Atrial Fibrillation

DEFINITION

Atrial fibrillation (AF) occurs when the electrical impulses in the atria degenerate from their usual organized rhythm into a rapid chaotic pattern. This disruption results in an irregular and often rapid heartbeat that is classically described as “irregularly irregular” and occurs because of the unpredictable conduction of these disordered impulses across the atrioventricular (AV) node.

AF may be classified on the basis of the frequency of episodes and the ability of an episode to convert back to sinus rhythm. One method of classification has been outlined in guidelines published by the American College of Cardiology (ACC), American Heart Association (AHA), and European Society of Cardiology (ESC), with the collaboration of the Heart Rhythm Society (HRS).¹ According to these guidelines, if a patient has two or more episodes, AF is considered to be recurrent. Recurrent AF may be paroxysmal or persistent. If the AF terminates spontaneously it is designated paroxysmal and if the AF is sustained, it is designated persistent. In the latter case, termination of the arrhythmia with electrical or pharmacologic cardioversion does not change its designation. The category of persistent AF also includes permanent AF, which refers to long-standing AF (generally >1 year), for which cardioversion was not indicated or attempted.

PREVALENCE

AF is the most common sustained tachyarrhythmia encountered by clinicians. It occurs in approximately 0.4% to 1.0% of the general population and affects more than 2 million Americans annually. Its prevalence increases with age, and it has been diagnosed at some point in up to 10% of the population older than 80 years. With the projected growth of the older adult population, the prevalence of AF will certainly increase.

PATHOPHYSIOLOGY

AF may be associated with physiologic stresses such as surgical procedures, pulmonary embolism, chronic lung diseases, hyperthyroidism, and alcohol ingestion. Disease states commonly associated with AF include hypertension, valvular heart disease, congestive heart failure (CHF), coronary artery disease, Wolff-Parkinson-White (WPW) syndrome, pericarditis, and cardiomyopathy. When no identifiable risk factor for AF is present, the condition is classified as lone AF.

New insights about the factors involved in the initiation and continuation of AF have led some investigators to propose a revised model of this complex arrhythmia. For many years, the focus had been on the substrate in the atria that supports the maintenance of AF. The multiple wavelet model has suggested that AF is sustained by multiple simultaneous wavelets wandering throughout the atria. Therefore, therapy was aimed at making these wavelets less likely to sustain and propagate. Such treatments included antiarrhythmic medications and surgical interruption of the atrial tissue.

More recently, it has been recognized that the initiation of AF in most cases occurs because of premature atrial contractions triggered by beats that arise from the pulmonary veins, usually near the junction with the left atrium. These triggers may also fire repetitively and contribute to the maintenance of AF, essentially becoming drivers of AF.

AF may have hemodynamic consequences. It can decrease cardiac output by as much as 20%, increase pulmonary capillary wedge pressure, and increase atrial pressures. These effects are caused by tachycardia, loss of atrial contribution to left ventricular (LV) filling, increased valvular regurgitation, and irregular ventricular response. Some investigators have suggested that the irregularity of the R-R intervals contributes more to the hemodynamic changes than the mere presence of tachycardia.

AF is associated with important morbidity and even mortality. AF can produce bothersome symptoms that affect quality of life, but patients with AF also have a substantial risk of thromboembolic stroke, as discussed later. It is less apparent, however, that AF is also associated with increased mortality, although the reason for this is unclear. Several studies have demonstrated an association of AF with reduced overall survival.^2,³

SIGNS AND SYMPTOMS

The clinical manifestation of AF is variable. Often, the symptoms are attributable to the rapid ventricular response. However, even when the ventricular response is controlled, symptoms can occur from loss of AV synchrony. This is particularly important for patients with LV dysfunction. Some patients are completely asymptomatic, even those with rapid heart rates. More often, however, patients report nonspecific symptoms such as fatigue, dyspnea, dizziness, and diaphoresis. Palpitations are a common feature. Occasionally, patients present with extreme manifestations of hemodynamic compromise, such as chest pain, pulmonary edema, or syncope. AF is present in 10% to 40% of patients with a new thromboembolic stroke.

DIAGNOSIS

The clinician must realize that an irregular pulse detected by physical examination or an irregular ventricular rhythm seen on the electrocardiogram (ECG) is not always AF. It is necessary to consider and exclude other types of irregular rhythm disturbances, including atrial or ventricular ectopy, atrial tachycardia or atrial flutter (Fig. 1) with variable AV conduction, multifocal atrial tachycardia (Fig. 2), and chaotic atrial rhythm, or wandering atrial pacemaker. Conversely, a regular pulse or rhythm does not exclude AF. For example, AF can manifest with a regular ventricular response in the presence of AV block or with a ventricular paced rhythm.

Figure 1 Typical atrial flutter.

Figure 2 Multifocal atrial tachycardia.

An ECG is essential for proper diagnosis. Electrocardiographic findings in AF include the absence of P waves, the presence of chaotic atrial activity and fibrillary waves (f waves), and an atrial rate in the range of 300 to 700 beats/min. In the absence of drug therapy, a patient with normal AV conduction has an irregularly irregular ventricular rhythm and often has a ventricular rate in the range of 120 to 180 beats/min. The baseline on the ECG strip often is undulating and occasionally has coarse irregular activity (Fig. 3). This activity may resemble atrial flutter, but it is not as uniform from wave to wave as atrial flutter.

Figure 3 Coarse atrial fibrillation.

TREATMENT

Most patients presenting with AF are not in critical condition. However, in some cases, the presence of AF or the way it is treated may be life threatening. It should be emphasized that for any unstable patient presenting with AF—for example, a patient with chest pain, pulmonary edema, or hypotension—the recommended therapy is rapid electrical cardioversion.

AF has particular importance in the setting of the WPW syndrome. Patients with WPW syndrome may be vulnerable to ventricular fibrillation and sudden death because of the development of AF, which can result in extremely rapid conduction over the accessory pathway (Fig. 4). Prompt electrical cardioversion is of utmost importance for these patients. Treatment with AV node–blocking medications such as verapamil or digoxin can facilitate rapid conduction over the accessory pathway and result in ventricular fibrillation. When intravenous (IV) pharmacologic therapy is required, the drug of choice is procainamide or amiodarone.

Figure 4 Wide complex tachycardia resulting from atrial fibrillation in a patient with Wolff-Parkinson-White syndrome.

The management of AF is directed at three basic goals: control of the ventricular rate, minimization of thromboembolism risk (particularly stroke), and restoration and maintenance of sinus rhythm. The first two management goals are essential for most patients, but the third management goal may not be necessary in every patient (see later). The ACC/AHA/ESC guidelines provide a more detailed review of the management of AF.¹

Control of the Ventricular Rate

The ventricular rate during AF may be rapid and therefore require control. This usually is accomplished with medications that slow conduction through the AV node (Table 1). If these medications are ineffective or their effectiveness is prohibited by the development of excessive bradycardia, then other measures may need to be considered. One option suitable for some patients is catheter ablation of the AV node and pacemaker implantation. A meta-analysis of 21 uncontrolled studies of the ablate-and-pace approach⁴ has shown demonstrated improvements in a number of clinical parameters, including symptoms, quality of life, exercise function, and cardiac performance. However, this approach usually results in pacemaker dependence. These patients may be exposed to the risks and complications of the implanted hardware. Pacemaker implantation without AV nodal ablation should be considered if the problem is simply excessive bradycardia that prohibits the effectiveness of rate-controlling medication. Strategies for suppression or cure of AF should be considered for appropriate patients before pursuing ablation of the AV node.

Table 1 Atrial Fibrillation Medications that Slow Conduction Through the Atrioventricular Node

Minimization of Thromboembolism and Stroke Risk

AF carries a considerable risk for thromboembolism and stroke. The Framingham study has shown that during a follow-up period of 30 years, the annual risk of stroke among AF patients is 4.2%; patients with nonvalvular AF had a more than fivefold higher risk of stroke. In the Framingham study, even patients with lone AF had a much higher incidence of stroke than controls over a period of almost 30 years.⁵ The annual risk of stroke may be even higher (7%-10%) in patients with AF who have one or more of the following risk factors: age older than 65 years, diabetes mellitus, hypertension, CHF, coronary artery disease, previous stroke, or transient ischemic attack. Findings of left atrial enlargement and reduced LV systolic function on echocardiography indicate an increase in thromboembolic risk.

Antithrombotic therapy for AF generally has consisted of the oral vitamin K antagonist warfarin or of the antiplatelet agent aspirin. A number of trials have studied the reduction of stroke risk in patients with AF, including some that compared the relative benefits and risks of warfarin and aspirin. Overall, warfarin has been shown to reduce the annual average relative risk of stroke by 68%, whereas the reduction with aspirin ranges from 0% to 44% (mean, approximately 20%). The combination of warfarin with aspirin increases the bleeding risk. Studies involving low-dose aspirin and clopidogrel in combination are under way to evaluate their potential efficacy when used as alternatives to warfarin.

Practice guidelines have been published regarding the recommended form of antithrombotic therapy for patients with AF.¹ In general, younger patients with no other risk factors have a low risk of stroke; therefore, aspirin may be an acceptable alternative to warfarin. Patients older than 65 years with or without other risk factors have a greater risk of stroke and should receive anticoagulation with warfarin, if it is not contraindicated. The goal of warfarin therapy for preventing stroke and thromboembolism from AF generally is an international normalized ratio (INR) between 2.0 and 3.0. Some older patients may be considered poor candidates for warfarin therapy because of excessive risk for bleeding complications, and these patients should be considered for aspirin therapy.

For patients who have been in AF for more than 48 hours and are not adequately anticoagulated, electrical or pharmacologic cardioversion should be delayed until appropriate measures are taken to reduce the thromboembolic risk. There are two approaches for patients being considered for cardioversion of AF longer than 48 hours’ duration. The conventional approach is to administer warfarin to achieve an INR value between 2.0 and 3.0 for at least 3 to 4 weeks before electrical or pharmacologic cardioversion. The second approach is the transesophageal echocardiography (TEE)–guided method. In some cases, cardioversion cannot be postponed for 3 or 4 weeks; in other cases, the patient, clinician, or both may prefer an expedited approach to achieving sinus rhythm. In such cases, once a therapeutic level of anticoagulation has been achieved with warfarin or IV heparin, TEE may be performed to rule out the presence of an intracardiac thrombus. If no thrombus is seen, cardioversion may be performed. TEE can detect the presence of a thrombus in the left atrium, particularly in the left atrial appendage, which is poorly seen on transthoracic echocardiography. The TEE-guided approach has been validated in several small multicenter trials as well as in a large, randomized, multicenter trial known as the Assessment of Cardioversion Using Transesophageal Echocardiography (ACUTE) trial.⁶

Warfarin should be continued after cardioversion until sinus rhythm has been maintained for at least 4 weeks to allow the atrial transport mechanism to recover. If the cardioversion was performed using the TEE-guided approach with IV heparin as the method of anticoagulation, it is advisable to continue IV heparin until a therapeutic INR is achieved with warfarin. The decision to initiate and continue anticoagulation for AF shorter than 48 hours’ duration should be based on the presence of other risk factors for thromboembolism.

Because of the relatively narrow therapeutic and safety window for warfarin, and the numerous potential drug and food interactions with this medication, there has been substantial interest in the development of an alternative antithrombotic medication. Studies are in progress with oral platelet inhibitors such as clopidogrel and factor Xa inhibitors such as idraparinux. Several studies have been completed regarding the use of ximelagatran, an oral direct thrombin inhibitor with few drug and dietary interactions that does not require anticoagulation monitoring. Ximelagatran has been shown to be not inferior to warfarin, with similar bleeding risks. However, an undefined risk of hepatotoxicity, among other factors, has led the U.S. Food and Drug Administration (FDA) to discontinue grant approval in 2006 for this medication until further study has been completed. At present, a suitable substitute for warfarin for patients requiring more than aspirin therapy has yet to be demonstrated.

Nonpharmacologic methods of stroke prevention for patients with AF are also being studied. Percutaneous left atrial appendage occlusion has shown early clinical promise, but further study is required.

Only gold members can continue reading. Log In or Register to continue