Overview of the presentation and management of atrial fibrillation

Sunday, July 19, 2009

Atrial fibrillation (AF) is a relatively common arrhythmia that can have adverse consequences related to a reduction in cardiac output and to atrial thrombus formation that can lead to systemic embolization [1-4]. There are four major issues that must be addressed in the treatment of AF:

· Reversion to sinus rhythm

· Maintenance of sinus rhythm

· Control of the ventricular rate in

patients with chronic AF

· Prevention of systemic

embolization

Therapy is also influenced by whether the AF is paroxysmal or chronic (show figure 1A-1B).

The following discussion will focus on three areas: a brief summary of these four treatment issues, each of which is discussed in detail separately; the presentation and management of recent onset AF; and the mortality risk associated with AF.

GENERAL TREATMENT ISSUES

Reversion to sinus rhythm - There are two standard and a number of experimental approaches to converting AF to sinus rhythm. The standard approaches are synchronized internal or external DC cardioversion and pharmacologic cardioversion with class IA (eg, quinidine, procainamide, disopyramide), IC (eg, flecainide, propafenone), or III antiarrhythmic agents (amiodarone, sotalol). The experimental approaches are surgical or percutaneous catheter ablation. (See "Restoration of sinus rhythm in atrial fibrillation: Therapeutic options" and see "Nonpharmacologic strategies to prevent recurrent atrial fibrillation").

DC cardioversion is indicated in patients who are hemodynamically unstable. In stable patients in whom spontaneous reversion due to correction of an underlying disease is not likely, either medical or electrical cardioversion can be performed. Rate control with an atrioventricular (AV) nodal blocker (calcium channel blocker, beta blocker, or, if the patient has heart failure or hypotension, digoxin) should be attained before instituting class IA drugs because of possible recurrence with atrial flutter and a very rapid ventricular rate. Successful reversion to and maintenance of sinus rhythm is more likely if the AF has been present for less than one year and if the left atrium is not enlarged [1,5].

Maintenance of sinus rhythm - Only 20 to 30 percent of patients who are successfully cardioverted maintain sinus rhythm for more than one year without chronic antiarrhythmic therapy [1,2,4]. This is more likely in patients with AF for less than one year, no enlargement of the left atrium, and a reversible cause of AF such as hyperthyroidism, pericarditis, and cardiac surgery.

It has been thought that the drugs that are most likely to maintain sinus rhythm suppress triggering ectopic beats and arrhythmias, and affect atrial electrophysiologic properties to diminish the likelihood of AF. There is therefore a strong rationale for prophylactic antiarrhythmic drug therapy in patients who have a moderate to high risk for recurrence, provided that it is effective and that both toxicity and proarrhythmic effects are low.

Class IA, IC, and III drugs are useful for maintenance of sinus rhythm. The choice may vary with the clinical setting (show algorithm 1) [6]. As an example, amiodarone may be preferred in patients with a reduced left ventricular ejection fraction, while disopyramide is generally avoided in patients with heart failure. Concurrent administration of an AV nodal blocker is indicated in patients who have demonstrated a moderate to rapid ventricular response to AF. (See "Antiarrhythmic drugs to maintain sinus rhythm after cardioversion in atrial fibrillation: Recommendations").

There are alternative methods to maintain sinus rhythm in selected patients who are refractory to conventional therapy. These include combined drug therapy, surgical and radiofrequency ablative procedures, and insertion of an implantable atrial defibrillator. (See "Nonpharmacologic strategies to prevent recurrent atrial fibrillation").

Slowing the ventricular rate in chronic atrial fibrillation - The administration of medications to control the ventricular rate in AF slow AV nodal conduction by the following physiologic mechanisms (show figure 2) [1,2]. (See "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy"):

· Further blockade of the calcium channel as occurs with calcium channel blockers, particularly verapamil and diltiazem

· Decreased sympathetic tone resulting from beta blockade

· Enhancement of parasympathetic tone with vagotonic drugs, the most important of which is digoxin

The factors that determine the choice between these drugs are discussed below (see "Initial rate control with mild to moderate symptoms" below). The nonpharmacologic therapies for achieving rate control in patients with AF who do not respond to pharmacologic therapy include surgery and radiofrequency catheter ablation. (See "Control of ventricular rate in atrial fibrillation: Nonpharmacologic therapy").

Prevention of systemic embolization - Separate issues are involved with anticoagulation during cardioversion to sinus rhythm and in patients with chronic AF.

Anticoagulation during restoration of sinus rhythm - Based upon observational studies, guidelines published in January 2001 by the Sixth American College of Chest Physicians (ACCP) Consensus Conference on Antithrombotic Therapy strongly recommended that outpatients without a contraindication to warfarin who have been in AF for more than 48 hours should receive three to four weeks of warfarin prior to and after cardioversion with a target INR of 2.5 (range 2.0 to 3.0) [7]. The rationale for this approach is that over 85 percent of left atrial thrombi resolve after four weeks of warfarin therapy [8].

Anticoagulation prior to cardioversion is also mandatory for patients with AF who have valvular disease, evidence of left ventricular dysfunction, recent thromboembolism, or when AF is of unknown duration, as in an asymptomatic patient. (See "Anticoagulation during restoration of sinus rhythm in atrial fibrillation").

An alternative approach that eliminates the need for prolonged anticoagulation prior to cardioversion, particularly in low risk patients who would benefit from earlier cardioversion, is the use of transesophageal echocardiographic-guided cardioversion (see "Role of transesophageal echocardiography" below).

A different approach may be used in patients with AF of less than 48 hours duration who do not have a history of a prior thromboembolic event, left ventricular dysfunction, or rheumatic heart disease. Such patients have a low risk (0.8 percent in one study) of clinical thromboembolism if converted early, even without screening TEE [9]. Acute anticoagulation with intravenous heparin is indicated only if the patient is admitted to the hospital and cardioversion is delayed beyond 48 hours (see "Indications for hospitalization" below).

The optimal therapy after cardioversion in this group is uncertain. Our current practice is to administer aspirin for a first episode of AF that converts spontaneously and warfarin for at least four weeks to all other patients.

Anticoagulation in chronic AF - In patients with chronic AF who are not anticoagulated, the incidence of clinically evident embolization is about 5 percent per year; in addition, the overall incidence of cerebrovascular embolization is 28 percent compared to 7 percent in patients in sinus rhythm [10]. The prevalence of stroke associated with AF increases strikingly with age.

Warfarin is associated with a 45 to 82 percent reduction in the risk of stroke in patients with chronic AF (show figure 3). Anticoagulation is beneficial in all age groups, including patients over age 75 (show figure 4), and is also effective as secondary prevention in patients with nonrheumatic AF who have had a recent transient ischemic attack or minor stroke [6,11]. The true efficacy of warfarin is likely to be even higher than suggested by these results, since many of the strokes in the warfarin-treated groups occurred in patients who were noncompliant at the time of the stroke. (See "Anticoagulation to prevent embolization in chronic atrial fibrillation: Recommendations").

Rhythm control versus rate control with anticoagulation - Most physicians prefer rhythm control, with the restoration and maintenance of sinus rhythm, to persistence of AF, with rate control and anticoagulation. However, there are few data available to suggest which approach is superior as both have strengths and weakness:

· Reversion of AF and maintenance of sinus rhythm restores normal hemodynamics and may prevent embolism. However, this approach usually requires chronic administration of antiarrhythmic drugs, which are not always effective and are associated with many side effects, including the risk of proarrhythmia. (See "Antiarrhythmic drugs to maintain sinus rhythm after cardioversion in atrial fibrillation: Clinical trials-I"). Although nonpharmacologic therapies are available, they are still investigational and their long-term efficacy and safety have not been demonstrated. (See "Nonpharmacologic strategies to prevent recurrent atrial fibrillation").

· Rate control with anticoagulation is not associated with chronic administration of antiarrhythmic drugs. However, this approach is associated with risks from anticoagulation, a continued small risk of embolism, and suboptimal hemodynamics that may be of particular importance for the patient with underlying left ventricular dysfunction. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm"). In addition, adequate rate control with pharmacologic therapy is occasionally difficult to achieve, and nonpharmacologic approaches, particularly radiofrequency ablation of the atrioventricular node and pacemaker insertion, may be necessary.

Two trials have compared these two approaches. In the PIAF trial, 252 patients with AF of 7 to 360 days duration were randomly assigned to rate control with diltiazem or rhythm control with amiodarone [12]. Patients who did not revert on amiodarone were electrically cardioverted and maintained on the drug; all patients received anticoagulation during the duration of the trial. After a one year follow-up, there was no difference in the quality of life between the two groups; patients with rhythm control had better exercise tolerance but required more frequent hospitalization.

In the STAF trial, 200 patients with chronic AF were randomly assigned to external or internal cardioversion followed by amiodarone or a class I antiarrhythmic drug or to rate control and anticoagulation [13]. After a mean follow-up of 20 months, there was no difference in the primary end point (death, stroke or transient ischemic attack, cardiopulmonary resuscitation, or systemic embolization) or in secondary end points (bleeding worsening heart failure, changes in left ventricular function, atrial size, or quality of life). However, the number of hospitalizations and length of stay was greater in the rhythm control group due to repeat cardioversions and adjustment of antiarrhythmic drug therapy. Furthermore, at three years, only 23 percent of patients remained in sinus rhythm.

These data suggest that both approaches are acceptable and that the choice should be individualized for the needs of the patient. Further information about the safety and efficacy of these two approaches will come from another ongoing trial, AFFIRM, which will include 5300 patients who will be followed for 3.5 years [14].

Cost-effectiveness - Attempts have been made to assess the cost-effectiveness of these two approaches. One study used a Markov decision-analytic model comparing no therapy, warfarin, cardioversion followed by quinidine, or cardioversion followed by amiodarone; the last approach was the best strategy [4].

A second report used the same model in a cohort of 70 year-old patients with different baseline risks of stroke [15]. The following results were noted:

· Strategies using cardioversion alone were more effective and less costly than other approaches.

· For patients at high risk for a stroke (5.3 percent per year), cardioversion was the most cost-effective approach ($9300 per quality-adjusted life-years), followed by repeated cardioversion plus amiodarone therapy upon relapse.

· The same strategy was preferred for patients at moderate risk of stroke (3.6 percent per year), but it was more costly ($18,900 per quality-adjusted life-years).

· For patients with the lowest risk of stroke (1.6 percent per year), cardioversion alone followed by aspirin therapy upon relapse was the best approach.

PRESENTATION AND MANAGEMENT OF RECENT ONSET ATRIAL FIBRILLATION - Most patients with recent onset AF present with symptoms related to the arrhythmia. Typical symptoms include palpitations, a sense of the heart racing, fatigue, lightheadedness, increased urination, or mild shortness of breath. More severe symptoms and signs include dyspnea, angina, hypotension, presyncope, or infrequently syncope. In addition, some patients present with an embolic event or the insidious onset of right-sided heart failure (as manifested by peripheral edema, weight gain, and ascites). Except for embolization, these symptoms are primarily due to a rapid ventricular rate.

A rationale approach to the management of patients with new onset AF is presented in algorithm 2 [16] and is in general agreement with guidelines for the acute management of recent onset AF were published in August 2000 by the American Heart Association in collaboration with the International Liaison Committee on Resuscitation (ILCOR) (show algorithm 2, show table 1 and show table 2) [17]. (See "Guidelines for advanced cardiovascular life support: Treatment of tachycardias").

Emergency room reversion of new onset AF - An important issue is whether patients who have an uncomplicated clinical status and are low-risk can be managed in the emergency room or an observational unit [18-21]. This issue was addressed in a study of 289 patients who were stable, did not have heart disease, and did not have another indication for hospital admission [20]. Chemical cardioversion was attempted in 62 percent and was successful in 50 percent; 28 percent underwent electric cardioversion with a success rate of 89 percent. Overall, 97 percent of patients were discharged home directly from the emergency room. Similar results were noted in another report of 51 patients who underwent attempted chemical cardioversion, followed by electrical reversion if AF was still present; all patients were successful reverted and discharged from the emergency room [21].

Thus, emergency room or observational unit treatment of new onset AF in clinically stable patients is safe and cost-effective [19]. (See "Restoration of sinus rhythm in atrial fibrillation: Recommendations", section on Atrial fibrillation and stable hemodynamics).

Indications for hospitalization - Traditionally, many patients with new onset AF, particularly those without spontaneous reversion, are admitted to the hospital. A frequent reason for admission to the hospital is to "rule out" an acute myocardial infarction. However, AF is rarely the manifestation of an asymptomatic acute ischemic event or myocardial infarction. As a result, there is no reason to admit the patient for this indication unless there are other clinical reasons to consider the diagnosis, such as classic ischemic chest pain or an electrocardiogram demonstrating an acute infarct or ischemia [22,23]. (See "Causes of atrial fibrillation", section on Coronary disease).

There are, however, several indications for which hospitalization is often required:

· For the treatment of an associated medical problem, which is often the reason for the arrhythmia

· For elderly patients who are more safely treated for AF in hospital

· For patients with significant underlying heart disease who have hemodynamic consequences from the AF or who are at risk for a complication resulting from therapy of the arrhythmia

Search for an underlying cause - When faced with a patient who presents with rapid AF, there needs to be a quick assessment for an underlying cause, such as heart failure, pulmonary problems, hypertension, or hyperthyroidism, and for the urgency for heart rate slowing. Therapy for a precipitating cause of AF may result in reversion to sinus rhythm and, unless the patient is hemodynamically unstable, should be initiated prior to therapy aimed at reverting AF. (See "Causes of atrial fibrillation").

Serum should be obtained for measurement of thyroid stimulating hormone (TSH). This should be done even if there are no symptoms suggestive of hyperthyroidism, since the risk of AF is increased up to threefold in patients with subclinical hyperthyroidism (show figure 5). Patients with low TSH values (<0.5 mU/L with the newer sensitive assays) and normal thyroid hormone levels probably have subclinical hyperthyroidism. In one series of 726 patients with recent onset AF, 39 (5.4 percent) had low serum TSH values; 14 of these patients were taking thyroxine supplements for previous hyperthyroidism or hypothyroidism [24]. (See "Subclinical hyperthyroidism").

In the patient in whom AF appears to have been precipitated by an acute and reversible medical problem, cardioversion should be postponed until the condition has been successfully treated, which will often lead to spontaneous reversion. If this treatment is to be initiated as an outpatient, anticoagulation with warfarin should be begun with cardioversion performed, if necessary, after three to four weeks of adequate anticoagulation. If the patient is to be admitted to hospital for treatment of the underlying disease, it is prudent to begin heparin therapy and then institute oral warfarin. Cardioversion is again performed after three to four weeks of adequate anticoagulation if the patient does not revert to sinus rhythm.

Spontaneous reversion of AF - Recent onset AF often spontaneously reverts to sinus rhythm, the incidence of which is related to the duration of the arrhythmia. This was illustrated in a study of 1822 patients admitted to the hospital because of AF: 356 had an arrhythmia duration less than 72 hours, 68 percent of whom spontaneously reverted to sinus rhythm [25]. Two-thirds of those with spontaneous reversion had an AF duration of less than 24 hours, which was the only predictor of spontaneous reversion. Identical findings were noted in another report of 375 patients with AF of less than 48 hours duration; two-thirds reverted spontaneously [9]. (See "Paroxysmal atrial fibrillation").

Indications for urgent cardioversion - There are settings in which the rapid heart rate produces complications requiring urgent cardioversion. These include:

· Active ischemia

· Significant hypotension, to which poor left ventricular systolic function, diastolic dysfunction, or associated mitral or aortic valve disease may contribute

· The presence of a preexcitation syndrome, which may lead to an extremely rapid ventricular rate (show table 2)

(See "Restoration of sinus rhythm in atrial fibrillation: Recommendations", section on DC electroversion).

Initial rate control with mild to moderate symptoms - Most patients with acute AF do not require immediate reversion. Initial treatment directed at slowing the ventricular rate will usually result in improvement or resolution of the associated symptoms. As noted above, this can be achieved with beta blockers, calcium channel blockers (primarily verapamil and diltiazem), or digoxin. The drug selected and the route of administration (oral versus intravenous) are dictated by the clinical presentation. (See "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy").

· Digoxin is usually the preferred drug in patients with AF due to heart failure. In addition to the direct vagotonic effect of digoxin on the AV node (which may require several hours to become apparent), the improvement in left ventricular function and systemic hemodynamics result in withdrawal of sympathetic tone and a further decrease in the ventricular rate. Not infrequently, the improvement in hemodynamics results in reversion of the arrhythmia. Digoxin can also be used in patients who cannot take or who respond inadequately to beta blockers or calcium channel blockers. The effect of digoxin is additive to both of these drugs.

· In most other situations, a beta blocker or calcium channel blocker is preferred since, in the absence of heart failure, digoxin is less effective for rate control than beta blockers and calcium channel blockers, is less likely to control the ventricular rate during exercise (when vagal tone is low and sympathetic tone is high), has little ability to terminate the arrhythmia, and often does not slow the heart rate in patients with recurrent AF.

Beta blockers and calcium channel blockers are also effective if heart failure or hypotension is due to the rapid arrhythmia. If, however, there is doubt about the origin of the heart failure, the initial dose should be small (since these drugs impair contractility), with upward titration based upon heart rate slowing, blood pressure, and symptomatic improvement.

The choice between a beta blocker or a calcium channel blocker is frequently based upon physician and patient preference, although it may be influenced by other problems that are present. As an example, beta blockers are particularly useful when the ventricular response increases to inappropriately high rates during exercise, after an acute myocardial infarction, and when exercise-induced angina pectoris is also present. On the other hand, a calcium channel blocker is preferred in patients with chronic lung disease. The use of both a beta blocker and calcium channel blocker should be avoided, if possible.

Elective cardioversion - The next step after control of the ventricular rate in patients with mild to moderate symptoms involves a decision about reversion of the AF. The role for cardioversion depends upon the duration of the arrhythmia as well as the presence of a reversible etiologic factor. (See "Cardioversion for specific arrhythmias-I").

Immediate cardioversion - If the duration of the arrhythmia is 48 hours or less and there are no associated cardiac abnormalities (particularly mitral valve disease or significant left ventricular enlargement due to a cardiomyopathy), there is a low risk of systemic embolization [9] and electrical or pharmacologic cardioversion can be attempted after systemic heparinization. Anticoagulation is indicated for three to four weeks after cardioversion because de novo thrombus formation and embolization can occur. (See "Anticoagulation during restoration of sinus rhythm in atrial fibrillation").

Delayed cardioversion - It is preferable to anticoagulate with warfarin, establishing an INR of 2 to 3 for approximately three to four weeks to allow any left atrial thrombi to resolve [8], before attempted cardioversion if:

· The duration of the arrhythmia is more than 48 hours or of unknown duration

· There is associated mitral valve disease or significant cardiomyopathy and heart failure

· The patient has a prior history of a thromboembolic event

During this time, rate control should be maintained with an oral AV nodal blocker as described above.

Role of transesophageal echocardiography - Transesophageal echocardiography (TEE) immediately prior to elective cardioversion should be considered for those patients at increased risk for left atrial thrombi (eg, rheumatic mitral valve disease, recent thromboembolism, severe left ventricular systolic dysfunction). Cardioversion should be delayed if thrombi are seen in any cardiac chamber.

The role of routine TEE prior to elective cardioversion in nonvalvular AF of more than 48 hours duration is uncertain. Several studies have found that stable patients receiving heparin in whom no thrombi are seen on TEE can be safely treated without prolonged anticoagulation prior to cardioversion (show table 3A-3B) [26-29]. (See "Anticoagulation during restoration of sinus rhythm in atrial fibrillation").

The ACUTE trial compared a TEE-guided strategy (anticoagulation with heparin immediately before TEE and cardioversion, and then continued with warfarin for four weeks after cardioversion) with a conventional strategy (three weeks of anticoagulation before cardioversion, followed by four weeks of anticoagulation after cardioversion) in 1222 patients with AF of more than two days duration who were undergoing electrical cardioversion [28]. There was no difference between the two groups in the incidence of ischemic stroke, TIA, or all embolic events within eight weeks of cardioversion (0.8 versus 0.5 percent for the conventional strategy). However, patients undergoing the TEE-guided strategy had a lower incidence of hemorrhagic events (2.9 versus 5.5 percent), a shorter mean time to cardioversion (3 versus 30.6 days), and a greater incidence of successful reversion (71 versus 65 percent).

These data suggest that the TEE-guided strategy is an alternative to a conventional approach and may be of particular use in the patient with AF of less than three weeks duration or who has an increased risk of hemorrhagic complications during prolonged warfarin therapy [30].

AF in underlying cardiomyopathy - Patients with an underlying cardiomyopathy who, as a result of AF, have severe heart failure that persists despite adequate slowing of the ventricular rate, often require rapid restoration of sinus rhythm. (See "Treatment of atrial fibrillation in congestive heart failure and cardiomyopathy").

There may be a role for TEE in this setting. Cardioversion is likely to be safe if there is no evidence for thrombus in the left atrium or appendage and no "smoke" in the left atrium (show echocardiogram). The patient should be placed on heparin prior to reversion and anticoagulated with warfarin for at least three to four weeks after restoration of sinus rhythm.

GENDER DIFFERENCES - The importance of gender differences in the presentation and treatment of AF was examined in a study of 900 men and women with new-onset AF who were followed for more than four years [31]. The following findings were noted:

· At the time of presentation, women were older than men (65.4 versus 60.5 years) and were more likely to seek medical advice because of symptoms perhaps due in part to higher heart rates during AF (126 versus 119 beats per min).

· The rate of cardioversion and use of cardiac medications was the same. However, women > or =75 years of age were 54 percent less likely to receive warfarin, but were twice as likely to receive aspirin therapy; this difference was the same even for those with one or more stroke risk factors.

· During follow-up, women were more likely to have recurrent episodes of paroxysmal AF (48 versus 31 percent at one year), but the progression to permanent AF at three years was the same (19 percent).

· There was no sex difference in the incidence of stroke, myocardial infarction, major bleeds, or cardiovascular death. However, among patients treated with warfarin, women were 3.4 times more likely to experience a major bleed than men.

MORTALITY - Although the morbidity associated with AF, primarily heart failure and stroke, is well established, it is not clear if AF itself results in excess mortality. Patients under the age of 60 who have AF but no apparent heart disease (called lone AF) have been considered a group with a better prognosis. (See "Causes of atrial fibrillation", section on Lone atrial fibrillation).

However, AF is a risk factor for increased mortality in otherwise healthy older individuals. Among subjects age 55 to 94 from the original 5209 subjects in the Framingham Heart Study, AF almost doubled the risk of death in both men and women without underlying cardiovascular disease [32]. After adjustment for other risk factors, AF was still associated with an increased risk of death (odds ratio 1.5 for men and 1.9 for women) (show figure 6).

The coexistence of cardiovascular disease and chronic AF worsens the patient's prognosis, doubling the cardiovascular mortality [33]. In patients with a recent myocardial infarction, for example, the presence of AF increases mortality [34-36]. However, this effect is primarily due to associated risk factors, such as heart failure and cardiogenic shock, not AF itself [35,36]. (See "Supraventricular arrhythmias after myocardial infarction").

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