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(Circulation. 1996;93:1262-1277.)
© 1996 American Heart Association, Inc.
Articles |
Management of Patients With Atrial Fibrillation
A Statement for Healthcare Professionals From the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association
 |
Executive Summary |
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Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice. Its incidence increases with age and the presence of structural heart disease. It is a major cause of stroke, especially in the elderly. Although the causes are diverse, hypertension is common. Most patients experience palpitations, but fatigue, dyspnea, and dizziness are not uncommon. Patients with an uncontrolled ventricular response during AF may occasionally develop a tachycardia-induced cardiomyopathy. There are three therapeutic goals to consider for patients with AF: rate control, maintenance of sinus rhythm, and prevention of thromboembolism. The risks and benefits of each treatment must be considered for each patient.
Restoration and Maintenance of Sinus Rhythm
Several drugs
effectively restore and maintain sinus rhythm
in patients with AF. To date few data are available to confirm
superiority of any particular drug over another for this purpose.
Agents such as digitalis, verapamil, diltiazem, and
ß-adrenergic blockers may be useful during AF to decrease the
ventricular response that occurs over the
atrioventricular (AV) node, but they rarely terminate
AF. Intravenous procainamide is the treatment of
choice for patients with Wolff-Parkinson-White syndrome who have a
preexcited ventricular response during AF, provided they
are hemodynamically stable. Patients who are unstable
(eg, those with hypotension or significant heart failure) may require
immediate cardioversion. Drugs selected for long-term oral therapy
should be given initially in low to moderate doses and titrated upward,
depending on effectiveness and side effects. Drug interactions with
warfarin and digoxin should be monitored. Proarrhythmia is
the most important risk associated with antiarrhythmic drug therapy.
Bradyarrhythmias, especially sinus bradycardia, and
ventricular tachyarrhythmias, especially
torsade de pointes, can occur. Proarrhythmia often occurs
during initiation of antiarrhythmic drug treatment. In patients without
heart disease who have a normal baseline QT interval,
ventricular proarrhythmia is relatively rare,
and outpatient initiation of treatment is reasonable. However, patients
with structural heart disease, especially those with a history of
congestive heart failure, are at highest risk for
proarrhythmia. Inpatient initiation of antiarrhythmic drug
therapy is recommended for these patients. Nonpharmacological
approaches to prevention of AF include surgery, atrial pacing, and
endocardial catheter ablation. Too few data are available to make any
specific recommendations.
Control of Ventricular Rate
In patients without ventricular
preexcitation,
acute rate control is most effective with intravenous
verapamil, diltiazem, or ß-blockers. ß-Adrenergic
blockers are especially effective in the presence of thyrotoxicosis and
increased sympathetic tone. Verapamil, diltiazem, and
ß-blockers are more effective than digoxin when given orally for
long-term rate control and should be the initial drugs of choice.
Digoxin should be considered as first-line treatment in patients
with congestive heart failure secondary to impaired systolic
ventricular function. Some patients may require
combinations of digoxin, calcium channel blockers, and
ß-adrenergic blockers to control ventricular response
during AF. Intravenous procainamide is the
treatment of choice if conduction is over an accessory pathway.
Nonpharmacological methods to control ventricular rate
include endocardial catheter ablation or modification of the AV
junction and surgically induced AV block. Surgery, however, is rarely
indicated. Catheter ablation is effective and is recommended in
patients who have not responded to or are intolerant of drugs used for
rate control.
Prevention of Thromboembolism
Patients at "low
risk" may be given aspirin 325 mg/d to
prevent stroke. "High-risk" patients who can safely receive
anticoagulation should be treated with warfarin. For high-risk AF
patients aged 75 years or younger, an International Normalized Ratio
(INR) range of 2.0 to 3.0 is safe and effective; for those older than
75, close surveillance of INR levels is recommended because of the
apparently greater likelihood of bleeding complications. Patients with
AF who cannot safely receive anticoagulation should be given aspirin.
The long-term recurrence rate for stroke is high, and
warfarin anticoagulation is recommended; aspirin is an alternative
therapy for those who cannot take anticoagulants. Regarding
cardioversion, in patients who have AF of unknown duration or for more
than 48 hours, anticoagulation should be given for 3 weeks before
electrical or pharmacological cardioversion and continued for 4 weeks
after cardioversion. An alternative approach involves use of
intravenous heparin and subsequent
transesophageal echocardiography
(TEE). Patients without atrial thrombi may undergo cardioversion and be
given warfarin for 4 weeks. Minimal data are available about embolic
risk and the need for anticoagulation in patients with AF of 48 hours'
duration or less.
|
Epidemiology |
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Atrial fibrillation is the most common sustained arrhythmia encountered in clinical practice. Recent data suggest that hospital stays for AF are markedly greater than for any other arrhythmia.1 Nevertheless, information about its incidence and prevalence in a general population is rather sparse. There are fewer data on atrial flutter. Data from clinical populations are subject to the influence of a number of factors that tend to introduce bias. The single best sources of data are reports from the Framingham Study.2 3 4 5 It should be noted that the Framingham population may not be representative of the ethnic and racial diversity found in other parts of the country.
Atrial fibrillation commonly occurs with rheumatic heart disease, particularly mitral stenosis. It also occurs with many other cardiac disorders, including coronary heart disease, congestive or hypertrophic cardiomyopathy, mitral valve prolapse, and mitral valve annular calcification. In the setting of acute myocardial infarction or following cardiac surgery, AF is a common but usually self-limited problem. A number of potentially reversible, noncardiac factors are also associated with transient AF. The latter include hyperthyroidism, acute alcohol intoxication, cholinergic drugs, noncardiac surgery or diagnostic procedures, and pulmonary conditions leading to hypoxemia. Continuing problems with AF are most commonly associated with rheumatic heart disease; hypertension, especially when left ventricular hypertrophy is present; and chronic coronary heart disease.2 Of course, AF can also occur in the absence of other preexisting conditions; in this situation it is called lone or primary AF.3 6 7
The reported frequency of lone AF, usually about 10% or less,3 6 7 may be lower than that currently observed in an office-based setting. At least two factors could be responsible: a referral bias caused by patients seen at tertiary medical centers, from which most data are reported, who are more sick; a change in the epidemiology of AF; or both. Other data (E.N. Prystowsky, unpublished data, 1996) demonstrate that approximately 28% of 172 consecutive outpatients referred for evaluation of AF had lone AF, defined as the absence of any known etiologic factors plus normal ventricular function by echocardiography. The majority of patients were younger than 65 years, although age was not used to define lone AF. Future investigations involving patients of various ages and from various types of practices should clarify this issue.
Prevalence of AF increases with age and is slightly more common in men than in women.2 The prevalence of AF is 0.5% for the group aged 50 to 59 years and rises to 8.8% in the group aged 80 to 89 years.5 In 1982 the cumulative incidence of development of AF over 22 years in the Framingham Study was 2.2% in men and 1.7% in women.2 Excluding persons with rheumatic heart disease, the 2-year incidence of development of AF in 1987 in Framingham was 0.04% for men and 0% for women aged 30 to 39 years; the corresponding figures in the 80-to-89 age group were 4.6% and 3.6%.4 In the more recently initiated Cardiovascular Health Study, a cross-sectional population study of Americans older than 65 years, the prevalence of AF on a 24-hour electrocardiographic (ECG) recording was approximately 5%.7 8 Because women have a greater life expectancy than men, the actual number of cases in elderly women (older than 75) is greater than it is in elderly men. Based on biennial examination in the Framingham Study, the age-adjusted prevalence of AF has increased substantially, particularly in men, over a 30-year period beginning in the mid 1950s (unpublished data, P.A. Wolf, 1995). The importance of this observation, if it can be generalized to the nation, is that the impact of AF with respect to stroke and other consequences may actually be much greater than estimated.
The cardiac precursors of AF were slightly different in men and women in the 1982 report from Framingham.2 In men the significant associations were stroke, cardiac failure, rheumatic heart disease, and hypertensive cardiovascular disease. The strongest associations of these were cardiac failure and rheumatic heart disease. In women the only two significant precursors were cardiac failure and rheumatic heart disease, and the latter was much stronger than in men. Echocardiographic correlates of these clinical features included left atrial enlargement, increased left ventricular wall thickness, and reduced left ventricular shortening.9 Cardiovascular risk factors significantly associated with AF in Framingham were diabetes and left ventricular hypertrophy.2
The importance of AF in a general population is that its appearance heralds a mortality rate double that of control subjects. Much of the morbidity and some of the mortality from AF are due to stroke. The risk of stroke is not due solely to AF, and it substantially increases in the presence of other cardiovascular disease. The attributable risk of stroke from AF is estimated to be 1.5% for the 50-to-59-year age group and approaches 30% for those aged 80 to 89.4 5
There is conflict in the literature concerning prognosis for lone or primary AF. In a 1985 report from Framingham, lone AF accounted for 11.4% of all cases of AF. Importantly, in these persons the relative risk for development of stroke was 4.1% compared with control subjects, whereas incidences for coronary heart disease events and congestive heart failure were the same in both groups.3 In Olmsted County, Minnesota, 2.7% of all patients aged 60 years or younger with AF were identified as having lone AF, and among these patients there was no increased risk of stroke.6 The major difference between the two studies is that the latter6 restricted observations to younger patients free of diabetes or hypertension, whereas in the former3 the majority of the cases of AF occurred in those older than 60 years, 31.5% of whom had hypertension, an important risk factor for stroke in patients with AF.3 Thus, it appears that there is an increased risk of stroke with lone AF in those older than 60 but not in younger patients. In the Cardiovascular Health Study, which included only patients over 65, 6% of cases of AF in women were categorized as lone AF; 9% of cases of AF in men were lone AF.7 The investigators have questioned the clinical usefulness of this diagnosis in the elderly.
Atrial fibrillation is relatively rare in the first 2 decades of life. It has been reported in the fetus, neonate, child, and adolescent, but except for the study by Radford and Izukawa,10 the reports have usually been single case. The rarity of cases has resulted in a limited clinical experience, which has hindered understanding of the etiology of AF, development of management strategies, and characterization of prognosis in the young patient.
Despite the rarity of cases, a few generalizations can be made. In the fetus and neonate, AF is almost always associated with an accessory AV connection.11 12 13 In this setting it is postulated that rapid AV reentry degenerates into AF14 ; the natural history favors spontaneous resolution of tachycardia during the first year of life.15 A similar mechanism has been proposed for development of AF during paroxysmal supraventricular tachycardia in adolescents.16 Atrial fibrillation has been reported in association with dilated and hypertrophic cardiomyopathy. The precise reason for this association has not been established, but it may be related to other aspects of the heart disease rather than as a consequence of the hemodynamic derangement. For example, Spirito et al17 noted that patients with hypertrophic cardiomyopathy and AF usually have the unobstructed type with mild left ventricular hypertrophy.
Long-standing, severe AV valve disease is a risk factor for development of AF. Such a problem is unusual in young persons in the industrialized world, but in areas in which rheumatic heart disease is prevalent, AF is common in young patients. Of note, AF is uncommon in young patients with tachycardia-bradycardia or sick sinus syndrome, which is relatively common following atrial surgery for congenital heart defects.18 Atrial fibrillation may occur in an adult with previous surgery to correct congenital heart disease. In this setting the tachycardia is usually atrial with some features of atrial flutter.19 Furthermore, when such patients undergo pacing conversion of atrial tachycardia, AF develops in about 25% of them, but this is transient and supervened by sinus rhythm within minutes.20 Finally, in ostensibly normal adolescents AF is rare, but in such cases hyperthyroidism has been noted.21 Atrial fibrillation has infrequently been reported in association with intracardiac tumor and muscular dystrophy.
|
Pathophysiology |
|---|
Atrial tachyarrhythmias in general and AF in particular occur in three distinct clinical circumstances: (1) as a primary arrhythmia in the absence of identifiable structural heart disease; (2) as a secondary arrhythmia in the absence of structural heart disease but the presence of a systemic abnormality that predisposes the individual to the arrhythmia; and (3) as a secondary arrhythmia associated with cardiac disease that affects the atria. At this time it is unclear whether the pathophysiological factors responsible for maintaining AF after it has been induced are common to all three, but it is likely that the initiating factors differ.
There are distinct differences between pathological findings in AF secondary to cardiac disorders and other forms of AF. Atrial dilatation and patchy fibrosis ranging from scattered foci to diffuse involvement, including evidence of destruction of the sinoatrial node, are commonly present when AF is associated with structural heart disease.22 23 In contrast, AF secondary to systemic disorders, such as thyrotoxicosis or electrolyte disturbances, is usually unaccompanied by pathological abnormalities or at most by nonspecific scattered fibrosis. From the limited information available, paroxysmal AF in otherwise healthy persons has no pathological correlate and has its basis in either abnormal function of atrial myocyte ion channels, a functional disorder of atrial myocardium, or is associated with unidentified nonpathological structural abnormalities. In some patients AF may be the earliest manifestation of sick sinus syndrome, often a panatrial disease.
There are defined clinical associations between patterns of AF and pathophysiology based on underlying cause. In the presence of heart disease, AF may be paroxysmal at onset and appears to begin when the disease has progressed to clinically significant levels. Over time it has a tendency to become chronic and fixed, rather than remaining paroxysmal. In contrast, systemic conditions that predispose a person to AF are usually associated with persistence of arrhythmia during the period of time that the abnormality persists, which is then followed by either spontaneous reversion after treatment of the predisposing condition or ability to maintain sinus rhythm after cardioversion. In the absence of cardiac or noncardiac disorders, AF is most commonly paroxysmal and recurrent and only occasionally more persistent.24
Electrophysiology of Atrial Fibrillation
The most widely
accepted theory of the mechanism of AF is the
multiple wavelet hypothesis of Moe.25 This hypothesis
envisions multiple reentrant impulses of various sizes wandering
through the atria, creating continuous electrical activity. The
wavelets are of the leading circle type, with a functionally determined
area of conduction block at the center of the circle preventing its
collapse and extinction.26 The critical number of wavelets
required for the perpetuation of AF is approximately
six26 ; the number of wavelets appears to be smaller with
longer wavelengths in coarse AF and greater with smaller wavelengths in
fine AF.
The wavelength, or the product of conduction velocity and refractory period, is a critical determinant for maintaining AF. Influences that increase the wavelength tend to prevent or terminate AF, whereas those that tend to shorten the wavelength of the atrial impulse tend to favor the onset and perpetuation of AF. Wavelength can be prolonged by antiarrhythmic drugs and shortened by increased parasympathetic tone, rapid atrial pacing, or intra-atrial conduction abnormalities.
Recent data suggest that AF may cause electrical changes in the atria, which may lead to persistence or recurrence of AF.27 In a chronic instrumented goat model, Wijffels et al27 noted that (1) artificial maintenance of AF resulted in a prolonged duration of subsequent episodes of AF; (2) atrial refractoriness was shortened markedly during the first 24 hours of AF; and (3) an inverse rate adaptation of atrial refractoriness was manifested by shortening of the effective refractory period at slower paced rates. Anatomic and genetic correlates of these findings remain to be elucidated. However, these exciting new observations may explain, in part, the clinical observation that maintenance of sinus rhythm is more difficult in patients who have had persistent AF for many months.
Functional Mechanisms of Atrial Fibrillation
It has long been
recognized that increased parasympathetic
tone predisposes otherwise normal hearts to the onset of
AF.28 This may occur through several mechanisms, but it is
clear that increased parasympathetic activity, as well as the
muscarinic agonist acetylcholine, can abruptly shorten the time course
of repolarization through activation of a muscarinic potassium channel
in atrial muscle.29 This action shortens the refractory
period of atrial tissue and therefore shortens the wavelength of the
atrial impulse. Increased sympathetic tone may also lead to AF. In
addition, a "maladaptation" of atrial refractory periods to
variations in heart rate has been associated with a propensity to
AF.30 The absence of physiological
shortening of the refractory period in response to an increased heart
rate has been observed and found highly predictive for atrial
tachyarrhythmias. This correlation appears to be at
variance with the mechanism related to the response to parasympathetic
stimulation, since maladaptation produces the reverse effect of the
shortening induced by acetylcholine. It is possible that two
fundamentally different mechanisms can both be responsible for
potentiation of atrial tachyarrhythmias under different
conditions, or that maladaptation to pacing may correlate with
increased response to parasympathetic surges, a possibility that has
not yet been studied. Furthermore, it is possible that changes in
refractoriness may differ in various parts of the atria.
Regardless, present knowledge suggests that one feature common to all patterns is the requirement for multiple wavelets of activation to sustain AF in normal and abnormal hearts. The possibility that multiple areas of focal automaticity could produce the same pattern should not be dismissed, particularly in the presence of underlying structural heart disease and the systemic abnormalities associated with AF. In this regard, a recent observation in a small group of patients suggests that a unifocal atrial mechanism may be the initiating factor in some patients with apparent lone AF. Such a mechanism could also produce multiple wavelets of activation, although by different pathophysiological mechanisms.
Atrioventricular Node Conduction
The AV node exhibits several
properties that tend to limit
ventricular rate during AF. First, the excitability of
cells within the AV node is significantly less than the adjacent atrial
myocardium.31 The inexcitable period of AV
nodal cells is delayed beyond the repolarization phase of the action
potential. Thus, the refractory period of the AV node tends to be
relatively prolonged. Second, the AV node demonstrates decremental
conduction properties; that is, the amplitude and rate of rise of
cardiac action potentials decrease progressively from cell to cell.
Therefore, as action potentials are conducted along the course of the
AV node, there is a progressive decrease in their ability to induce new
action potentials in the cells that lie ahead.32 Because
of this property of decremental conduction, impulses may traverse a
portion of the AV node before encountering conduction block. Among the
clinical manifestations of this property is the phenomenon of concealed
conduction, in which an atrial impulse that itself does not conduct to
the ventricles may impair conduction of subsequent
impulses.33 Thus, a premature electrical impulse may slow
conduction of another impulse through the AV node, blocking an impulse
that otherwise would have conducted.34 The conduction
interval through the AV node is inversely related to the coupling
interval of the preceding atrial impulses, with short atrial cycles
resulting in longer AV nodal conduction intervals than longer atrial
cycles. Moe and colleagues35 observed that when the atrial
rate during AF was relatively slow, there was a tendency for the
ventricular rate to increase; conversely, when the atrial
rate increased, the ventricular rate slowed. The combined
properties of concealed conduction, delayed refractoriness, and the
rapid, variable cycle length of the wavelets of atrial activation
tend to slow conduction of impulses through the AV node in AF. The
result is a significantly slower ventricular rate than
atrial rate. Accessory AV pathways typically do not share these
electrophysiological properties of the
normal AV node, and patients with Wolff-Parkinson-White syndrome
require special therapeutic considerations.
The electrophysiological properties of the AV node are profoundly affected by autonomic influences. Withdrawal of vagal inhibition or an increase in sympathetic stimulation facilitates AV nodal conduction. Exercise is associated with both of these changes in autonomic tone, and the ventricular response during AF may substantially increase along with the metabolic demands of the individual. Changes in AV nodal conduction will reflect the adequacy of heart rate control in patients with AF during varying levels of exertion, emotion, and other metabolic stresses. The marked variation in AV nodal conduction properties as a consequence of varying autonomic tone often presents a therapeutic dilemma for physicians treating patients with AF in whom the ventricular rate may be excessively rapid during exercise, yet inappropriately slow during rest.
Hemodynamic Effects Related to Loss of
Atrioventricular Synchrony and Irregular RR
Intervals
In addition to an inappropriately rapid heart rate, patients
with AF experience the loss of normal AV synchrony and an irregular
ventricular rhythm. The loss of effective atrial
contraction may result in a marked decrease in cardiac output,
especially for persons with impaired diastolic filling of
the ventricles. Patients with mitral stenosis, restrictive or
hypertrophic cardiomyopathy, pericardial diseases,
or ventricular hypertrophy are especially
likely to experience hemodynamic deterioration with
development of AF. In contrast, patients with impaired systolic
function with elevated filling pressures and dilated, compliant
ventricles may experience only minor hemodynamic
deterioration as a consequence of losing AV synchrony.
The random variation in RR intervals during AF results in a constantly changing diastolic filling interval. This fluctuation in diastolic filling interval results in a widely varying stroke volume. Naito and colleagues36 studied the effects of an irregular ventricular rhythm on cardiac output in dogs with complete AV block during ventricular pacing. These investigators found that an irregular ventricular rhythm was associated with a 15% decline in cardiac output compared with a regular rhythm at the same average pacing rate. Mitral regurgitation was observed in these animals during an irregular paced rhythm but not with constant-rate pacing. Thus, it appears that both loss of AV synchrony and irregularity of the ventricular rhythm have an adverse impact on cardiac output. It is quite likely that many symptoms related to AF are due to the variation in left ventricular stroke volume as a result of irregular RR intervals. Chronically elevated ventricular rates during AF or any supraventricular tachycardia may result in a reversible form of ventricular dysfunction characterized by global hypokinesis and dilatation. Persons with continuously elevated ventricular rates (usually greater than 130 beats/min) for a period of several months are at risk of developing a tachycardia-induced cardiomyopathy.37 This form of cardiomyopathy is often reversible following effective control of the ventricular rate. In fact, several investigators have found this to be true in patients with AF when pharmacological or nonpharmacological methods are used to control ventricular rate.38 39 40
|
Clinical Presentations |
|---|
Symptoms associated with AF vary and depend on several factors, including ventricular rate, cardiac function, concomitant medical problems, and individual patient perceptions. Most patients experience palpitations, but presyncope, dizziness, fatigue, and dyspnea are not uncommon. Furthermore, a minority of patients are asymptomatic and AF is discovered by chance. Although asymptomatic patients usually have a relatively controlled ventricular rate, even in the absence of drugs, in some instances the ventricular rate is greater than 100 beats/min. Some patients may have left ventricular dysfunction presumably secondary to a persistently fast ventricular rate during AF.38 Three specific, although relatively uncommon clinical presentations, are noted below.
Tachycardia-Induced
Tachycardia
Tachycardia-induced tachycardia
is the phenomenon in which one tachycardia degenerates into
another.14 For example, atrial flutter and certain atrial
tachycardias often degenerate into AF. More interesting is
the induction of AF as a result of a nonatrial tachycardia;
for example, AV or AV node
reentry.14 41 42 43 44
Even
ventricular tachycardia, with or without
ventriculoatrial conduction, can initiate AF.14 The
mechanism of tachycardia-induced
tachycardia in nonatrial arrhythmias is unclear and
probably multifactorial. Rate of tachycardia, accessory
pathway electrophysiological properties,
intrinsic atrial vulnerability, and contraction-excitation
feedback45 may be causative. In patients who underwent
surgery for Wolff-Parkinson-White syndrome, Chen et al42
reported that cycle length of AV reentry was shorter in patients with a
history of AF. Spach et al46 showed that micro-reentry
based on anisotropy can occur in very small muscle bundles in the
atrial appendage, and in patients with AV reentry, spontaneous
degeneration into AF during
electrophysiological study commonly occurs
first on the high right atrial recording.14 47
Sudden dilatation of the atria, which can be observed at surgery after
onset of AV reentry, can affect cardiac membrane
potential45 and lead to development of AF. Whatever the
exact mechanism for tachycardia-induced
tachycardia in patients with otherwise normal atria, it is
important to be aware of its occurrence. In patients with a history of
regular palpitations preceding AF, AV or AV node reentry may be a cause
of AF. In these persons, elimination of the primary arrhythmia
almost always prevents further episodes of AF.14
Atrial Fibrillation in Wolff-Parkinson-White
Syndrome
Atrioventricular reentry can initiate AF,
which can lead to disastrous consequences if the patient is capable of
sustaining a very rapid preexcited ventricular response
with conduction over the accessory pathway. The rapid heart rate can
produce syncope or, more important, AF may cause
ventricular fibrillation and sudden cardiac
death.48 49 50 Patients who have been
resuscitated from
ventricular fibrillation have a rapid preexcited
ventricular response as demonstrated during induction of AF
in electrophysiological
study.48 49 These patients require aggressive
therapy,
most commonly radiofrequency catheter ablation of the accessory
pathway. Sudden cardiac death in patients with ventricular
preexcitation who have symptomatic arrhythmias
should be preventable, and these persons should undergo
electrophysiological evaluation. If they
are capable of sustaining a rapid preexcited ventricular
response during AF (eg, the shortest preexcited RR interval is less
than 260 ms), catheter ablation of the accessory pathway or aggressive
antiarrhythmic drug therapy to prevent conduction over the accessory
pathway is necessary.
Neurogenic Atrial Fibrillation
Coumel51
described a vagal and adrenergic
form of AF. Vagal origin of AF is characterized by (1) predominance in
men rather than in women (approximately 4:1); (2) age at onset
approximately 40 to 50 years; (3) lone AF with minimal tendency to
permanent AF; (4) occurrence at night, during rest, after eating, or
with absorption of alcohol; and (5) AF usually preceded by progressive
bradycardia. Importantly, both ß-adrenergic blocking drugs and
digitalis may increase frequency of AF.
According to Coumel,51 adrenergic AF has the following features: (1) occurs less frequently than vagal AF; (2) onset is exclusively during daytime; (3) often preceded by exercise and emotional stress; (4) polyuria is common; (5) onset typically occurs with a specific sinus rate, often near 90 beats/min. In contrast to vagally induced AF, ß-adrenergic blockers are usually the treatment of choice.
Patients with "pure" vagally dependent or adrenergic AF are very uncommon. However, history taking may reveal a pattern of onset of AF that has elements of one of these syndromes. This is important because it allows the clinician to select agents that are more likely to prevent episodes of AF in these patients.
|
Approach to Treatment |
|---|
Patient symptoms often direct the physician's therapeutic decisions. For example, a patient with bothersome palpitations in the presence of a rapid ventricular response requires treatment directed at AV nodal conduction to decrease the rate, and if this cannot be achieved with drugs, then nonpharmacological methods may be needed. Restoration and maintenance of sinus rhythm may also be appropriate. In contrast, a patient with a controlled ventricular response during AF and fatigue or shortness of breath often requires maintenance of sinus rhythm as the primary therapeutic goal. In this instance, nonpharmacological methods to control ventricular rate often will not ameliorate symptoms. Asymptomatic persons, especially those with good rate control and depending on the circumstances, may not need further therapy or may be considered candidates for anticoagulation.
In summary, three therapeutic goals should be considered for each patient: rate control, maintenance of sinus rhythm, and prevention of thromboembolism. Heart rate control is a requisite for all patients. The risks and benefits of other therapy must be considered for each patient. A recently initiated NIH trial (AFFIRM) will evaluate the merits and problems of rate control versus maintenance of sinus rhythm.
|
Restoration of Sinus Rhythm and Primary Prevention of Atrial Fibrillation |
|---|
Pharmacological Therapy
Restoration of sinus rhythm may improve symptoms and hemodynamics and has even been associated with an increase in cerebral blood flow.52 Several antiarrhythmic drugs with disparate electrophysiological effects on atrial tissue often restore sinus rhythm. About 50% of patients with new-onset AF will convert spontaneously to sinus rhythm within 24 to 48 hours of presentation.53
Digitalis, verapamil, propranolol, and esmolol rarely terminate AF.53 54 55 Falk et al53 noted no difference in acute reversion of AF in patients with and without digitalis. Agents such as quinidine or procainamide will frequently terminate paroxysmal AF.56 57 The ability to acutely terminate and maintain sinus rhythm over the long term may be enhanced when pharmacological therapy is instituted before electrical cardioversion and then continued after sinus rhythm is restored.
Several antiarrhythmic drugs that affect atrial electrophysiology can terminate or prevent AF.56 57 58 59 60 61 62 63 64 65 66 67 68 69 These include quinidine, procainamide, disopyramide, propafenone, sotalol, flecainide, and amiodarone. Few comparative data exist to assess the efficacy of these agents in maintaining sinus rhythm. In one study sotalol was equally as effective as quinidine.65 Sinus rhythm will be maintained in more than 50% of patients treated with propafenone, flecainide, or sotalol, often with fewer side effects than quinidine.60 61 64 Amiodarone is considered by some the most effective agent for drug-refractory, symptomatic, recurrent AF, although minimal prospective comparative drug data are available. Nearly two thirds of patients treated remained in sinus rhythm for up to 1-year follow-up.66 67 68 69 70 Frequent use of amiodarone for AF is limited by its potentially severe and life-threatening side effects, which may be minimized with lower daily doses.69
Recurrence of AF is common, although antiarrhythmic drugs often effectively decrease the frequency of AF as measured by time to first recurrence and the arrhythmia-free interval.60 63 Thus, successful drug therapy should be evaluated by the decrease in number and duration of AF episodes and not its mere recurrence. Patients with long-standing AF, large left atrial size, or those with multiple previous drug failures will have the highest recurrence rates. Concomitant ventricular rate control therapy with oral digoxin, verapamil, diltiazem, or a ß-blocker should be considered.
Recommendation
There are minimal data from randomized clinical
trials that
confirm superiority of efficacy of any particular drug over the others.
Therefore, selection of an antiarrhythmic agent should be
individualized and will depend in part on renal and hepatic function,
concomitant illnesses and drugs, and cardiovascular
function. Initially, drug dosages should be in the low to moderate
range and titrated upward if efficacy is not achieved and side effects
are not limiting. Certain agents interact with warfarin and digoxin,
and close observation is warranted in these circumstances.
Wolff-Parkinson-White Syndrome
Patients with anterograde
conduction over an
accessory pathway during AF may be hemodynamically
stable and may not require emergency electrical cardioversion. However,
these patients represent the one subgroup with
supraventricular tachyarrhythmias that
may be at risk for sudden cardiac death if the preexcited
ventricular response is rapid (see above). Drugs such as
digitalis, calcium channel blockers, and ß-adrenergic blockers
typically will be ineffective in blocking conduction over the accessory
pathway and frequently enhance conduction resulting in hypotension or
precipitation of cardiac arrest.55 71 72
These drugs
should not be given in such a situation. Lidocaine typically will not
terminate AF and may rarely enhance conduction over the accessory
pathway. Intravenous procainamide is the treatment
of choice. Patients who are hemodynamically unstable
require direct-current cardioversion.
Recommendation
Intravenous administration of procainamide may
decrease conduction over the accessory pathway and terminate AF. In
patients who are hemodynamically unstable,
direct-current cardioversion is the treatment of choice. As noted
previously, these patients require
electrophysiological evaluation and
aggressive antiarrhythmic treatment, preferably catheter ablation of
the accessory pathway.
Risks Associated With Antiarrhythmic Drug Therapy for Atrial
Fibrillation
It is assumed that antiarrhythmic drug treatment will
reduce
recurrence of AF and thus morbidity. This hypothesis has not
been well tested. Asymptomatic short-term
recurrence of AF episodes appears to be common.73
It is not known if these asymptomatic
recurrences are associated with an increased risk for stroke.
In addition, data suggest that use of antiarrhythmic drugs may be
associated with increased
risk.56 74 75 76 77 78 79
In a
meta-analysis study, Coplen et al56 reported
that use of quinidine was associated with a 2.9% mortality, compared
with only 0.9% in patients not treated with quinidine
(P<.05). However, many deaths were due to noncardiac
causes. In the Stroke Prevention in Atrial Fibrillation trial, Flaker
et al77 noted enhanced mortality in AF patients with
associated heart failure who were treated with drugs such as quinidine
and procainamide. The results of the Cardiac Arrhythmia
Suppression Trial (CAST) indicate that flecainide should be avoided in
the post–myocardial infarction setting.80 Pritchett
et al81 reported that in patients with
supraventricular tachycardia, flecainide and
encainide were not associated with enhanced mortality.
Because of its vagolytic effect and resultant rapid ventricular response, quinidine should not be given without prior administration of agents that slow AV nodal conduction. Many antiarrhythmic agents, especially flecainide and propafenone, may slow the atrial rate, allowing more atrial impulses to be conducted through the AV node, which results in a faster ventricular rate.74 In fact, many episodes of wide QRS tachycardia in patients with AF treated with flecainide or propafenone appear to be secondary to atrial flutter with 1:1 AV node conduction associated with QRS widening.82 83 The resultant arrhythmia is often misdiagnosed as ventricular tachycardia. This situation can be prevented or treated by the addition of agents that slow AV node conduction, for example, digitalis, ß-adrenergic blockers, or calcium channel blockers. Occasionally, treatment of patients with tachycardia-bradycardia syndrome worsens sinus node function, resulting in symptomatic bradyarrhythmias that require pacemaker support.
The most common proarrhythmic event reported with antiarrhythmic drug therapy for AF is torsade de pointes, a rapid polymorphic ventricular tachycardia74 78 that occurs with agents that prolong ventricular repolarization (QT interval) (eg, quinidine). Patients most at risk are those with ventricular dysfunction, hypokalemia, or baseline prolongation of the QT interval. Torsade de pointes usually occurs after sinus rhythm has been restored.74 75 Thus, for patients at risk, it is recommended that therapy be initiated in the hospital and the patient observed for 24 to 48 hours in sinus rhythm. Recent data suggest that patients with ventricular hypertrophy may be at increased risk of developing torsade de pointes,74 and drugs that prolong the QT interval should be used with caution in these patients.
Drugs such as propafenone and flecainide do not prolong ventricular repolarization but may cause other forms of life-threatening ventricular tachyarrhythmias. This usually occurs with rapid dose escalations, coexisting potentially lethal ventricular arrhythmias, or left ventricular dysfunction.84 These patients should also be monitored in hospital during drug titration for unexpected proarrhythmic responses. Finally, development of incessant atrial arrhythmias or atrial arrhythmias not previously documented is a rare but well-described atrial proarrhythmic response.78 These arrhythmias are frequently resistant to pharmacological and/or electrical cardioversion, with spontaneous conversion occurring after the drug is metabolized. Because it is difficult to predict the hemodynamic and ventricular responses to an incessant atrial proarrhythmia after the drug is discontinued, treatment is most safe when done in the hospital with telemetry monitoring. Digitalis may cause more frequent episodes of AF in certain patients, possibly because of its vagomimetic effect.
Recommendation
Proarrhythmia is the most important risk
associated
with antiarrhythmic drug therapy in patients with AF. Both
bradyarrhythmias, especially sinus bradycardia, and
ventricular tachyarrhythmias, especially
torsade de pointes, can occur. Proarrhythmia is relatively
rare in patients without heart disease, and outpatient initiation of
antiarrhythmic treatment is reasonable. Patients with heart disease are
most at risk for proarrhythmia, especially those with a
history of congestive heart failure. Inpatient initiation of
antiarrhythmic therapy is recommended for these patients.
Nonpharmacological Therapy
Several surgical approaches have
been used to treat patients
with AF.85 86 87 The left atrial
isolation technique and
"corridor" operation85 86 have met with
less
enthusiasm compared with the maze procedure.87 In the maze
operation, multiple atrial incisions are made to channel sinus impulses
through a path, or "maze," to reach the AV node. This prevents a
critical mass of contiguous atrial tissue from sustaining AF while
maintaining atrial contractility. Early results have
been optimistic, but long-term follow-up of substantial numbers
of patients with a variety of causes of AF is lacking. A substantial
number of patients may require implantation of a permanent pacemaker
after the maze procedure.
Results from surgical approaches suggest that large areas of the atria must be isolated electrically from each other to prevent AF. Endocardial radiofrequency catheter ablation can be used to create long linear lesions for this purpose and is under extensive study by many investigators. A recent case report documenting short-term success of catheter ablation of the right atrium only to prevent AF is noteworthy.88 It is possible that different ablation approaches may be required, depending on the etiology of AF.
Permanent pacing has also been championed as a method to prevent AF. In this regard, dual-chamber AV systems have been considered superior to single-chamber ventricular demand pacemakers.89 90 However, few prospective data are available that document the efficacy of pacing in preventing AF. Even fewer data are available on implantable atrial defibrillators. Newer pacing methods such as biatrial pacing require further investigation.
Recommendation
Nonpharmacological approaches to prevention of
AF include surgery,
atrial pacing, and endocardial catheter ablation. Too few data are
available to recommend pacing or ablation. Preliminary data with the
maze operation are encouraging, but longer follow-up in a more
diverse patient population is required before any specific
recommendations can be made. Recommendations on the use of implantable
atrial defibrillators await results from clinical trials.
Prevention of Postoperative Atrial
Arrhythmias
Postoperative atrial arrhythmias are most commonly
seen after thoracic surgery, especially pneumonectomy and
open-heart surgery.91 92 Up to 30% of patients may
develop an episode that is most often AF. Acute treatment to restore
sinus rhythm is often ineffective or associated with early
recurrence. However, most patients who develop postoperative AF
will have sinus rhythm restored either spontaneously or with
pharmacological therapy within 1 week of surgery and will rarely
require long-term treatment. Hemodynamic and
embolic complications from postoperative paroxysmal AF are rare.
Multiple studies have shown that perioperative
prophylaxis with low-dose ß-blockers frequently prevents
acute episodes.92
|
Control of Ventricular Rate in Atrial Fibrillation |
|---|
Pharmacological Control of Atrioventricular Conduction During Atrial Fibrillation
Pharmacological agents that depress conduction and prolong refractoriness in the AV node are frequently required for control of symptoms and improvement of hemodynamics during AF. Commonly used drugs that prolong refractoriness and decrease conduction velocity in the AV node include digoxin, ß-adrenergic antagonists, and calcium channel blockers. The electrophysiological actions of digoxin on the AV node are indirect and depend on cardiac innervation, with minimal direct effects noted.93 The physician attempting to slow the ventricular rate during AF must consider two phases of treatment: an acute phase that involves rapid control of ventricular rate and a long-term phase that involves drugs given orally.
Patients with an episode of AF often develop rapid ventricular rates and may be highly symptomatic. In the presence of important clinical symptoms, such as chest pain or exacerbation of congestive heart failure, that are related to a rapid ventricular response, intravenous drug therapy to slow the heart rate relatively quickly is often required. Although intravenous digoxin may effectively slow the ventricular rate at rest, there is a delay in onset of the therapeutic effect of at least 60 minutes in most patients, with the full effect delayed for up to 6 hours. In addition, digoxin is no more effective than placebo for converting AF to sinus rhythm53 and may prolong duration of paroxysmal AF.94 Thus, except in heart failure, it is not first-line therapy.
For patients with severe symptoms related to a rapid ventricular rate, intravenous diltiazem, verapamil, esmolol, propranolol, or metoprolol provide rapid control of heart rate. Each of these drugs has a potential role in acute management of symptomatic individuals with AF and rapid ventricular rates. For example, an intravenous bolus of diltiazem (20 to 25 mg) resulted in a slowing of ventricular rate during AF or atrial flutter in 94% of patients in one multicenter study.95 The median time to therapeutic response was 4 minutes, and a continuous infusion of diltiazem (10 to 15 mg/h) maintained control of ventricular rate in 74%. Intravenous verapamil is also effective for slowing ventricular rate during AF.55 96 97 98 An initial bolus of 5 to 15 mg reduces the ventricular rate within 5 minutes and can be followed by a maintenance infusion of 0.05 to 0.2 mg/min.55 96 97 98 The major adverse effects of intravenous diltiazem and verapamil include hypotension (in up to 7.5% of patients receiving diltiazem).99 Intravenous esmolol, an ultrashort-acting ß-adrenergic antagonist, may effectively control ventricular response during AF within 15 minutes.100 Intravenous metoprolol (5 to 15 mg intravenously over 5 to 15 minutes) and propranolol (1 to 12 mg intravenously over 5 to 12 minutes) can also be administered for control of rapid heart rates in AF. Adenosine is a naturally occurring substance with a half life of approximately 10 seconds that produces marked inhibition of AV nodal conduction. Although adenosine is very effective for terminating reentrant arrhythmias using the AV node,101 this agent has no role in the management of AF because of its transient duration of action.
The control of rapid preexcited ventricular rates during AF in patients with Wolff-Parkinson-White syndrome requires reemphasis. As stated earlier, drugs such as digoxin, adenosine, calcium channel blockers, and ß-adrenergic antagonists should be avoided. Prompt electrical cardioversion is indicated for patients with severe symptoms. Others may be treated with intravenous procainamide.
In the absence of significant symptoms related to a rapid ventricular response to AF, intravenous medications are not indicated because of the potential for adverse effects such as hypotension or precipitation of congestive heart failure. In these less symptomatic persons, the ventricular rate is usually controlled with orally administered medications. Calcium channel blockers and ß-adrenergic antagonists are preferred over digoxin in patients without heart failure. In the presence of thyrotoxicosis or factors associated with increased sympathetic tone, such as exercise or metabolic stress, rapid ventricular rates during AF are most effectively controlled with ß-adrenergic blockers. When there are contraindications to the use of ß-adrenergic antagonists, such as bronchospasm, calcium channel blockers should be considered.
The choice of a drug for long-term ventricular rate control during AF requires consideration of several clinical factors. Some patients with depressed AV nodal function may have adequate rate control and do not require drug therapy. Since AV node conduction is markedly influenced by changes in autonomic tone, the ventricular rate may be well controlled during rest, yet excessive during physical exertion. Thus, although digoxin is useful for slowing the ventricular rate during AF at rest, it provides little control during exercise.102 For patients without heart failure, ß-adrenergic or calcium channel blockers are preferred for rate control.55 103 104 105 Perhaps the most clearly defined role for digoxin in the management of AF is for concomitant congestive heart failure related to impaired systolic ventricular function or in combination with other agents. In the latter circumstance, digoxin provides additive effects with calcium channel or ß-adrenergic blockers for ventricular rate control.102 103 104 The balance of rate control during varying levels of physical activity can be especially challenging for patients who have episodes of paroxysmal AF associated with rapid ventricular rates that alternate with periods of sinus rhythm with sinus node dysfunction (tachycardia-bradycardia syndrome).22 Permanent pacing is often required for these patients to allow use of pharmacological agents that slow AV nodal conduction. In some patients with tachycardia-bradycardia syndrome, pindolol, a ß-adrenergic blocker with intrinsic sympathomimetic activity, may provide rate control without the need for permanent pacing. Last, if sotalol or amiodarone is chosen to prevent AF, in some patients no other agent may be needed because these drugs also depress AV node conduction.
Recommendation
It is important to control ventricular
response during
AF to decrease the patient's symptoms as well as prevent a
tachycardia-induced cardiomyopathy.
Acute rate control is most effective with intravenous
verapamil, diltiazem, or ß-blockers.
Intravenous procainamide is the treatment of choice
if conduction is over an accessory pathway. Some patients may require
immediate cardioversion. ß-Adrenergic blockers are especially
effective in the presence of thyrotoxicosis and increased sympathetic
tone. For long-term rate control, verapamil, diltiazem,
and ß-blockers are more effective than digoxin and should be the
initial drugs of choice. Digoxin should be considered as first-line
treatment only in patients with congestive heart failure secondary to
impaired systolic ventricular function. In some
patients, combinations of digoxin, calcium channel blockers, and
ß-adrenergic blockers may be needed to control
ventricular response.
Nonpharmacological Control of Ventricular Rate During
Atrial Fibrillation
Many persons with either paroxysmal or chronic AF
will remain
significantly symptomatic despite the use of drugs that
slow AV nodal conduction or attempt to maintain sinus rhythm. In some
patients with severe symptoms that cannot be improved with adequate
trials of antiarrhythmic medications, AV nodal ablation and permanent
pacemaker implantation may provide symptomatic
relief.106 107 This procedure has been demonstrated
to
improve exercise tolerance and quality of life for selected individuals
with either paroxysmal or chronic AF.108 Several methods
for ablating AV nodal conduction have been described, including
surgical cryoablation, catheter ablation with direct-current
shocks,109 intracoronary ethanol infusion, or
radiofrequency energy.110 Radiofrequency catheter ablation
has emerged as the most commonly used technique for ablating the AV
node. There are several important clinical considerations regarding use
of AV nodal ablation for treatment of AF. First, there is no evidence
that this technique influences survival in patients with AF. In fact,
there has been some concern about a very small possible risk of sudden
death after AV junctional ablation in these patients, but it is not
clear whether this is not simply the natural history of the underlying
cardiac disease. Second, the results of this procedure cannot be
reversed. Third, patients with fatigue who have good rate control may
receive minimal benefit from this procedure. Fourth, many patients are
pacemaker dependent after AV nodal ablation. For this reason, the
long-term reliability of pacing leads and pulse generators must be
considered. Finally, AV nodal ablation does not change the risk of
systemic emboli or the need for anticoagulation. Recently, ablation
techniques that modify AV conduction without inducing complete AV block
have been described.111 112
Recommendation
Nonpharmacological methods to control
ventricular rate
include endocardial catheter ablation or modification of the AV
junction and surgically induced AV block. Catheter ablation is
recommended in patients who have not responded to or are intolerant of
drugs used to control ventricular response. Surgery is
rarely indicated for rate control.
|
Preventing Thromboembolism in Atrial Fibrillation |
|---|
 TopExecutive Summary Epidemiology Pathophysiology Clinical Presentations Approach to Treatment Restoration of Sinus Rhythm...Control of Ventricular Rate... Preventing Thromboembolism in... References |
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Atrial fibrillation is a common cardiac arrhythmia of the elderly, and stroke is its most devastating complication. The high risks of thromboembolism in AF associated with mitral stenosis and prosthetic mitral valves have long been appreciated. However, AF even in the absence of these valvular disorders carries a substantially increased risk of ischemic stroke.5 The rate of ischemic stroke among elderly people with AF averages 5% per year, about six times that of people without AF.4 5 113 Considering transient ischemic attacks (which often cause radiographic evidence of brain infarction) and clinically occult stroke detected radiographically, the rate of brain ischemia accompanying nonvalvular AF exceeds 7% per year, an impressive threat to the brain.113 114 115 116 117 However, the absolute rate of stroke varies importantly with patient age and coexistent cardiovascular disease.6 113 118 119 Stratification of AF patients into those at high and low risk for thromboembolism is a crucial determinant of optimal antithrombotic prophylaxis, as discussed in detail below.
The prevalence of AF increases with advancing age, and the incidence of stroke in AF patients is similarly age related. Thus, AF is most frequent and more threatening in the very elderly.4 5 120 About half of AF-associated strokes occur in patients older than 75, and AF may be the most frequent cause of disabling stroke in elderly women.5 121 122 In short, AF-associated stroke is particularly a problem for the very elderly (older than 75 years). Special consideration of stroke prophylaxis in this age group is critical to prevention.
Most ischemic strokes associated with AF are probably due to embolism of stasis-induced thrombi forming in the left atrium and particularly its appendage. Transesophageal echocardiography shows left atrial thrombi to be more frequent in AF patients with ischemic stroke compared with AF patients without stroke. However, perhaps 25% of AF-associated stroke is due to associated intrinsic cerebrovascular diseases, other cardiac sources of embolism, or aortic arch atheroma.123 124 About half of elderly AF patients have chronic hypertension, a major risk factor for primary cerebrovascular disease.113 About 12% of elderly AF patients harbor cervical carotid artery stenosis, but the frequency of carotid artery stenosis is not substantially greater in AF patients with stroke, suggesting that carotid artery stenosis is a minor contributor to AF-associated stroke.125 Routine screening of AF patients without symptoms of brain ischemia for cervical carotid artery stenosis does not appear warranted.
Atrial Fibrillation Patients With High and Low Rates of
Thromboembolism
The absolute rate of ischemic stroke in
patients with AF is critically influenced by coexistent
cardiovascular disease. Identification of
subpopulations of AF patients who have relatively high or low absolute
rates of stroke determine which patients gain the greatest benefit from
anticoagulant therapy, offsetting its disutility. Because clinical
classification of etiologic subtypes of ischemic stroke is
imperfect and not adequately validated,123 risk
stratification schemes are presently based on combined
analysis of all ischemic strokes. Such stratification
schemes for AF patients have been extensively pursued, using clinical
and echocardiographic
parameters.6 113 118 119 122 126 127 128 129 130
Two prospective studies included sufficient numbers of patients and
strokes, analyzed by multivariable techniques, and
provide the most reliable stratification schemes available
(Table
).113 118 The differences in the
two
schemes (presence of age versus heart failure) are not contradictory or
even substantially conflicting, as clinical variables overlap (age
is related to heart failure, hypertension, and diabetes).
Interestingly, intermittent (ie, paroxysmal) AF was not an independent
predictor of thromboembolic risk in either study. In summary, the five
clinical variables listed in the Table are independently
predictive
of thromboembolic risk and are clinically useful for characterizing AF
patients with high and low risks for stroke. Other studies support the
notion that AF-associated stroke is related to patient age,
hypertension, coexistent heart disease, and perhaps female
gender.122 126 Echocardiographic
predictors of increased thromboembolic risk in AF are enlarged left
atrial size (mitigated by mitral regurgitation) and,
independently, impaired left ventricular
function.119 131 Impaired left ventricular
function may further contribute to stasis within the left atrium in AF
patients.132 133 Precordial
echocardiographic findings can be combined with
clinical risk stratifiers to identify AF patients with very low
inherent rates of thromboembolism.119
|
Transesophageal echocardiography offers better visualization of the left atrium and its appendage than conventional transthoracic echocardiography. When TEE is used, left atrial appendage thrombi and spontaneous echogenic densities ("smoke") possibly indicative of stasis are more often found in AF patients with thromboembolism than those without thromboembolism.134 Stoddard et al135 used TEE to evaluate the frequency of left atrial thrombus in 143 patients with AF of less than 3 days' duration. Twenty patients (14%) had left atrial thrombus and 56 (39%) had spontaneous echocardiographic contrast. A recent systemic embolus occurred in 24 patients, 5 of whom had documented left atrial thrombus. Fatkin et al136 showed that thromboembolic complications can occur after cardioversion in patients without left atrial thrombus identified with TEE before cardioversion, an observation confirmed in a multicenter study.137 However, the predictive value of TEE findings for subsequent stroke has yet to be validated by adequate clinical studies. Thus, data are insufficient to recommend routine TEE to stratify thromboembolic potential in AF patients.
Antithrombotic Therapies to Prevent Stroke
Anticoagulation
with oral vitamin K antagonists
such as warfarin is highly effective for reducing ischemic
stroke in AF patients. Five recent randomized clinical trials using INR
ranges of approximately 1.8 to 4.2 showed a mean reduction in
ischemic stroke of nearly 70% in patients assigned to receive
anticoagulation (Fig 1); on-therapy
analysis indicated an even greater benefit.113 The
incremental risk of serious bleeding was less than 1% per year among
patients on anticoagulation who were selected to participate in these
clinical trials and followed carefully on protocols. In a more
generalized outpatient population, risk of bleeding may be
greater.138 Low-intensity anticoagulation (INR 2.0 to
3.0) clearly confers benefit.113 139 Warfarin is very
effective in subgroups of AF patients with a high inherent risk of
thromboembolism (Table
).113 140 Safe
anticoagulation
requires monitoring with the INR that corrects for varying
thromboplastin sensitivities.
|
The safety and tolerability of long-term anticoagulation titrated to conventional levels has been less clear in the very elderly (older than 75), the age group encompassing perhaps half of AF-associated stroke patients. All but one of the placebo-controlled clinical trials testing anticoagulation enrolled AF patients with a mean age in the late 60s.113 The single placebo-controlled trial involving AF patients with a mean age of 75 reported a 38% withdrawal rate from anticoagulation after 1 year, although withdrawal was not related merely to age.141 A recent clinical trial comparing anticoagulation in AF patients younger and older than 75 years found that risk of major hemorrhage during anticoagulation (INR range 2.0 to 4.5; mean INR, 2.7) was substantially increased in AF patients older than 75 compared with younger AF patients who received anticoagulation of similar intensities.140 In contrast, the pooled data from five AF trials demonstrated only one intracranial hemorrhage in 223 patients older than 75 receiving warfarin.113 Further, in the European Atrial Fibrillation Trial,142 a secondary prevention study, 63% of patients were more than 70 years old, and no intracranial hemorrhages occurred during warfarin therapy (mean INR 2.9). Importantly, the yearly incidence of major bleeding complications was significantly higher during warfarin treatment versus control (2.8% versus 0.7%).142 Thus, particular caution should be taken and INR levels closely monitored when warfarin is used in the very elderly.
The efficacy of aspirin, an antiplatelet agent,
for
stroke prevention in AF patients is less clear and remains
controversial.113 The effect of aspirin in doses between
75 and 325 mg/d has been assessed in three randomized,
placebo-controlled clinical trials with a statistically significant
risk reduction of about 25% (range 14 to 44%) in aspirin-treated
patients, based on pooled
data.114 142 143 However,
aspirin was significantly less effective than anticoagulation in two of
these clinical trials142 143 and also by secondary
on-therapy analysis of the third trial144 (Fig 2).
There is no compelling evidence that the specific dose
of aspirin between 75 and 325 mg/d confers more or less benefit. In
short, aspirin has some degree of efficacy for preventing AF-associated
stroke, but it is clearly less than that of anticoagulation.
|
Selecting Antithrombotic Therapy to Prevent Stroke
There is
persuasive evidence that antiplatelet agents
and anticoagulants differentially affect cardioembolic and
noncardioembolic stroke in AF patients.123 145
Aspirin has
a greater effect on noncardioembolic stroke than on those presumed to
be cardioembolic.123 In cardioembolic strokes, aspirin
exerted a lesser and nonsignificant effect.123 Aspirin may
be particularly effective in AF patients under 75 years old with a
history of diastolic hypertension, who are at special risk
for noncardioembolic stroke.145 Antiplatelet
agents do appear to be effective in reducing stasis-induced thrombi
in the lower extremities,144 and aspirin may offer some
degree of protection against cardioembolic stroke in AF
patients.123 Most AF-related stroke, particularly in
women, is due to cardiogenic embolism, and these strokes are more
effectively prevented by
anticoagulation.145 146
Recommendation
Pending further clinical studies now ongoing,
low-risk AF
patients may be given 325 mg aspirin daily to prevent stroke and may be
carefully followed unless high-risk criteria (including
systolic blood pressure 
160 mm Hg) develop (the Table).
This
can be strongly recommended for low-risk AF patients younger than
65. High-risk patients who can safely receive anticoagulation
should be treated with warfarin. For high-risk AF patients 75 or
younger, an INR range of 2.0 to 3.0 is safe and effective; for those
over 75, close surveillance of INR levels is recommended because of the
apparently greater likelihood of bleeding complications. Patients with
AF who cannot safely receive anticoagulation should be given aspirin.
The value of other antiplatelet agents has not been assessed in
patients with AF.
Secondary Prevention of Stroke in Atrial Fibrillation
Patients
The conventional wisdom has been that most ischemic
strokes in AF patients are large and disabling, but it is now clear
that minor stroke and transient ischemic attacks (TIAs)
frequently accompany AF.113 AF-related stroke carries a
particularly high 30-day mortality rate related to advanced patient age
and associated heart disease.124 147 Stroke in AF
patients
is usually due to cardiogenic embolism, but an important minority is
caused by other mechanisms.123 124 In patients with
acute
stroke who have previously unrecognized AF, atrial fibrillation can be
the consequence of brain infarction mediated by other
mechanisms.148
Recent studies indicate that risk of early recurrent stroke (within 2 weeks) is low in patients with AF.124 149 Initiating oral anticoagulation within a few days in submassive infarcts seems reasonable; a delay of 1 week or more in starting warfarin in AF patients with large infarcts may be prudent to avoid accentuating secondary brain hemorrhage. Prophylaxis for deep venous thrombosis with low-dose, subcutaneous heparin and/or aspirin in those with lower limb paresis is safe.124
The sequence and extent of diagnostic evaluation is aimed at identifying patients who should receive long-term anticoagulation for secondary prevention (most patients) or carotid endarterectomy (few). Carotid sonography shows ipsilateral cervical carotid stenosis in about 15% of AF patients with stroke.123 124 Transthoracic echocardiography at the time of stroke is seldom helpful in defining stroke mechanism, as left atrial thrombi are not reliably detected with this technique. Transesophageal echocardiography is more sensitive for detection of left atrial thrombi. In AF patients with brain ischemia who have ipsilateral carotid artery stenosis, TEE is recommended to exclude atrial thrombi before considering carotid endarterectomy. In AF patients with acute stroke or TIA with or without carotid artery stenosis, anticoagulation is optimal for secondary prevention in all who can safely take it. The long-term rate of recurrent stroke is high, exceeding 10% per year.142 149 A large randomized trial demonstrated long-term anticoagulation (INR 2.5 to 4.0) to be highly effective (significantly more effective than aspirin) and relatively safe.142 Because of the substantial rate of recurrent stroke, the absolute risk reduction by anticoagulation for secondary prevention clearly favors its use in most patients, with a target INR value of 3.0.142 150 Aspirin offers a lesser benefit for those who cannot receive anticoagulants for secondary prevention.142
Recommendation
The long-term recurrence rate for stroke is
high, and
warfarin anticoagulation is recommended. Aspirin is alternative therapy
for those who cannot receive anticoagulants.
Anticoagulation for Cardioversion
Systemic embolism is a
complication of electrical and
pharmacological cardioversion of AF to sinus
rhythm.151 152 Prior anticoagulation appears to
decrease
the embolic risk,152 153 although randomized
prospective
trials to evaluate the effectiveness of anticoagulation in
this setting have not been performed. Current recommendations are to
give anticoagulants to patients who have AF of unknown duration or more
than 48 hours for approximately 3 weeks before and 4 weeks after
cardioversion.154 Because pharmacological cardioversion
may lead to systemic emboli, antiarrhythmic agents to restore sinus
rhythm should be withheld until anticoagulation has been achieved.
An alternative approach using TEE has been suggested for inhospital patients with AF lasting for more than 2 days.155 In this prospective study, patients were given intravenous heparin, and TEE was used to determine whether atrial thrombi were present. Patients without atrial thrombi underwent pharmacological or electrical cardioversion, and warfarin was prescribed for 1 month after cardioversion. No clinical embolic events were noted. Patients with atrial thrombi were given warfarin therapy, and cardioversion was deferred. Thus, this approach can be used for patients when earlier cardioversion is desired.
The need for anticoagulation in patients with short-duration AF (less than 48 hours) is less clear. These patients can have left atrial thrombi and systemic emboli.135 Administration of intravenous heparin before cardioversion and warfarin anticoagulation for 3 to 4 weeks after cardioversion may be useful, but supporting data are not available.
Recommendation
A newly formed thrombus may take at least 2
weeks to become
firmly attached to the atrial myocardium.
Furthermore, after cardioversion, forceful atrial contractions
may not resume for 2 weeks or longer. Thus, in patients with AF of
unknown duration or for more than 48 hours, anticoagulation should be
given for 3 weeks before cardioversion (electrical or pharmacological)
and continued for 4 weeks after cardioversion. An alternative approach
involves the use of intravenous heparin and subsequent TEE.
Patients without atrial thrombi may undergo cardioversion and be given
warfarin for 4 weeks. Minimal data are available regarding embolic risk
in patients with AF of short duration (less than 48 hours).
|
Footnotes |
|---|
"Management of Patients With Atrial Fibrillation" was approved by the American Heart Association SACC/Steering Committee on October 19, 1995.
Requests for reprints should be sent to the Office of Scientific Affairs, American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231-4596.
|
References |
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A. Capucci, G.Q. Villani, N. Marrazzo, and M. Piepoli The complementary role of drug, ablation and device in the electrical therapy of atrial fibrillation Eur. Heart J. Suppl., November 1, 2001; 3(suppl_P): P47 - P52. [Abstract] [PDF]
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V. Fuster, L. E. Ryden, R. W. Asinger, D. S. Cannom, H. J. Crijns, R. L. Frye, J. L. Halperin, G. N. Kay, W. W. Klein, S. Levy, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary 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 Circulation, October 23, 2001; 104(17): 2118 - 2150. [Full Text] [PDF]
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G. C. Fonarow Quality Indicators for the Management of Heart Failure in Vulnerable Elders Ann Intern Med, October 16, 2001; 135(8_Part_2): 694 - 702. [Full Text] [PDF]
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K. A. Glatter, P. C. Dorostkar, Y. Yang, R. J. Lee, G. F. Van Hare, E. Keung, G. Modin, and M. M. Scheinman Electrophysiological Effects of Ibutilide in Patients With Accessory Pathways Circulation, October 16, 2001; 104(16): 1933 - 1939. [Abstract] [Full Text] [PDF]
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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 Eur. Heart J., October 2, 2001; 22(20): 1852 - 1923. [PDF]
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V. Frykman, B. Beerman, L. Ryden, and M. Rosenqvist Management of atrial fibrillation: discrepancy between guideline recommendations and actual practice exposes patients to risk for complications Eur. Heart J., October 2, 2001; 22(20): 1954 - 1959. [Abstract] [PDF]
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V. Fuster, L. E. Ryden, R. W. Asinger, D. S. Cannom, H. J. Crijns, R. L. Frye, J. L. Halperin, G. N. Kay, W. W. Klein, S. Levy, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary: 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., October 1, 2001; 38(4): 1231 - 1265. [Full Text] [PDF]
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A. L. Klein, R. A. Grimm, R. D. Murray, C. Apperson-Hansen, R. W. Asinger, I. W. Black, R. Davidoff, R. Erbel, J. L. Halperin, D. A. Orsinelli, et al. Use of Transesophageal Echocardiography to Guide Cardioversion in Patients with Atrial Fibrillation N. Engl. J. Med., May 10, 2001; 344(19): 1411 - 1420. [Abstract] [Full Text] [PDF]
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C. Ozcan, A. Jahangir, P. A. Friedman, P. J. Patel, T. M. Munger, R. F. Rea, M. A. Lloyd, D. L. Packer, D. O. Hodge, D. L. Hayes, et al. Long-Term Survival after Ablation of the Atrioventricular Node and Implantation of a Permanent Pacemaker in Patients with Atrial Fibrillation N. Engl. J. Med., April 5, 2001; 344(14): 1043 - 1051. [Abstract] [Full Text] [PDF]
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M. Fukuchi, J. Watanabe, K. Kumagai, Y. Katori, S. Baba, K. Fukuda, T. Yagi, A. Iguchi, H. Yokoyama, M. Miura, et al. Increased von Willebrand factor in the endocardium as a local predisposing factor for thrombogenesis in overloaded human atrial appendage J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1436 - 1442. [Abstract] [Full Text] [PDF]
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B. F. Gage, S. D. Fihn, and R. H. White Warfarin Therapy for an Octogenarian Who Has Atrial Fibrillation Ann Intern Med, March 20, 2001; 134(6): 465 - 474. [Abstract] [Full Text] [PDF]
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A. L. Klein, R. D. Murray, and R. A. Grimm Role of transesophageal echocardiography-guided cardioversion of patients with atrial fibrillation J. Am. Coll. Cardiol., March 1, 2001; 37(3): 691 - 704. [Abstract] [Full Text] [PDF]
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H. S. Friedman Serum Homocysteine and Stroke in Atrial Fibrillation Ann Intern Med, February 6, 2001; 134(3): 253 - 254. [Full Text] [PDF]
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K. L. Grady, K. Dracup, G. Kennedy, D. K. Moser, M. Piano, L. W. Stevenson, and J. B. Young Team Management of Patients With Heart Failure : A Statement for Healthcare Professionals From the Cardiovascular Nursing Council of the American Heart Association Circulation, November 7, 2000; 102(19): 2443 - 2456. [Full Text] [PDF]
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M. J. P. Raatikainen, T. E. Morey, P. Druzgala, P. Milner, M. D. Gonzalez, and D. M. Dennis Potent and Reversible Effects of ATI-2001 on Atrial and Atrioventricular Nodal Electrophysiological Properties in Guinea Pig Isolated Perfused Heart J. Pharmacol. Exp. Ther., November 1, 2000; 295(2): 779 - 785. [Abstract] [Full Text]
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G E Kochiadakis, N E Igoumenidis, M E Marketou, M D Kaleboubas, E N Simantirakis, and P E Vardas Low dose amiodarone and sotalol in the treatment of recurrent, symptomatic atrial fibrillation: a comparative, placebo controlled study Heart, September 1, 2000; 84(3): 251 - 257. [Abstract] [Full Text] [PDF]
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R. L. Page Beta-blockers for atrial fibrillation: must we consider asymptomatic arrhythmias? J. Am. Coll. Cardiol., July 1, 2000; 36(1): 147 - 150. [Full Text] [PDF]
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L.-P. Lai, J.-L. Lin, W.-P. Lien, Y.-Z. Tseng, and S. K. S. Huang Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes J. Am. Coll. Cardiol., May 1, 2000; 35(6): 1434 - 1441. [Abstract] [Full Text] [PDF]
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S. Mittal, S. Ayati, K. M. Stein, D. Schwartzman, D. Cavlovich, P. J. Tchou, S. M. Markowitz, D. J. Slotwiner, M. A. Scheiner, and B. B. Lerman Transthoracic Cardioversion of Atrial Fibrillation : Comparison of Rectilinear Biphasic Versus Damped Sine Wave Monophasic Shocks Circulation, March 21, 2000; 101(11): 1282 - 1287. [Abstract] [Full Text] [PDF]
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M. A. Wood, C. Brown-Mahoney, G. N. Kay, and K. A. Ellenbogen Clinical Outcomes After Ablation and Pacing Therapy for Atrial Fibrillation : A Meta-Analysis Circulation, March 14, 2000; 101(10): 1138 - 1144. [Abstract] [Full Text] [PDF]
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H Nakazawa, D.A Lythall, J Noh, N Ishikawa, K Sugino, K Ito, and S.M.C Hardman Is there a place for the late cardioversion of atrial fibrillation?. A long-term follow-up study of patients with post-thyrotoxic atrial fibrillation Eur. Heart J., February 2, 2000; 21(4): 327 - 333. [Abstract] [PDF]
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A Capucci, G.Q Villani, D Aschieri, A Rosi, and M.F Piepoli Oral amiodarone increases the efficacy of direct-current cardioversion in restoration of sinus rhythm in patients with chronic atrial fibrillation Eur. Heart J., January 1, 2000; 21(1): 66 - 73. [Abstract] [PDF]
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S. H. Hohnloser, Y.-G. Li, B. Bender, and G. Gronefeld Review : Pharmacological Management of Atrial Fibrillation: An Update Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 2000; 5(1): 11 - 16. [Abstract] [PDF]
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P. Schauerte, B. J. Scherlag, M. A. Scherlag, S. Goli, W. M. Jackman, and R. Lazzara Ventricular rate control during atrial fibrillation by cardiac parasympathetic nerve stimulation: a transvenous approach J. Am. Coll. Cardiol., December 1, 1999; 34(7): 2043 - 2050. [Abstract] [Full Text] [PDF]
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L Frost, G Engholm, H Moller, and S. Husted Decrease in mortality in patients with a hospital diagnosis of atrial fibrillation in Denmark during the period 1980-1993 Eur. Heart J., November 1, 1999; 20(21): 1592 - 1599. [Abstract] [PDF]
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M Gasparini, M Mantica, M Brignole, L Gianfranchi, C Menozzi, F Pizzetti, G Magenta, P Delise, A Proclemer, S Tognarin, et al. Thromboembolism after atrioventricular node ablation and pacing: long term follow up Heart, October 1, 1999; 82(4): 494 - 498. [Abstract] [Full Text] [PDF]
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W. G. Stevenson and L. W. Stevenson Atrial Fibrillation in Heart Failure N. Engl. J. Med., September 16, 1999; 341(12): 910 - 911. [Full Text]
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P. J. Zimetbaum and M. E. Josephson The Evolving Role of Ambulatory Arrhythmia Monitoring in General Clinical Practice Ann Intern Med, May 18, 1999; 130(10): 848 - 856. [Abstract] [Full Text] [PDF]
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M. A. Gatzoulis, M. A. Freeman, S. C. Siu, G. D. Webb, and L. Harris Atrial Arrhythmia after Surgical Closure of Atrial Septal Defects in Adults N. Engl. J. Med., March 18, 1999; 340(11): 839 - 846. [Abstract] [Full Text] [PDF]
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G. E. Kochiadakis, N. E. Igoumenidis, F. I. Parthenakis, G. I. Chlouverakis, and P. E. Vardas Amiodarone versus propafenone for conversion of chronic atrial fibrillation: results of a randomized, controlled study J. Am. Coll. Cardiol., March 15, 1999; 33(4): 966 - 971. [Abstract] [Full Text] [PDF]
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P. B. Sparks, S. Jayaprakash, H. G. Mond, J. K. Vohra, L. E. Grigg, and J. M. Kalman Left atrial mechanical function after brief duration atrial fibrillation J. Am. Coll. Cardiol., February 1, 1999; 33(2): 342 - 349. [Abstract] [Full Text] [PDF]
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N. S PETERS Atrial fibrillation: towards an understanding of initiation, perpetuation, and specific treatment Heart, December 1, 1998; 80(6): 533 - 534. [Full Text]
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R. S. Stafford, D. C. Robson, B. Misra, J. Ruskin, and D. E. Singer Rate Control and Sinus Rhythm Maintenance in Atrial Fibrillation: National Trends in Medication Use, 1980-1996 Arch Intern Med, October 26, 1998; 158(19): 2144 - 2148. [Abstract] [Full Text] [PDF]
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M. Brignole, C. Menozzi, L. Gianfranchi, G. Musso, R. Mureddu, N. Bottoni, and G. Lolli Assessment of Atrioventricular Junction Ablation and VVIR Pacemaker Versus Pharmacological Treatment in Patients With Heart Failure and Chronic Atrial Fibrillation : A Randomized, Controlled Study Circulation, September 8, 1998; 98(10): 953 - 960. [Abstract] [Full Text] [PDF]
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M. Haissaguerre, P. Jais, D. C. Shah, A. Takahashi, M. Hocini, G. Quiniou, S. Garrigue, A. Le Mouroux, P. Le Metayer, and J. Clementy Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins N. Engl. J. Med., September 3, 1998; 339(10): 659 - 666. [Abstract] [Full Text] [PDF]
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M. H. Eckman, R. H. Falk, and S. G. Pauker Cost-effectiveness of Therapies for Patients With Nonvalvular Atrial Fibrillation Arch Intern Med, August 10, 1998; 158(15): 1669 - 1677. [Abstract] [Full Text]
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A. L. Gullov, B. G. Koefoed, P. Petersen, T. S. Pedersen, E. D. Andersen, J. Godtfredsen, and G. Boysen Fixed Minidose Warfarin and Aspirin Alone and in Combination vs Adjusted-Dose Warfarin for Stroke Prevention in Atrial Fibrillation: Second Copenhagen Atrial Fibrillation, Aspirin, and Anticoagulation Study Arch Intern Med, July 27, 1998; 158(14): 1513 - 1521. [Abstract] [Full Text] [PDF]
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F. Gaita, R. Riccardi, L. Calo, M. Scaglione, L. Garberoglio, R. Antolini, M. Kirchner, F. Lamberti, and E. Richiardi Atrial Mapping and Radiofrequency Catheter Ablation in Patients With Idiopathic Atrial Fibrillation : Electrophysiological Findings and Ablation Results Circulation, June 2, 1998; 97(21): 2136 - 2145. [Abstract] [Full Text] [PDF]
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M BRIGNOLE Ablate and pace: a pragmatic approach to paroxysmal atrial fibrillation not controlled by antiarrhythmic drugs Heart, June 1, 1998; 79(6): 531 - 533. [Full Text]
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B. F. Gage, A. B. Cardinalli, and D. K. Owens Cost-Effectiveness of Preference-Based Antithrombotic Therapy for Patients With Nonvalvular Atrial Fibrillation Stroke, June 1, 1998; 29(6): 1083 - 1091. [Abstract] [Full Text] [PDF]
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A. A. Grace and A. J. Camm Quinidine N. Engl. J. Med., January 1, 1998; 338(1): 35 - 45. [Full Text] [PDF]
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