Control of ventricular rate in patients with atrial

fibrillation who do not have heart failure:

Pharmacologic therapy
Author: Rachel Kaplan, MD, MS
Section Editor: Bradley P Knight, MD, FACC
Deputy Editor: Susan B Yeon, MD, JD

Contributor Disclosures

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

Literature review current through: Jan 2024. | This topic last updated: Nov 09, 2023.

INTRODUCTION

In patients with atrial fibrillation (AF), the ventricular rate is modulated by the
conduction properties of the atrioventricular (AV) node. In the typical patient with
untreated AF, the ventricular rate can reach 150 beats/min or higher.

The use of pharmacologic therapies to achieve rate control in AF will be reviewed

here. Nonpharmacologic therapies for rate control in AF are discussed separately.
(See "Atrial fibrillation: Atrioventricular node ablation".)

Further information regarding the overall management of patients with AF, including
anticoagulation and choice of rhythm versus rate control, is discussed separately:

● (See "Atrial fibrillation in adults: Use of oral anticoagulants".)

● (See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)
● (See "Atrial fibrillation: Overview and management of new-onset atrial
fibrillation".)
● (See "Management of atrial fibrillation: Rhythm control versus rate control".)

The control of ventricular rate of AF in patients with heart failure is discussed

separately; thus, this topic focuses only on patients with AF who do not have heart
failure. (See "The management of atrial fibrillation in patients with heart failure".)
PATHOPHYSIOLOGY

Atrial fibrillation — During AF, electrical activity in the atria can exceed 400
beats/min. The majority of these impulses do not conduct to the ventricles because of
the electrophysiologic properties of the AV node. (See "Mechanisms of atrial
fibrillation", section on 'Role of the atrioventricular node'.)

AV nodal tissue consists of so-called "slow response" fibers, giving it decremental

conduction properties. In most myocardial tissue, the initial depolarizing phase of the
action potential (phase 0) is mediated by rapid sodium channels. In contrast, in the
slow response fibers of the AV node, phase 0 is mediated by an inward calcium
current, which uses a kinetically slow channel. (See "Cardiac excitability, mechanisms
of arrhythmia, and action of antiarrhythmic drugs".)

The relatively slow kinetics of the inward calcium current limit conduction velocity
through the AV node, and therefore the ventricular rate during AF. In addition to
these intrinsic properties, the AV node is also richly supplied and affected by both
components of the autonomic nervous system. AV conduction is enhanced by
sympathetic fibers and slowed by parasympathetic fibers ( figure 1).

In the typical patient with untreated AF, the ventricular rate during the day varies
between 90 and 170 beats/min. The ventricular rate may be slower (eg, less than 60
beats/min) in the following settings:

● Increased vagal tone

● Drugs that affect AV nodal conduction
● AV nodal disease, which should be suspected if the ventricular rate is below 60
beats/min in the absence of a drug that slows AV conduction

A ventricular rate above 200 beats/min suggests one or more of the following:

● Catecholamine excess
● Enhanced AV nodal conduction
● Parasympathetic withdrawal
● Hyperthyroidism
 ● An accessory pathway as occurs in the preexcitation syndrome (see
"Atrioventricular reentrant tachycardia (AVRT) associated with an accessory
pathway")

Drug mechanisms of action — The ventricular rate in AF is slowed using beta

blockers or calcium channel blockers, and to a lesser extent digoxin or amiodarone. In
general, calcium channel blockers are effective at rest and during exercise, beta
blockers are similarly effective at rest but more effective during exercise, and digoxin
is reasonably effective at rest but less effective than the other drugs during exercise.
Thus, it is particularly important to assess ventricular rate with exertion in patients
treated with digoxin alone. These agents slow AV nodal conduction based upon the
following physiologic mechanisms ( figure 2) [1,2]:

● Calcium channel blockade – Blockade of the calcium channel with the

nondihydropyridine calcium channel blockers verapamil and diltiazem.

● Beta blockade – Decreased sympathetic tone and slowed AV nodal conduction

with beta blockers.

● Enhancement of parasympathetic tone – This is done with vagotonic drugs, the

most important of which is digoxin.

RATIONALE FOR RATE LOWERING

Specific reasons for slowing the ventricular rate in patients with AF include the
following:

● Hemodynamic instability – This may be acute and may require urgent therapy.
This is discussed in detail separately. (See "Hemodynamic consequences of atrial
fibrillation and cardioversion to sinus rhythm".)

● Symptoms – Patients with AF may or may not have associated symptoms, and
the spectrum of symptoms is broad. Typical symptoms include palpitations,
tachycardia, fatigue, weakness, dizziness, lightheadedness, reduced exercise
capacity, increased urination, or mild dyspnea. Symptoms of AF are discussed in
 detail separately. (See "Atrial fibrillation: Overview and management of new-onset
atrial fibrillation", section on 'Symptoms'.)

● Tachycardia-mediated cardiomyopathy – Persistently increased ventricular

rates in AF have been associated with left ventricular cardiomyopathy. While this
issue has not been well studied, we believe that this phenomenon is unlikely to
occur if the ventricular rate is kept below 110 beats/min, which is the
recommended ventricular rate goal. This is discussed in detail separately. (See
"Arrhythmia-induced cardiomyopathy".)

● Potential mortality benefit – There is some evidence to suggest a mortality

benefit from rate control. In a large, population-based cohort study in Taiwan,
mortality in individuals receiving beta blockers (43,879), nondihydropyridine
calcium channel blockers (18,466), and digoxin (38,898) was compared with
mortality in individuals not taking a rate-control drug. Patients were excluded if
they were taking more than one rate-slowing drug. After adjustment for baseline
differences, the risk of death was lower in patients receiving beta blockers
(adjusted hazard ratio [HR] 0.76; 95% CI 0.74-0.78) and calcium channel blockers
(adjusted HR 0.93; 95% CI 0.90-0.96). However, the risk of death was higher in the
group receiving digoxin (adjusted HR 1.12; 95% CI 1.10-1.14). We recommend
caution in applying to clinical practice the findings in this nonrandomized study.

● Spontaneous conversion to sinus rhythm – Some patients whose rate has been
slowed and who then tolerate AF may spontaneously convert to normal sinus
rhythm without the need for electrical cardioversion. Spontaneous conversion is
most likely to occur in patients with a duration of AF of less than 48 hours, or in
patients with a history of short, self-limited episodes [3]. The rate of spontaneous
conversion has been reported to be around 50 percent at 48 hours [3]. In a
retrospective study of 438 patients with AF, if the AF onset was <48 hours,
spontaneous conversion occurred in 77 percent compared with 36 percent in the
group with first onset AF >48 hours [4]. In a separate study of 943 patients,
spontaneous conversion was shown to occur most frequently in patients with
first-onset AF <24 hours, a lower body mass index, and normal left atrial size [5].
EVALUATION AND GOAL VENTRICULAR RATE
● Evaluation and monitoring of ventricular rate – In practice, the ventricular rate
can be assessed by measurement of both the resting ventricular rate and use of
one of the following to assess exercise:

• Six-minute walk test (at moderate exercise) ( table 1).

• Either submaximal or maximal exercise electrocardiogram (ECG) testing. (See

"Exercise ECG testing: Performing the test and interpreting the ECG results".)

• A 24-hour ambulatory monitor can also be used to evaluate efficacy. (See

"Ambulatory ECG monitoring".)

● For patients with an implantable pacemaker or defibrillator, device interrogation

provides useful diagnostic data to assess rate control, including a ventricular rate
histogram during episodes of AF.

For young active patients, we recommend either an exercise ECG test or

ambulatory monitoring during exercise. For older or sedentary patients,
measuring ventricular rate after walking briskly around the office or upstairs may
provide sufficient information. Wearable devices, such as an electronic watch that
connects with a smartphone application, also can provide ventricular rate data.
Caution is advised with relying entirely on photoplethysmography, which may
undersense individual beats in AF and report an inaccurately low heart rate [6].
Heart rate reports should be verified with ECG strips, which may also be
obtainable from some wearable technologies.

These methods of assessing ventricular rate can be used both at the start of therapy
and for long-term follow-up.

In the assessment of ventricular rate control, average ventricular rate is

considered the most important parameter. Ventricular rates during peak exercise
may also be valuable. Assessment of rate control can be confusing when using
monitors that display continuous beat-to-beat ventricular rate rather than
average ventricular rate.
● Goal ventricular rate – The optimal long-term ventricular rate for patients in AF
has not been firmly established [7]. For most symptomatic patients with AF, we
suggest a ventricular rate goal of 85 beats/min. In general, the goal is to control
the rate during activity to prevent or treat symptoms. If the ventricular rate
during AF is faster than would be expected during sinus rhythm and occurs at a
time that correlates with the patient's symptoms, then rate control medications
are usually titrated upwards.

In the subset of patients with AF who are asymptomatic and have permanent AF,
a less strict rate control goal of <110 beats/min may be reasonable. These
patients should be monitored for the development of tachycardia-mediated
cardiomyopathy. (See "Arrhythmia-induced cardiomyopathy".)

Alternative goal rates that are similar to those recommended for patients in sinus
rhythm with heart disease can also be used: resting heart rate ≤80 beats/min and
≤110 beats/min during moderate exercise such as with the six-minute walk. Goals
similar to these were used in many of the trials of rate versus rhythm control,
such as AFFIRM [8]. The AFFIRM study is discussed in detail separately. (See
"Management of atrial fibrillation: Rhythm control versus rate control", section on
'High cardiovascular risk'.)

The prevention of symptoms during normal activities or exercise is a primary goal

of therapy. It is important to consider that symptoms may be due to either
inadequate rate control or relative bradycardia (eg, in patients with tachycardia-
bradycardia syndrome). (See "Sinus node dysfunction: Epidemiology, etiology,
and natural history".)

Thus, for those patients in whom a lenient strategy is chosen but who remain
symptomatic, an attempt should be made to decrease symptoms by setting a
lower rate goal. A more lenient rate-control strategy offers the advantages of less
medication (fewer drug side effects, lower cost) and fewer outpatient visits to
achieve ventricular rate control.

The recommended goal rate is based on the observation that 85 beats/min was
the mean achieved rate for patients assigned lenient rate control in the RACE
study [9]. In this trial of patients with permanent AF, adhering to a strict rather
than lenient rate-control strategy did not improve cardiovascular or safety
outcomes. This study also supports our practice in which achieving strict rate
control is not necessary in many physically active patients with AF who are
minimally symptomatic. In the RACE study, 614 physically active patients with
permanent AF were randomly assigned either lenient rate control (resting heart
rate <110 beats/min) or a strict rate control (resting heart rate <80 beats/min and
heart rate during moderate exercise <110 beats per minute). Patients were
followed for the primary outcome of cardiovascular death, hospitalization for
heart failure, stroke, systemic embolism, bleeding, and life-threatening
arrhythmic events. The following findings were noted:

• Similar efficacy of lenient and strict rate control – After three years, the
estimated cumulative incidence of the primary outcome was similar in both
groups (12.9 versus 14.9 percent, respectively; hazard ratio [HR] 0.84; 90% CI
0.58-1.21).

• Fewer people in strict versus lenient group met heart rate target – The
percentage of patients was 98 and 75 percent, respectively [10].

• More medical visits in strict rate-control group – There were nearly nine
times as many visits (684 versus 75) to achieve rate control target(s) in the
strict control.

• Low resting heart rates were achieved in the lenient group too – In
patients assigned to lenient rate control, the mean resting rates at the end of
follow-up was 85+14 beats/min compared with 76+14 beats/min in those
assigned to strict control.

The results of the RACE trial must be tempered given that the lenient-control
group was in fact treated more aggressively than the protocol required. In
addition, RACE included only patients with permanent AF, so the results are not
generalizable to those with paroxysmal or persistent AF.
INITIAL CONSIDERATIONS

The initial management of patients with AF and a rapid ventricular response involves
the following:

● Determining if urgent therapy is needed

● Choosing between a rate and rhythm control strategy
● Determining if there is preexcitation

Determining urgency — In a patient with new or recurrent AF with a rapid

ventricular response, the immediate goals are to stabilize hemodynamics (if
necessary) and to improve symptoms. Thus, the intensity of initial rate control therapy
(eg, inpatient versus outpatient or oral versus intravenous therapy) depends upon the
clinical scenario.

● Urgent therapy – In patients who are clinically or hemodynamically unstable (eg,

myocardial ischemia, pulmonary edema, hypotension) due to AF and a rapid
ventricular response, treatment options include intravenous rate-control
medications and/or immediate cardioversion. (See 'Urgent therapy' below.)

● Elective therapy – Patients who have mild or no symptoms and whose

ventricular rate is mildly to moderately elevated (eg, ≤120 beats/min) can be
managed with the addition or increase of oral rate-control medications. (See
'Elective and long-term management' below.)

Deciding on rate control — The advantages and disadvantages of rhythm and rate
control, as well as whether there are subgroups of patients for whom one or the other
should be preferred, are discussed separately. (See "Management of atrial fibrillation:
Rhythm control versus rate control".)

Caution in preexcitation syndrome — Among patients with AF and preexcitation,

initial therapy is aimed at reversion to sinus rhythm. Usual treatments for rate control
(ie, calcium channel blockers, beta blockers, digoxin, and amiodarone) should not be
given because they may paradoxically increase the ventricular response in patients
with AF. Intravenous procainamide or ibutilide should be given if hemodynamics are
stable, and direct current cardioversion should be performed if the patient is
unstable. This is discussed in detail separately. (See "Treatment of arrhythmias
associated with the Wolff-Parkinson-White syndrome", section on 'When to avoid AV
nodal blockers'.)

The preferred long-term therapy of preexcited AF is ablation of the accessory

pathway. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White
syndrome", section on 'Catheter ablation'.)

URGENT THERAPY

This section describes our approach to urgent ventricular rate control in patients with
AF who do not have heart failure ( algorithm 1). Rate control of patients who have
AF and heart failure is discussed separately. (See "The management of atrial
fibrillation in patients with heart failure", section on 'Acute decompensation'.)

Choice of initial urgent therapy — Patients who require urgent therapy need to be
in a monitored setting. In patients without symptomatic hypotension (eg, in those
with ischemia without hypotension), we select diltiazem as the initial agent.
Intravenous (IV) esmolol, verapamil, or other IV beta blockers such as metoprolol are
reasonable alternatives to diltiazem. If it is uncertain whether the patient will become
hypotensive with a beta blocker, we use esmolol since this medication has a very
short half-life and can be immediately discontinued if needed. (See 'Hypotensive
patient' below.)

In the absence of larger randomized trials, much of the current management relies
on clinical experience rather than evidence. Diltiazem may have a less pronounced
negative inotropic effect than verapamil [11]. The IV preparation is convenient and
effective for acute control of the ventricular rate in AF [12-14], while oral therapy is
effective for chronic rate control [15,16]. In our experience, either a beta blocker or
calcium channel blocker could result in hypotension, and therefore careful blood
pressure monitoring is needed regardless of the choice of medication. Small,
heterogenous studies of urgent control of ventricular rate in AF suggest higher
efficacy for IV diltiazem versus IV beta blocker therapy:
 ● One meta-analysis of three studies including 160 patients and comparing effects
of IV diltiazem versus IV metoprolol showed an average of 9 mm lower systolic
blood pressure with metoprolol at 15 minutes following treatment but no
differences at earlier or later timepoints (ie 5, 10, or 30 minutes) [17].

● In a meta-analysis of 17 randomized and cohort studies (1214 patients), patients

given IV diltiazem compared with IV metoprolol had higher efficacy of successful
rate control (relative risk [RR] 1.11; 95% CI 1.06-1.16). Efficacy was defined
differently in various studies (eg, achieving a heart rate <100 beats/min or
lowering heart rate by at least 20 percent). Those treated with IV diltiazem also
had shorter average onset time (RR per minute of onset -1.13; 95% CI -1.97 to
-0.28) and lower ventricular rate (RR difference in beats/min -9.48; 95% CI -12.13
to -6.82) and less impact on (weighted mean difference 3.76 mmHg; 95% CI 0.20-
7.33). There was no significant difference in adverse events between treatment
regimens [17].

Normotensive patient — In most normotensive patients with AF with a rapid

ventricular rate, we first try IV diltiazem ( table 2).

The suggested regimen for IV diltiazem is derived from the Diltiazem Atrial
Fibrillation/Atrial Flutter Study Group [12-14]. The efficacy of this regimen was
evaluated in a report of 84 consecutive patients with AF, atrial flutter, or both [14]. The
overall response rate was 94 percent. The continuous infusion maintained adequate
rate control for 10 hours or longer in a dose-dependent fashion: 47 percent at 5
mg/hour; 68 percent after titration to 10 mg/hour; and 76 percent after titration to 15
mg/hour ( figure 3). Hypotension occurred in 13 percent and was symptomatic in
almost 4 percent. All such patients responded to an infusion of normal saline. Weight-
based dosing of IV diltiazem is further supported in a study of 252 patients who
received IV diltiazem for acute rate control in the emergency department. Weight-
based dosing (0.25 mg/kg) was associated with higher rates of rate control without
increased adverse effects [18].

Hypotensive patient
Asymptomatic and not on a vasopressor — If the patient is mildly hypotensive but
asymptomatic and does not require a vasopressor, we typically start metoprolol
tartrate (short-acting) 25 mg by mouth every six hours and up-titrate as needed and
as tolerated by 12.5 mg every six hours until the rate is controlled. Other IV beta
blockers and calcium channel blockers may cause worsening hypotension.

Patients with inadequate response

● Urgent combination therapy – In patients who do not adequately respond to

initial therapy with either an IV calcium channel blocker or IV beta blocker, we
suggest the addition of IV digoxin as the second drug in combination therapy
( table 2). Digoxin should not be used if preexcitation is present.

● Urgent alternative therapy – In patients who do not respond to or are

intolerant of IV calcium channel blockers, beta blockers, and/or digoxin, we
suggest IV amiodarone for acute control of the ventricular rate ( table 2). In
such patients, the use of amiodarone for rate control is a short-term strategy (eg,
hours to days). The drug should not be used if preexcitation is present. Careful
attention to anticoagulation is also necessary because there is a small chance of
cardioversion with amiodarone.

If none of these therapies work, we typically opt for acute cardioversion rather
than continued attempts at rate control (with evaluation of the left atrial
appendage thrombus if warranted and clinically feasible and appropriate
anticoagulation strategy).

Symptomatic hypotension and/or on a vasopressor — If the hypotension is

symptomatic and requires a vasopressor, we typically opt for acute cardioversion
rather than rate control (with evaluation of the left atrial appendage thrombus if
warranted and appropriate anticoagulation strategy). (See "Prevention of
embolization prior to and after restoration of sinus rhythm in atrial fibrillation".)

If the patient is on a vasopressor that can exacerbate tachycardia (eg, epinephrine or

norepinephrine), we may elect to switch the vasopressor to a vasoconstrictor (eg,
phenylephrine) if this is a reasonable alternative. (See "Use of vasopressors and
inotropes".)

Management of patients in whom cardioversion is unsuccessful is discussed

separately. (See "Atrial fibrillation: Cardioversion", section on 'Electrical cardioversion'.)

Alternative therapies we do not suggest — We do not use IV magnesium for

control of ventricular rate in AF despite a small body of supporting evidence because
very few patients are refractory to other therapies and would require it. Magnesium
does have physiologic properties suggesting that it might have efficacy for rate
control in AF. Initial small studies provided the rationale for a clinical trial in which 199
patients presenting with rapid AF (mean baseline ventricular rate 142 beats/min) were
treated with usual therapy for rate control (most often digoxin) and randomly
assigned to IV magnesium sulfate (2.5 g over 20 minutes followed by 2.5 g over two
hours) or placebo [19]. Magnesium therapy increased the likelihood of achieving a
ventricular rate <100 beats/min (65 versus 34 percent with placebo) and conversion to
sinus rhythm (27 versus 12 percent with placebo). However, the difference in mean
ventricular rate never exceeded 12 beats/min. The benefit of magnesium was modest,
preferred primary therapies (calcium channel blocker, beta blocker) were used in only
12 to 13 percent of the patients, and magnesium was associated with side effects
such as flushing and hypotension. A separate meta-analysis of six trials and 745
patients showed similar results [20].

Ivabradine blocks the pacemaker current, which is primarily thought to affect the
sinoatrial node; however, some studies have shown that this current is also expressed
in the atrioventricular node. Accordingly, a few studies are investigating the use of
ivabradine for ventricular rate control in AF. One retrospective study of 18 patients
with permanent AF showed average reduction in ventricular rate from 104.6 to 89
[21]. The BRAKE-AF trial randomized patients with permanent AF to ivabradine or
digoxin. Ivabradine was found to reduce the average ventricular rate by an average of
11.6 beats/minute, which was significantly less than the reduction observed with
digoxin (19.6 beats/minute). Though the number of serious adverse events were
similar in each group, ivabradine was better tolerated and had a higher compliance
through the study [22]. At present, there is insufficient evidence to recommend the
routine use of ivabradine for ventricular rate control in AF; it can be used if more
commonly used rate control agents are unsuccessful or not tolerated [23].

Transition to oral medications — When making a transition from IV to oral therapy,

we first ensure that the patient has tolerated the IV medication well. For instance,
beta blockers may have a variety of adverse effects that can be important in patients
with AF. (see "Major side effects of beta blockers")

When transitioning from IV to oral medications, we generally convert the total daily
dose of the IV medication to an equivalent divided or long-acting oral dose of a
medication in the same class. We often use pharmacy or pharmacist-based reference
for appropriate conversion dosages. For example, if a patient is placed on IV
diltiazem, we will usually convert the patient to a short or long-acting oral formulation
of diltiazem that gives an equivalent daily dose of the medication. A general formula
for approximate conversion from IV diltiazem to the daily oral dose is [(infusion rate
x3)+3]x10 [24]. Example conversions from IV to oral dosing for diltiazem and
metoprolol are shown in a table ( table 2). Other nuances of long-term rate control
medications are discussed separately. (See 'Elective and long-term management'
below.)

ELECTIVE AND LONG-TERM MANAGEMENT

Choice of nonurgent therapy — Although there are differences in the efficacy of the
various drugs, it is likely that monitoring and adjustments to therapy are more
important components of successful rate-control strategies than the initial drug
selection. Studies of specific pharmacologic agents for management of AF are small
and heterogeneous.

A study of 25 clinical trials showed no difference in effectiveness for different

diltiazem or verapamil formulations (eg, immediate release, sustained release, or
controlled delivery). There was also no evidence of differences in effectiveness for
extended-release diltiazem and verapamil [25]. Long-acting or sustained-release
formulations are typically preferred for chronic management to facilitate medication
compliance.
One study reviewed 54 trials that evaluated 17 different agents used for rate control
[26]. The studies were all relatively small (6 to 239 patients) and had relatively short
follow-up periods of eight weeks or less. Most compared single agents with placebo.
Due to extensive variability in methods and outcome assessments, a meta-analysis of
the trials could not be performed.

However, the following observations were noted:

● Both beta blockers and calcium channel blockers were effective – Diltiazem,
verapamil, and most beta blockers (atenolol, metoprolol, timolol, pindolol, and
nadolol) were all effective in reducing the ventricular rate during rest and
exercise. The beta blockers labetalol, xamoterol, and celiprolol were less effective
at rest but did reduce ventricular rates during exercise.

● Mixed results for digoxin versus placebo – Trials comparing digoxin with
placebo reported inconsistent results, particularly when heart rate during
exercise was assessed.

● Digoxin was effective when added to beta blocker or calcium channel blocker
– The combination of digoxin with a beta blocker or calcium channel blocker
reduced heart rate both at rest and with exertion.

Thus, pharmacologic therapy can achieve adequate rate control in approximately 80

percent of patients. However, achieving this goal requires close monitoring,
medication adjustments, and often combination therapy. Although there are
differences in the efficacy of the various drugs, it is likely that monitoring and
adjustments to therapy are more important components of successful rate-control
strategies than the initial drug selection.

● AFFIRM trial – Among evaluations of rate-control drugs, the study with the
largest sample size and longest follow-up is a post-hoc analysis from the AFFIRM
trial [27]. The original AFFIRM trial assigned patients with AF to either rate or
rhythm control, and a post-hoc analysis compared the efficacy of various rate-
control medications. In this post-hoc study, over 2000 patients assigned to rate
control were given medications according to physician preference. Effectiveness
 of rate control was defined as a resting heart rate ≤80 beats/minute, exertional
heart rate ≤110 beats/min during six-minute walk test or average heart rate
during 24-hour ambulatory Holter monitoring ECG ≤100 beats/min (at least 18
hours of interpretable monitoring), and no heart rate >110 percent maximum
predicted age-adjusted exercise heart rate.

The overall effectiveness (meeting both rest and exertion heart rate goals) of
initial monotherapy therapy was most effective for beta blockers (59 percent),
followed by digoxin (58 percent), and then calcium channel blockers (38 percent).

At five-year follow-up, adequate rate control increased from approximately 60 to

80 percent of patients. Only 58 percent of patients had adequate rate control with
the first drug or combination used. Patients initially treated with a beta blocker
were significantly less likely than those treated with calcium channel blockers or
digoxin to have their drug regimen changed.

Limitations of this study included nonrandom assignment of specific rate-control

medication and an inadequate baseline assessment of heart rate.

Initial therapy — In patients who do require elective management or in those

transitioning to long-term therapy, we usually suggest an oral beta blocker or
nondihydropyridine calcium channel blocker. Reasons for these preferences are
discussed below.

● Beta blockers – We prefer beta blockers in the following groups of patients:

• Recent myocardial infarction.

• Heart failure due to systolic dysfunction.

• Inappropriate increase in ventricular rate during exercise.

• Surges in sympathetic function that trigger AF. Beta blockers may be

particularly useful in states of high adrenergic tone (eg, postoperative AF)
[28,29].
In the first two settings, beta blockers improve patient survival. (See "Acute
myocardial infarction: Role of beta blocker therapy" and "Primary pharmacologic
therapy for heart failure with reduced ejection fraction", section on 'Beta
blocker'.)

Oral beta blockers are widely used as primary therapy for rate control in chronic
AF. Beta blockers decrease the resting ventricular rate and blunt the ventricular
rate response to exercise. Most beta blockers appear to have similar efficacy. For
patients with heart failure with systolic dysfunction, the preferred agents for
treatment are metoprolol succinate, carvedilol, carvedilol continuous release,
and bisoprolol. (See "Primary pharmacologic therapy for heart failure with
reduced ejection fraction", section on 'Beta blocker'.)

In a post-hoc analysis of the AFFIRM trial of rate versus rhythm control in patients
with AF, beta-blocker therapy was shown to be effective in achieving goal
ventricular rate in 59 percent of people [27]. The AFFIRM trial is discussed in
greater detail separately. (See 'Choice of nonurgent therapy' above.)

There is the most supporting evidence for metoprolol, atenolol, and nadolol.
Atenolol and nadolol have the advantages of a long half-life and are typically
given once daily. Long-acting propranolol can be effective. Bisoprolol and
carvedilol are also used ( table 2).

It should be noted that beta blockers are contraindicated or relatively

contraindicated in some patients, and others cannot tolerate the side effects. (See
"Major side effects of beta blockers".)

Beta blockers have additional properties that may make them preferred to other
rate-control drugs in some AF patients:

• Patients with systolic dysfunction – This is discussed separately. (See "The

management of atrial fibrillation in patients with heart failure" and "Primary
pharmacologic therapy for heart failure with reduced ejection fraction", section
on 'Beta blocker'.)
 • Patients with AF triggered by sympathetic dysfunction – Beta blockers may
reduce the incidence of AF recurrence in patients with episodes of AF that are
triggered by surges in sympathetic activity [28,29].

Some patients with paroxysmal AF also have sinus node dysfunction, with
tachycardia-bradycardia syndrome. In such patients, beta blockers with intrinsic
sympathomimetic activity may be useful since they are less likely to worsen
bradycardia than standard beta blockers. (See "Sinus node dysfunction:
Epidemiology, etiology, and natural history".)

● Calcium channel blocker – A nondihydropyridine calcium channel blocker is

preferred in patients with chronic lung disease and in patients who do not
tolerate beta blockers. Among the calcium channel blockers, verapamil has a
somewhat greater blocking effect on the AV node than diltiazem, and the choice
between these drugs is often dictated by side effects ( table 2).

In a post-hoc analysis of the AFFIRM trial of rate versus rhythm control in patients
with AF, calcium channel blocker therapy was shown to be effective in achieving
goal ventricular rate in 38 percent of people [27]. The AFFIRM trial is discussed in
greater detail separately. (See 'Choice of nonurgent therapy' above.)

Calcium channel blockers have a number of characteristics that need to be

considered when they are administered to patients with AF:

• Variable effect on sinoatrial (SA) nodal function – Although both verapamil

and diltiazem have an inhibitory effect on the sinus node, their vasodilator
effects cause a reflex release of catecholamines that usually maintains or
slightly accelerates the SA nodal rate. However, patients with the sinus node
dysfunction may be particularly sensitive to the effects of calcium channel
blockers. (See "Sinus node dysfunction: Epidemiology, etiology, and natural
history".)

• Negative ionotropic effects – Both verapamil and diltiazem have negative

inotropic effects, although this is less pronounced with diltiazem. As a result,
these drugs should be used with caution in patients with heart failure and in
 patients taking other negative inotropes, such as beta blockers. They should
not be given if the patient is hypotensive.

• Side effects in older patients – With either verapamil or diltiazem, it should

be remembered that older patients are more likely to develop side effects,
especially those that are cardiac in nature. Although the same maximum doses
may be tolerated, it is usually appropriate to titrate more slowly.

In summary, diltiazem and verapamil should not be given to patients with severe
heart failure (New York Heart Failure class III or IV), preexcitation syndrome, or
significant hypotension. In addition, these drugs should be given with caution to
patients with sinus node dysfunction, significant liver disease, mild hypotension,
marked first-degree heart block, or the concurrent intake of other drugs that
inhibit SA nodal function or slow AV nodal conduction. Considerations for patients
with heart failure are discussed separately. (See "The management of atrial
fibrillation in patients with heart failure", section on 'Rate control in heart failure
with reduced ejection fraction' and "The management of atrial fibrillation in
patients with heart failure", section on 'Rate control in heart failure with
preserved ejection fraction'.)

Combination therapy

● Combination therapy – In patients initially tried on a beta blocker or calcium

channel blocker with persistently high ventricular rates, the combination of a
beta blocker and a calcium channel blocker can be tried in most patients. In a
post-hoc analysis of the AFFIRM trial of rate versus rhythm control in patients
with AF, this combination was shown to be effective in achieving goal ventricular
rate in 59 percent of people [27]. The AFFIRM trial is discussed in greater detail
separately. (See 'Choice of nonurgent therapy' above.)

● Adding digoxin – In patients who do not achieve adequate rate control on

maximum-tolerated doses of a beta blocker and nondihydropyridine calcium
channel blocker together, we suggest adding digoxin if AV nodal ablation,
pharmacologic rhythm control, or catheter ablation of AF are not being
 considered. (See "Atrial fibrillation: Atrioventricular node ablation", section on
'Indications'.)

When digoxin is added to either a beta blocker or calcium channel blocker or to

both, patients should be carefully monitored for bradycardia and hypotension.
Also, patients with significant left ventricular dysfunction may not tolerate triple
therapy ( table 2).

Digoxin levels should be obtained periodically for the purpose of detecting

potentially high levels. We attempt to keep the level in the lower half of the
normal range. Digoxin toxicity is discussed in detail separately. (See "Digitalis
(cardiac glycoside) poisoning" and "Cardiac arrhythmias due to digoxin toxicity".)

Combination therapy with digoxin was studied in a post-hoc analysis of the

AFFIRM rate versus rhythm control trial. The overall effectiveness (meeting both
rest and exertion ventricular rate goals) of combination therapy with digoxin was
described as follows:

• Beta blocker plus digoxin – 68 percent

• Calcium channel blocker plus digoxin – 60 percent
• Beta blocker plus calcium channel blocker plus digoxin – 76 percent

The AFFIRM trial is discussed in greater detail separately. (See 'Choice of nonurgent
therapy' above.)

In patients with AF, the following summarizes evidence regarding the efficacy and
safety of digoxin as a combination drug for rate control:

• Three large observational studies of digoxin use among patients with AF have
yielded mixed results, with at least two finding an increase in all-cause
mortality of about 20 percent [30,31] and one finding no increase [32].

• The best available evidence regarding the relationship between digoxin use in
AF patients (either alone or in combination with a beta blocker or calcium
channel blocker) and mortality comes from a post-hoc subgroup analysis of the
 ARISTOTLE trial of anticoagulant therapy [33]. The following findings were
reported:

- Baseline digoxin use was not associated with an increased risk of death
(adjusted hazard ratio [HR] 1.09; 95% CI 0.96-1.23)
- Digoxin concentration ≥1.2 ng/mL was associated with an increased risk of
death (adjusted HR 1.56; 95% CI 1.20-2.04)
- New digoxin use was associated with a higher risk of death (adjusted HR
1.78; 95% CI 1.37-2.31)
- Having heart failure versus not having heart failure did not change these
effects.

The use of digoxin in patients with AF and heart failure is discussed separately.
(See "The management of atrial fibrillation in patients with heart failure", section
on 'Rate control in heart failure with reduced ejection fraction'.)

Alternative medications

● Amiodarone – For patients with AF, there is a limited role for amiodarone as a
long-term agent for rate control. Due to the increased risk of side effects, the
2014 American Heart Association/American College of Cardiology/Heart Rhythm
Society AF guideline states that amiodarone can be used as second-line therapy
for chronic rate control only when other therapies are unsuccessful or
contraindicated [34,35]. We agree with this guideline, and for patients treated
with amiodarone for long-term rate control of AF, we require careful follow-up,
including monitoring for known medication side effects. (See "Amiodarone:
Adverse effects, potential toxicities, and approach to monitoring".)

Data supporting the use of amiodarone as a rate-control agent for AF are more
limited compared with evidence supporting its use for pharmacologic rhythm
control of AF. In one study, IV amiodarone (7 mg/kg), flecainide, or placebo were
given to 98 patients with recent-onset AF (0.5 to 72 hours) [36]. Even when AF did
not revert to sinus rhythm, amiodarone promptly slowed the ventricular rate
during the eight-hour observation period ( figure 4). In addition, in critically ill
 patients, amiodarone may be less likely to cause systemic hypotension than IV
diltiazem [37].

● Digoxin monotherapy – In patients without hypotension or severe heart failure,

we do not generally use digoxin as a single agent for the following reasons
[34,35]:

• Association with higher mortality in patients with high digoxin levels.

• It may not be appropriate for use in older patients. There are additional
reasons that digoxin should not be used as an initial drug for rate control in
most settings.

• Generally less effective rate control compared with beta blockers or calcium
channel blockers, particularly during exercise when vagal tone is low and
sympathetic tone is high [38]. This is because the drug slows the ventricular
rate during AF, primarily by vagotonic inhibition of AV nodal conduction.

• Digoxin is only rarely effective at terminating AF.

One study suggests that digoxin may have a similar efficacy for rate control as
bisoprolol [39]. However, the higher toxicity profile and risk of mortality prevent
us from using it as monotherapy.

Refractory to rate-control medications — Some patients will not achieve adequate

ventricular rate control with pharmacologic therapy due to poor response to or
intolerance of initial, combination, and alternative medications. In such cases, the
options are as follows:

● AV nodal ablation with permanent pacemaker placement – If a patient has

high refractory ventricular rates despite initial therapy, combination, and other
pharmacotherapies, they may be referred for AV nodal ablation with pacemaker
placement to achieve adequate rate control of their AF. This is discussed in detail
separately. (See "Atrial fibrillation: Atrioventricular node ablation".)

● Switching to rhythm control – In some patients, it is prudent to reconsider a

rhythm-control strategy to control the ventricular rate. This is discussed in detail
 separately. (See "Management of atrial fibrillation: Rhythm control versus rate
control" and "Atrial fibrillation: Atrioventricular node ablation".)

Monitoring and adjustments — These are more important components of

successful rate-control strategies than initial drug selection. Once an effective rate
control regimen has been developed, it is reasonable to periodically assess adequacy
of rate control; monitoring for both bradycardia and tachycardia is important. (See
"Atrial fibrillation: Overview and management of new-onset atrial fibrillation", section
on 'Additional cardiac testing' and 'Evaluation and goal ventricular rate' above.)

It is also reasonable to monitor left ventricular function in patients treated with a

pharmacologic rate-control strategy to make sure that a tachycardia-related
cardiomyopathy has not developed. Some experts perform an echocardiogram every
two to three years in asymptomatic patients with higher average ventricular rates
while others do not. (See "Tests to evaluate left ventricular systolic function".)

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".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, “The Basics” and “Beyond
the Basics.” 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.)

● Basics topic (see "Patient education: Medicines for atrial fibrillation (The Basics)")

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

SUMMARY AND RECOMMENDATIONS

● Rationale and rate goal – We slow the ventricular rate in patients with atrial
fibrillation (AF) to treat symptoms, stabilize hemodynamics symptoms, and/or to
avoid tachycardia-mediated cardiomyopathy. (See 'Rationale for rate lowering'
above.)

We target a mean rate-control goal of <85 beats/min for symptomatic patients

with AF. For asymptomatic patients with permanent AF, a more lenient mean
rate-control goal of <110 beats/min may be reasonable. (See 'Evaluation and goal
ventricular rate' above.)

● Caution in preexcitation syndrome – In these patients, initial therapy is aimed

at reversion to sinus rhythm rather than rate control. Amiodarone, digoxin,
verapamil, diltiazem, and adenosine are contraindicated with preexcited AF, and
beta blockers also should not be used. (See "Treatment of arrhythmias associated
with the Wolff-Parkinson-White syndrome", section on 'When to avoid AV nodal
blockers'.)

● Urgent therapy

• Normotensive patients – In these patients, we suggest intravenous

nondihydropyridine calcium channel blockers such as diltiazem ( table 2 and
algorithm 1) (Grade 2B). (See 'Urgent therapy' above and 'Normotensive
patient' above.)
 In patients who do not adequately respond to initial therapy with either an IV
calcium channel blocker or IV beta blocker, we suggest the addition of IV
digoxin as the second drug in combination therapy (Grade 2C). (See
'Combination therapy' above.)

● Asymptomatic hypotensive patients who do not require vasopressor – We

typically start oral metoprolol tartrate (short-acting) until the rate is controlled.

- In patients who do not adequately respond to initial therapy with either IV

calcium channel blocker or IV beta blocker, we suggest the addition of IV
digoxin as the second drug in combination therapy ( table 2). (See
'Asymptomatic and not on a vasopressor' above.)

- In patients who do not respond to or are intolerant of IV calcium channel

blockers, beta blockers, and/or digoxin, we suggest IV amiodarone as a
short-term rate-control strategy ( table 2). Careful attention to
anticoagulation is also necessary because there is a small chance of
cardioversion with amiodarone.

- If none of these therapies work, we typically opt for acute cardioversion

rather than continued attempts at rate control (with evaluation of the left
atrial appendage thrombus if warranted and appropriate anticoagulation
strategy).

• Symptomatic hypotensive patients and/or those requiring vasopressors –

If the hypotension is symptomatic and requires a vasopressor, we typically opt
for acute cardioversion rather than rate control (with evaluation of the left
atrial appendage thrombus if warranted and appropriate anticoagulation
strategy). (See 'Symptomatic hypotension and/or on a vasopressor' above and
"Prevention of embolization prior to and after restoration of sinus rhythm in
atrial fibrillation".)

● Elective and long-term management – We start an oral beta blocker or

nondihydropyridine calcium channel blocker ( algorithm 2). (See 'Choice of
nonurgent therapy' above.)
 • Combination therapy – We try a combination of oral beta blocker and calcium
channel blocker if monotherapy is not effective. (See 'Combination therapy'
above.)

• Alternative short-term therapy – In patients who do not respond to or are

intolerant of IV calcium channel blockers, beta blockers, and/or digoxin, we
suggest IV amiodarone for acute control of the ventricular rate (Grade 2C).
(See 'Alternative medications' above.)

• Refractory to rate control – In patients who have a poor response or

intolerance to pharmacologic therapy, options are:

- Atrioventricular (AV) nodal ablation with permanent pacemaker placement.

(See "Atrial fibrillation: Atrioventricular node ablation".)

- Switching to rhythm control. (See "Management of atrial fibrillation:

Rhythm control versus rate control" and "Atrial fibrillation: Atrioventricular
node ablation".)

• Monitoring – Careful follow-up for side effects such as bradycardia or

persistent tachycardia is imperative. (See 'Monitoring and adjustments' above.)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who
contributed to an earlier version of this topic review.
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Topic 938 Version 75.0

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