarin.
Dabigatran is approved by the FDA to reduce the risk of stroke and systemic
embolism in patients with nonvalvular AF.
In the Re-Ly trial, dabigatran 110 mg
twice daily and 150 mg twice daily was compared with warfarin in patients with a
CHADS2 score of 1 or more (average CHADS2 score of 2.1). The CHADS2 score is
a tool used to estimate stroke risk. In this study the lower dose of dabigatran was
noninferior to warfarin for stroke prevention but was associated with less bleeding.
High-dose dabigatran was superior to warfarin for stroke prevention but comparable
86 The most common nonbleeding adverse event in this study was GI
upset. It should also be noted that dabigatran capsules should not be chewed or
The three oral factor Xa inhibitors that are currently approved for prevention of
stroke and systemic embolus in patients with AF include rivaroxaban, apixaban, and
edoxaban. Each of these agents have been compared directly to warfarin using fairly
82–84 Rivaroxaban and edoxaban were found to be noninferior to
warfarin in stroke/systemic embolus prevention, while apixaban was found to be
superior to warfarin in efficacy. Major bleeding occurred less frequently with
edoxaban and apixaban and at a similar rate with rivaroxaban, compared to warfarin.
Although efficacy and safety of all of the new agents differed when compared with
warfarin, there are no direct comparisons between any of the newer antithrombotic
options. As such, no firm conclusions can be drawn regarding the optimal agent to
choose. However, in a patient who is perceived to have a high bleeding risk, it is
reasonable to select apixaban or edoxaban, given the bleeding risk advantage of these
Some differences between the newer agents could be considered when selecting an
anticoagulant regimen for a patient. For example, each agent has different
recommendations for use with kidney dysfunction. None of the newer oral agents
should be used in patients with a CrCl less than 15 mL/minute. The “renal doses” of
rivaroxaban (15 mg/day with CrCl of 15–49 mL/minute) and edoxaban (30 mg/day
with CrCl of 15–50 mL/minute) were evaluated in the ROCKET AF and ENGAGE
AF TIMI 48 studies, whereas the renal dose adjustment recommended for dabigatran
(75-mg twice daily dose for those with a CrCl of 15–30 mL/minute) was based on
extrapolated pharmacokinetic data.
82,84,87 Apixaban does not require dosage
adjustment based on a CrCl, but adjustment should occur if the patient has two or
more high-risk characteristics (body weight <60 kg, serum creatinine >1.5 or age >80
years). Interestingly, edoxaban is less effective and should not be used when CrCl is
greater than 95 mL/minute. Therefore, edoxaban, apixaban, or rivaroxaban may be a
more evidence-based option than dabigatran for a patient with poor kidney function
and edoxaban would be an inappropriate choice for the patient with very good kidney
The drug interaction profiles of the oral direct thrombin inhibitor or oral factor Xa
inhibitors are favorable compared to that of warfarin. All of the newer anticoagulant
options interact with rifampin. Rivaroxaban and apixaban also interact with other
strong inhibitors and inducers of both the P-glycoprotein and CYP 3A4 systems.
Dabigatran interacts with inhibitors of P-glycoprotein (ketoconazole, dronedarone);
however, no change in therapy is required unless the interacting drugs are used in a
patient who also has a CrCl less than 50 mL/minute. At this time, no notable
interactions have been identified with edoxaban, other than the interaction with
rifampin. Although the number of interactions with the newer anticoagulants is fewer
than with warfarin, it will still be important to evaluate for the presence of
interactions at therapy initiation and when the drug therapy regimen is changed. An
advantage of dabigatran and the oral factor Xa antagonists is that these agents do not
require frequent monitoring and dosage adjustment in order to assure an appropriate
anticoagulation. A potential disadvantage is that it is often not possible to monitor
the extent of anticoagulation in the setting of bleeding or when an urgent procedure or
surgery is needed. In addition, strategies for reversal of these agents are not well
defined, in contrast to the reversal approach with warfarin. Best available evidence
suggests that concentrated blood factor products (4-factor prothrombin complex
concentrates and FEIBA) may be options for reversing the effects of these agents;
however, specific reversal agents are likely to be commercially available in the near
88 Hemodialysis can also be used to remove dabigatran, in the setting of lifethreatening bleeding.
Generally, patients with a CHA2DS2
-VASc score of 2 or greater should receive
anticoagulant therapy for stroke prophylaxis.
7 Warfarin (INR target 2–3), dabigatran,
rivaroxaban, apixaban are all recommended as antithrombotic agents for stroke
7 Edoxaban was not approved at the time of publication of the 2014
guidelines for AF and is not currently included, but has FDA approval. No therapy,
an antithrombotic agent, or aspirin alone could be used in patients with a CHA2DS2
VASc score of 1 and stroke prophylaxis is not required if a patient’s CHA 2DS2
VASc score is 0. If a patient’s INR is difficult to control on warfarin, a direct
thrombin inhibitor or oral Xa antagonist could be used.
patients with AF and valvular disease should only be treated with warfarin for stroke
prophylaxis as data with valvular AF are either unfavorable or unavailable with the
newer agents in this patient population.
Even though J.K. is in normal sinus rhythm at this time, in the AFFIRM trial, only
73% and 63% of patients randomized to rhythm control remained in sinus rhythm at 3
26 As such, the use of an antiarrhythmic drug does not
eliminate the risk of stroke, and in fact, patients may return to AF and not be aware
they are no longer in normal sinus rhythm. J.K. has a CHA2DS2
does not appear to have any factors that would suggest a high bleeding risk (no recent
history of GI bleeding, etc.). Therefore, he should continue to receive anticoagulation
7 Although J.K. is currently taking warfarin, there would be no
reason he could not receive any of the other available anticoagulants.
the treatment of AF and what is the role of radiofrequency catheter ablation for M.P.?
Atrial flutter is an unstable rhythm that often reverts to sinus rhythm or progresses
to AF. If atrial flutter is episodic, its underlying cause should be identified and
treated if possible. If a patient remains in atrial flutter, the treatment goals (control of
ventricular rate, return to normal sinus rhythm) are the same as those for AF. Similar
agents and doses can be used to control the ventricular response. Chemical
conversion, low-energy (<50 J) DC cardioversion, or rapid atrial pacing may acutely
convert atrial flutter back to sinus rhythm, but the recurrence of atrial flutter is high.
Radiofrequency catheter ablation therapy could be used as a nonpharmacologic
treatment for atrial flutter and AF.
7 With both atrial flutter and AF, an EP study is
performed to identify whether ablation can be performed. Various sections of the
atria and pulmonary veins (where they intersect with the atria) are probed with a
catheter that delivers cardiac pacing. If an area is stimulated with pacing and an
atrial ectopic or reentrant focus is recognized, that area could be ablated. Ablation
destroys tissue that is integral either to the initiation or to the maintenance of the
arrhythmia by delivering electrical energy through electrodes on the catheter. If the
focus of the arrhythmia is in the atrial tissue (typically for atrial flutter), then the
focus itself is ablated. This procedure is successful in 75% to 90% of cases and can
the pulmonary veins can often initiate the arrhythmia. In this case, circumferential
ablation, in which a circle of ablated tissue is made around the pulmonary veins, is
performed. Circumferential ablation does not prevent the ectopic impulses from the
pulmonary veins from occurring; however, it does prevent propagation of the impulse
into the atria and may reduce the recurrence of AF. Recent data comparing ablation to
antiarrhythmic drug therapy in patients with PAF suggest that ablation is more
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