Download Atrial Fibrillation - Kaiser Permanente Provider

KAISER PERMANENTE OHIO
ATRIAL FIBRILLATION
Methodology: Evidence-Based
Champion: Cardiology
Key Stakeholders: Cardiology, IM
Issue Date:
3-97
Most Recent Updates: 9-03,12-05, 2-07, 1-09
Next Update:
3-11
BACKGROUND
Atrial fibrillation (AF) is associated with an increased risk of thromboembolism, especially to the brain.
Two basic strategies have evolved for reducing the risk of stroke in atrial fibrillation: cardioversion and
antithrombotic therapy. This discussion will center on these two basic strategies. The vast majority of
patients with atrial fibrillation have organic heart disease. Less than 10% of atrial fibrillation cases are
defined as lone atrial fibrillation; (i.e., patients with atrial fibrillation without organic heart disease,
hypertension or diabetes mellitus). Valvular heart disease accounts for 15% to 30% of the cases of atrial
fibrillation; nonvalvular heart disease accounts for 50% to 80% with causes including coronary artery
disease, cardiomyopathy, congenital heart disease, hypertension, and thyrotoxic heart disease.
Most patients presenting to the physician's office or to the Emergency Department with atrial fibrillation do
not require hospital admission. AF not occurring in a setting of reversible cause (e.g., myocardial
infarction, pericarditis and cardiac surgery) can be classified in the following categories: new-onset AF,
1
paroxysmal AF, persistent AF, and permanent AF.
ƒ
New-onset AF is defined as AF not previously documented.
ƒ
Paroxysmal AF is if the arrhythmia terminates spontaneously not dependent upon pharmacologic or
nonpharmacologic interventions. The duration of the paroxysmal AF is normally less then 24 to 48
hours. Paroxysmal AF may occur only once or may be recurrent.
ƒ
Persistent AF is defined as AF with duration of seven days or longer.
ƒ
Permanent AF is defined as long standing AF in which no further attempts will be made to restore or
maintain sinus rhythm.
The recommendations contained in this guideline can be followed for most patients without inpatient
hospitalization. Cardioversion can be performed in an outpatient monitored setting. Anticoagulation with
warfarin can be initiated and followed in outpatients. Acute myocardial infarction needs to be ruled out in
few patients with atrial fibrillation. When uncertainty exists, contact the Cardiologist on-call. The use of
electrical cardioversion in the outpatient monitored setting can be expected to decrease hospital
admissions and shorten stays in monitored areas.
RECOMMENDATIONS
Rhythm Control vs. Heart Rate control
Reasons for restoration and maintenance of sinus rhythm in patients with AF include relief of symptoms,
prevention of embolism, and avoidance of cardiomyopathy. Conversion to and maintenance of sinus
rhythm offers the theoretical advantages of reducing the risk of thromboembolism and consequently the
need for chronic anticoagulation. Several recently published clinical trials (AFFIRM, RACE) have been
completed with data suggesting no clear advantage of one approach over the other with similar outcomes
in total mortality and ischemic stroke.
New-Onset Atrial Fibrillation (see Figures 1 & 2)
When atrial fibrillation duration has been less than 48 hours, no anticoagulation is required and
cardioversion can be performed. Rate control with beta blockers, calcium blockers, or digoxin is
suggested to obtain a resting heart rate <100 before attempted chemical cardioversion with
antiarrhythmic medications such as 1A drugs (e.g., quinidine, procainamide, disopyramide), or 1C drugs
(propafenone, flecainide). Type 1C drugs should not be used in patients with prior myocardial infarction or
with decreased left ventricular function. Emergency direct current cardioversion for new onset atrial
fibrillation should be considered in hemodynamically unstable patients or patients with congestive heart
failure or myocardial infarction with rapid ventricular response.
After 48 hours, or if one is uncertain as to the duration of the new onset AF, the patient should be given
warfarin therapy for at least 3 to 4 weeks at an INR of 2-3 and schedule for an elective cardioversion.
During this period, rate control should be established with standard therapy including digoxin, calcium
channel blockers, or beta blockers (see Fig 3). Hospitalization is not required in these patients when
starting warfarin therapy to establish therapeutic levels. This can be accomplished in an outpatient
setting.
Recurrent Paroxysmal Atrial Fibrillation (See Fig. 3)
For patients who experience brief or minimally symptomatic recurrences of paroxysmal AF, it is
reasonable to avoid antiarrhythmic drugs unless troublesome symptoms occurs. Rate control and
prevention of thromboembolism are appropriate in both situations.
Recurrent Persistent Atrial Fibrillation (See Fig. 3)
Defined as patient who have undergone at least 1 attempt to restore sinus rhythm and may remain in AF
after its second occurrence with minimal or no symptoms. These patients should be treated with therapy
for rate control and prevention of thromboembolism as needed. Alternatively, those with symptoms
favoring sinus rhythm should be treated with an antiarrhythmic agent (in addition to medications for rate
control and anticoagulation) before cardioversion.
Permanent Atrial Fibrillation (See Fig. 3)
The treatment of permanent AF is given to patients in which sinus rhythm cannot be sustained after
cardioversion of AF or when the patient and physician have decided to allow AF to continue without
further efforts to restore sinus rhythm. It is important to maintain control of the ventricular rate and to use
antithrombotic therapy , as outlined in TABLE 2 for all patients in this category.
Preventing Thromboembolism (See Table 1)
The rate of stroke in patients with AF is related to coexistent cardiovascular disease. Adjusted-dose oral
anticoagulation (Warfarin) is more efficacious then aspirin for prevention of stroke in patients with AF. All
patients with AF should be administered antithrombotic therapy (Warfarin or Aspirin), except those with
lone AF, to prevent thromboembolism.
Those with coumadin include those with an allergy to coumadin, recent surgery (6 weeks), proten c
deficiency frequent falls especially those with a history of head trauma or fracture other than hip and
pregnancy. The selection of antithrombotic agent (Warfarin or Aspirin) should be individualized based
upon assessment of the absolute risks of stroke and bleeding and the relative risk and benefit for the
particular patient (See TABLE 2). Chronic oral anticoagulant therapy (Warfarin) should be dose adjusted
to achieve a target INR of 2 to 3 in patients at high risk of stroke, unless contraindicated. Aspirin in a dose
of 325 mg daily may be used as an alternative in low-risk patients or in those with certain
contraindications to oral anticoagulation. Oral anticoagulation with Warfarin is indicated for all patients
with AF associated with rheumatic mitral valve disease or prosthetic heart valves (mechanical or tissue
valves).
The use of anticoagulation in those patients age 85+ or those with severe functional impairment needs to
be tempered by clinical judgment, given the known risks of anticoagulation.
Adapted from KP Southern California
Page
2
Cardioversion
Cardioversion is usually performed electively to restore sinus rhythm in patients with persistent AF.
Cardioversion without prior anticoagulation may be attempted in patients with new-onset AF less then 24
hours or when acute AF produces hemodynamic instability in the form of angina pectoris, MI, shock, or
pulmonary edema. Otherwise, anticoagulation with warfarin with an INR of 2-3 is recommended for 3 to 4
weeks before and after cardioversion for patients with AF of unknown duration or with AF for more then
48 hours.
Asymptomatic patients with controlled atrial fibrillation of more than 24 hours duration who are considered
for cardioversion do not require hospitalization for anticoagulant therapy. They can be treated with 3
weeks of warfarin therapy with INR of 2-3. After this treatment, they may have chemical or electrical
cardioversion. Rate control should be attempted with beta blockers or calcium channel blockers. Digoxin
used as monotherapy is a poor drug for rate control. Underlying etiologic mechanisms for atrial fibrillation
must be investigated, such as thyrotoxicosis and congestive heart failure.
The role of echocardiography in atrial fibrillation is to exclude anatomic disease. When history and
physical exam suggest valvular, myocardial, or pericardial disease the study is indicated. It should not be
used solely to determine left atrial size, which in itself does not predict the initial success of cardioversion.
Chemical Cardioversion (see Table 2)
Chemical cardioversion, if preferred to electrical cardioversion, may be attempted in an
electrocardiographically monitored setting. This may be emergency room, telemetry unit, or other in or
outpatient monitored area. Patients without ventricular dysfunction or ischemia are at low proarrhythmic
risk. Electrical cardioversion is preferred by many physicians because of the risk of proarrhythmia
associated with anti-arrhythmic agents. New regimens such as single dose oral flecainide at 300 mg
exist to supplement or supplant the older regimens of quinidine and procainamide. Intravenous Ibutilide is
an option in patients without cardiomyopathy but requires electrocardiographic monitoring for six hours
after administration. Chemical cardioversion should be successful in 24 hours or less. After cardioversion,
discharge to outpatient follow-up can usually be accomplished promptly in low risk patients and within 24
hours in high risk patients.
Rate control is defined as a resting ventricular rate of atrial fibrillation < 110 beats/minute. Initial therapy
with usual loading dose of digoxin 0.75-1 mg followed by maintenance digoxin should be used in patients
with rapid atrial fibrillation. Additional rate control should be accomplished with either beta blockers or
calcium channel blockers. The calcium channel blockers most commonly used are dilitiazem or
verapamil. Digoxin should not be pushed to high doses. Digoxin is not a good drug for rate control in atrial
fibrillation, particularly during enhanced sympathetic states such as physical activity, because the rate
control of digoxin is solely from vagotonic action. Once rate control is established, chemical cardioversion
can be attempted with a 1A, 1C, or type III drug. If the patient should develop "torsade de pointes" (i.e., a
rapid polymorphic ventricular tachycardia, or an exacerbation of ventricular ectopy secondary to the
drug), the patient should be assessed and the drug stopped. A second drug could be tried. If chemical
cardioversion with a 1A, IC or type III drug is not successful, electrical cardioversion should be attempted
unless digitoxicity is suspected.
In the patient with chronic atrial fibrillation, if the duration has exceeded 6 months, cardioversion is not
usually recommended. A return to sinus rhythm is unlikely. Rate control should be established. Warfarin
therapy should be continued for 4 weeks after successful cardioversion to normal sinus rhythm.
Antiarrhythmic therapy may be continued for 6-12 months after successful conversion. Therapy should be
reassessed after this time. Caution: Antiarrhythmic drugs may cause proarrhythmia and may lead to
increased mortality rates.
Adapted from KP Southern California
Page
3
Table 1. Risk-Based Antithrombotic Therapy in Patients With Atrial Fibrillation
Patient Features
Age < 60, no heart disease (Lone AF)
Age < 60, heart disease but no risk factors*
Age ≥ 60 , no risk factors*
Age ≥ 60, with diabetes or CAD
Recommended Antithrombotic Therapy
Aspirin (325 mg per day) or no therapy
Aspirin (325 mg per day)
Aspirin (325 mg per day)
Oral anticoagulation (INR 2.0-3.0),
addition of aspirin (81-162 mg) per day is optional
Oral anticoagulation (INR = 2.0)
Oral anticoagulation (INR 2.0-3.0)
Age ≥ to 75 , especially women
Heart failure, LV ejection fraction ≤ 35%,
thyrotoxicosis, and hypertension
Rheumatic heart disease (mitral stenosis)
Oral anticoagulation (INR 2.5-3.5 or higher may be
Prosthetic heart valves
appropriate)
Prior thromboembolism
Persistent atrial thrombus on TEE
* Risk factors for thromboembolism include heart failure, LV EF < 35%, history or hypertension.
Table 2. Recommended Drugs for Pharmacological Cardioversion of Atrial Fibrillation
Drug
Amiodarone
Route of
Administration
Oral
Intravenous/oral
Dofetilide
Oral
Flecainide
Oral
Intravenous
Oral
Intravenous
Oral
Propafenone
Quinidine
Dosages
Inpatient: 1.2-1.8 g per day in divided dose until
10 g total, then 200-400 mg per day
maintenance or 30 mg/kg as single dose
Outpatient: 600-800 mg per day divided dose
until 10 g total, then 200-400 mg per day
maintenance
5-7 mg/kg over 30-60 min, then 1.2-1.8 g per day
continuous IV or in divided oral doses until 10g
total, then 200-400 mg per day maintenance
Creatinine Clearance
Dose
(mL/min)
(mcg BID)
>60
500
40-60
250
20-40
125
<20
Contraindicated
200-300 mg
1.5-3.0 mg/kg over 10-20 min
450-600 mg
1.5-2.0 mg/kg over 10-20 min
0.75-1.5 g in divided doses over 6-12 h,
usually with a rate-slowing drug
Adapted from KP Southern California
Potential Adverse Effects
Hypotension, bradycardia,
QT prolongation, tosade de
pointes (rare), GI upset,
constipation, phlebitis (IV)
QT prolongation, torsade
de pointes; adjust dose for
renal function, body size,
and age
Hypotension, rapidly
conducting atrial flutter
Hypotension, rapidly
conducting atrial flutter
QT prolongation, tosade de
pointes, GI upset,
hypotension
Page
4
Figure 1. Treatment Algorithm – New-Onset Atrial Fibrillation
New-Onset AF
Paroxysmal
Persistent
Accept
permanent AF
1. No therapy needed
unless severe symptoms
(e.g., hypotension, HF,
angina)
Yes
No
*Anticoagulation
and rate control
as needed
Consider
Antiarrhythmic
drug therapy
2. Treat associated HD
*Anticoagulation as
needed
Cardioversion
Long-term
antiarrhythmic
drug therapy
unnecessary
* The use of anticoagulation in those patients age 85+ or those with severe functional impairment
needs to be tempered by clinical judgment, given the known risks of anticoagulation.
Adapted from KP Southern California
Page
5
Figure 2. Antiarrythmic Drug Selection for Rhythm
Heart Disease
Yes
No or minimal
Flecainide
Propafenone
Sotalol
CHF
or
LVEF < 0.35%
CAD
Hypertension
Amiodarone,
Dofetilide
Amiodarone,
Dofetilide
Sotalol
LVH ≥ 1.4 cm
Yes
Disopyramide
Procainamide
Quinidine
Consider
nonpharmacological
options, i.e. AV ablation,
AV nodal ablation with
permanent pacemaker,
Focal RFA
Adapted from KP Southern California
Amiodarone
Dofetilide
No
Amiodarone
Flecainide
Propafenone
Amiodarone
Dofetilide
Sotalol
Disopyramide
Procainamide
Quinidine
Disopyramide
Procainamide
Quinidine
Page
6
Figure 3. Treatment Algorithm: Recurrent and Permanent Atrial Fibrillation
Recurrent
Paroxysmal AF
Recurrent
Persistent AF
Permanent AF
Minimal or no
Symptoms
Disabling
symptoms in AF
Minimal or no
Symptoms
Disabling
symptoms in AF
*Anticoagulation
and rate control
as needed
*Anticoagulation
and rate control
as needed
*Anticoagulation
and rate control
as needed
*Anticoagulation
and rate control
as needed
No drug for
prevention of AF
Antiarrhythmic
drug therapy
Anticoagulation
and rate control
as needed
Continue
anticoagulation
as needed and
therapy to
maintain sinus
rhythm
Electrical
cardioversion
as needed
* The use of anticoagulation in those patients age 85+ or those with severe functional impairment
needs to be tempered by clinical judgment, given the known risks of anticoagulation.
Adapted from KP Southern California
Page
7
SOURCES
1.
Kaiser Permanente, Southern California. Guideline for Atrial Fibrillation 12-2000.
2.
Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC guidelines for the management of patients
with atrial fibrillation A report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines and the European Society of Cardiology Committee for Practice
Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of
Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of
Pacing and Electrophysiology. J Am Coll Cardiol. 2001;38:1-70.
3.
Van Gelder IC, Hagens VE, et al. A Comparison of Rate Control and Rhythm Control in Patients with
Recurrent Persistent Atrial Fibrillation. NEJM. 2002; 347: 1834-1840.
Adapted from KP Southern California
Page
8