Atrial Fibrillation Part 1

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia defined by rapid, irregular atrial activation. This disordered atrial activation results in loss of coordinated atrial contraction; irregular electrical input to the atrioventricular (AV) node typically leads to sporadic ventricular contractions. On an electrocardiogram, AF is characterized by the absence of visible discrete P waves, the presence of irregular fibrillatory waves, or both, and an irregularly irregular ventricular response [see Figure 1].

AF may occur by itself or with other arrhythmias, notably, atrial flutter. Atrial flutter is more organized than AF, involving regular atrial activation that often produces a characteristic sawtooth pattern on ECG. Cardiac rhythm may alternate between AF and atrial flutter, AF may trigger atrial flutter, or atrial flutter may degenerate into AF.

Classification

Numerous classification schemes have been used to characterize AF patients, and the lack of a consistent classification scheme across studies has led to difficulties in comparison of analyses and an inability to extrapolate results to all patients. Consequently, the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC), in collaboration with the North American Society of Pacing and Electrophysiology, have established guidelines for the classification of AF.1 The ACC/AHA/ESC guidelines include the following categories:


• Recurrent—AF occurring in a patient who has experienced an episode of AF in the past.

• Lone—AF occurring in a patient younger than 60 years who has no clinical or echocardiographic evidence of cardiopul-monary disease.

• Valvular or nonvalvular—Valvular AF is AF that occurs in a patient who has evidence or history of rheumatic mitral valve disease or who has a prosthetic heart valve; all other forms of AF are classified as nonvalvular.

• Paroxysmal—AF that typically lasts 7 days or less and that converts spontaneously to sinus rhythm.

• Persistent—AF that typically lasts longer than 7 days or requires pharmacologic or direct current (DC) cardioversion.

• Permanent—AF that is refractory to cardioversion or that has persisted for longer than 1 year.

Paroxysmal, persistent, and permanent AF categories do not apply to episodes of AF lasting 30 seconds or less or to episodes precipitated by a reversible medical condition. Reversible conditions include acute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism, and acute pulmonary disease.

Epidemiology

AF is the most common sustained arrhythmia, currently affecting more than 2.2 million persons in the United States.2 The incidence is approximately 0.1% per year for the entire population; however, the incidence of AF increases steadily with age. As a result, one out of 11 Americans older than 80 years has AF.

AF is associated with significant morbidity and mortality. The annual incidence of ischemic stroke in patients with AF is 5%, which is two to seven times higher than the incidence in the general population. In addition, the mortality in patients with AF is approximately twice that of patients without AF.3,6,7 AF frequently leads to reduced functional capacity, dyspnea, palpitations, fatigue, tachycardia-induced cardiomyopathy, heart failure, and angina, significantly impairing quality of life.8

Finally, AF results in tremendous health care expenditures. There are more than 370,000 hospital admissions for AF annual-ly.9 After the first diagnosis of AF, hospitalization costs are typically 35% higher for patients with AF than for age-matched control subjects.10

Pathophysiology

Central to the pathophysiology of AF are two factors: the electrical trigger that initiates the arrhythmia and the abnormal myocardial substrate that allows AF to be maintained. A spectrum of triggers is thought to initiate AF, ranging from premature atrial contractions to atrial tachycardias; ultimately, AF may be self triggering.11-13 Ectopic atrial foci, frequently located in the pulmonary veins, have been shown to trigger AF.

For AF to persist, the atrial tissue must be primed to allow the propagation of multiple wavelets of electrical depolarization throughout the atria.14 If a wavelet encounters refractory tissue, the wavelet can extinguish, divide into additional wavelets, or change direction. If the underlying atrial substrate leads to the extinction of the wavelets, then AF will not persist. In contrast, if the underlying atrial substrate promotes the generation of additional wavelets or the maintenance of the existing wavelets, then AF will continue. Fibrosis, hypertrophy, and fatty infiltration of atrial tissue likely allow for abnormal atrial electrical conduction and the maintenance of AF wavelets.

Diagnosis

Clinical manifestations

AF can result in a wide variety of signs and symptoms. Some patients are asymptomatic, although they may have an irregularly irregular pulse. Other patients experience strokes, palpitations, fatigue, dyspnea, reduced exercise capacity, heart failure, angina, presyncope, or syncope. Additional complications include thromboembolism and tachycardia-induced cardiomyopathy.15 The effect of AF on the patient’s quality of life is often a critical component that guides decisions regarding AF management.

An electrocardiographic tracing shows characteristic features of atrial fibrillation, with absent P waves, irregular fibrillatory waves, and an irregularly irregular ventricular response.

Figure 1 An electrocardiographic tracing shows characteristic features of atrial fibrillation, with absent P waves, irregular fibrillatory waves, and an irregularly irregular ventricular response.

Table 1 Initial Clinical Evaluation of Atrial Fibrillationi

Evaluation

Features to Assess

History and physical examination

Presence, frequency, onset, duration, termination, exacerbating and alleviating factors of AF; date of AF onset; AF classification; associated symptoms; reversible and irreversible contributing conditions; thromboembolic and hemorrhagic risk factors; response to pharmacologic or mechanical interventions

Laboratory studies

Thyroid function,* serum electrolytes, hemoglobin or hematocrit

Chest radiography

Lung parenchyma for intrinsic lung disease; abnormal pulmonary vasculature for pulmonary hypertension; cardiac size and shape for heart failure and pericardial disease

ECG

AF verification; P wave morphology for atrial flutter; preexcitation; atrial arrhythmias besides AF, as possible AF triggers; LVH, for hypertension and hypertrophic cardiomy-opathy; bundle branch block and previous MI as markers for CAD, left ventricular dysfunction, and conduction system disease; RR, QRS, and QT intervals to guide antiarrhyth-mic drug therapy

Transthoracic echocardiography

Left and right atrial size and function; left ventricular size, function, and hypertrophy; valvular heart disease, including rheumatic heart disease; right ventricular systolic pressure for pulmonary hypertension; left atrial thrombus; spontaneous echocardiographic contrast (low sensitivity); pericardial disease; aortic plaque (low sensitivity)

‘Reassessment of thyroid function should be considered if ventricular rate becomes difficult to control or atrial fibrillation recurs unexpectedly after conversion to sinus rhythm.

AF—atrial fibrillation

CAD—coronary artery disease

ECG—electrocardiogram

LVH—left ventricular hypertrophy

MI—myocardial infarction

Clinical evaluation

The initial evaluation of a patient with AF focuses on the following tasks: (1) confirming the diagnosis of AF, (2) classifying the type of AF, (3) identifying factors (both reversible and irreversible) that contribute to or cause AF, (4) establishing the risk of thromboembolism and additional adverse outcomes, and (5) defining the most effective treatment strategy. In taking the history, the clinician should try to determine whether this is the first episode of AF. If more than one episode of AF has occurred, the AF is defined as recurrent. If no reversible condition is detected in recurrent AF, the clinician may be able to classify the AF as paroxysmal, persistent, or permanent [see Classification, above].

Laboratory studies

The standard blood tests that are recommended by the ACC/AHA/ESC are thyroid function tests and measurement of serum electrolytes and hemoglobin or hematocrit. Other recommended laboratory studies include chest radiography, ECG, and transthoracic echocardiography [see Table 1]. Additional tests that may be indicated in specific situations are event and Holter monitoring, exercise testing, trans-esophageal echocardiography (TEE), and electrophysiologic study (EPS).

Event and Holter Monitors

Event monitors are of particular use for documenting infrequent symptomatic episodes in patients in whom AF has not been confirmed previously. In addition to their diagnostic utility for documenting AF, Holter monitors may be used for therapeutic follow-up to evaluate rate control.16

Exercise Testing

Exercise testing can confirm the presence of ischemic heart disease and may unmask exercise-mediated AF. In addition, exercise testing can be used to explore the safety of using specific antiarrhythmic medications and to assess rate control.

Transesophageal Echocardiography

TEE is of greatest use in establishing the risk for embolic stroke, most notably in association with cardioversion to sinus rhythm. Risk factors for cardiogenic embolism that are best identified with TEE include the following: left atrial and left atri-al appendage thrombus, left atrial and left atrial appendage spontaneous echo contrast (smoke), left atrial appendage flow velocity, and aortic plaque.17

Electrophysiologic Study

EPS can define specific forms of AF that are amenable to catheter-based intervention (i.e., radiofrequency ablation). In addition, EPS allows for assessment of the underlying conduction system to determine the etiology of wide-complex tachycardias, whether supraventricular or ventricular in origin.

Management

Treatment of AF includes either restoration and maintenance of sinus rhythm or control of ventricular rate if AF is persistent or if future paroxysmal events are likely to occur. In ad-dition, antithrombotics are used to reduce embolic risk [see Figures 2 through 4].10 Treatment decisions involve a synthesis of research results with the characteristics of the individual patient.

Management of newly discovered atrial fibrillation.1 (AF—atrial fibrillation)

Figure 2 Management of newly discovered atrial fibrillation.1 (AF—atrial fibrillation)

Management of recurrent paroxysmal, recurrent persistent, or permanent atrial fibrillation.10 (AF—atrial fibrillation)

Figure 3 Management of recurrent paroxysmal, recurrent persistent, or permanent atrial fibrillation.10 (AF—atrial fibrillation)

Several trials have compared restoration of sinus rhythm with control of ventricular rate in patients with AF. Outcomes evaluated have included overall mortality, stroke, symptoms, and quality of life. Contrary to the expectations of many experts, maintenance of sinus rhythm provided no survival advantage and possibly a higher mortality when compared with ventricular rate control.18,19 Maintenance of sinus rhythm frequently requires the use of antiarrhythmic medications that may precipitate ventricular arrhythmias, bradycardia, and depression of left ventricular function. It was theorized that maintenance of sinus rhythm would reduce rates of thromboembolism and the need for anticoagulation; however, trial results demonstrated no significant reduction in thromboembolic risk. Peak exercise capacity may improve with maintenance of sinus rhythm, but both treatment strategies result in a similar degree of perceived symptomatic impairment.8,20,21

Nevertheless, ventricular rate control frequently is not feasible because of the complications that patients experience while in AF. Clinical scenarios in which AF often is not tolerated include unstable angina, acute myocardial infarction, heart failure, and pulmonary edema. In addition, patients in whom atri-al contraction provides a significant proportion of ventricular filling because of impaired ventricular relaxation often need to be maintained in sinus rhythm.

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