Chapter 1 Atrial Fibrillation
Definition
Epidemiology
The prevalence of Afib increases with age, from <1% in patients under age 60, to >6% in patients above age 80. Afib is also more common in males than in females, and in Caucasians than in African Americans. The incidence for Afib is under 0.1% annually for persons under age 40, rising to 1.5% to 2% annually in persons over age 80. In a large study of almost 2 million members of a health maintenance organization (HMO), the overall prevalence of Afib was 1%, but ranged from 0.1% in patients under age 55 to 9% in patients over age 80. The prevalence of Afib also increases with the severity of heart failure.
The ischemic stroke risk for persons with nonvalvular Afib ranges from 2 to 7 times that of persons without Afib. For persons with rheumatic heart disease and Afib, the stroke risk is even higher, up to 17 times that of persons without Afib. For untreated patients, the stroke risk increases with age, from 1.5% annually in patients between the ages of 50 and 59, to 23.5% in patients between the ages of 80 and 89.
Pathogenesis
Potential Mechanisms
Afib is thought to be due to either enhanced automaticity of atrial foci or the presence of reentry circuits.
The success rate of cardioversion for Afib is the highest within the first 24 hours of onset of Afib. With longer duration of Afib, electrophysiological remodeling occurs, resulting in decreased atrial refractory periods and perhaps increasing the sinus node recovery time. In addition, prolonged duration of Afib may result in an increased recovery time for atrial contractility after cardioversion.
Afib is often initiated by other supraventricular arrhythmias or atrial premature beats. Atrioventricular (AV) nodal reentry and atrioventricular reentry tachycardias may also result in Afib.
Pathophysiologic Effects
Ventricular Rate
Conduction of electrical impulses to the ventricle via the AV node is related to autonomic tone, AV nodal refractory period, and concealed conduction (atrial impulses may enter the AV node, but are not transmitted to the ventricle).
Hemodynamic Effects
Afib results in the loss of atrial systole (causing decreased ventricular filling) and the potential for a rapid ventricular response. Both have the potential to lower cardiac output.
Loss of atrial systole may have pronounced consequences in patients with decreased ventricular compliance (i.e., left ventricular hypertrophy, hypertrophic cardiomyopathy) or mitral stenosis.
Rapid ventricular response to Afib may result in decreased cardiac output due to lack of ventricular filling time compounded by loss of atrioventricular synchrony and suboptimal contractility.
Over time, atrial and ventricular tachycardia result in atrial and dilated ventricular cardiomyopathy, respectively. Atrial cardiomyopathy leads to decreased myocyte contractility and propensity for the development of sustained Afib. Ventricular cardiomyopathy may lead to signs and symptoms of heart failure. Both are potentially reversible with control of Afib.
Embolic Complications
Thrombus formation tends to occur in the left atrial appendage, accessible to examination by transesophageal echocardiography. Although the precise mechanism of thrombus formation remains unclear, a combination of decreased blood flow through the atrial appendage and regional coagulopathy likely play a role.
Risk factors for stroke in patients with Afib include:
Risk Factors and Potential Causes
Patients without Cardiac Disease
Metabolic factors (such as obesity and hyperthyroidism) and drugs (such as adenosine, theophylline, and alcohol) may cause Afib. Noncardiac (particularly thoracic) surgery may induce Afib. Pulmonary embolism, chronic obstructive pulmonary disease, and obstructive sleep apnea are associated with Afib, as well. Obstructive sleep apnea does not initiate Afib but has been found to increase the risk of Afib recurrence.
Autonomic dysfunction may be associated with Afib. Vagally mediated Afib tends to occur during periods of heightened parasympathetic tone, such as mealtimes, or during sleep. Adrenergically mediated Afib usually happens during the day, with exercise, or during emotional or physical stress.
Patients with Cardiac Disease
Hypertension, coronary artery disease, and valvular heart disease are the most common cardiac disorders associated with Afib, and are found in roughly 21%, 17%, and 15% of patients with Afib, respectively. Afib is an unusual presentation of cardiac ischemia or infarction, with the latter occurring in 5.5% of patients seen in an emergency department. For valvular heart disease, mitral valve disorders have a higher association with Afib than do aortic valve disorders.
Other cardiac diseases associated with Afib include hypertrophic cardiomyopathy, heart failure, pericarditis, myocarditis, presence of other supraventricular arrhythmias, cor pulmonale, cardiac surgery, and transplantation.
Clinical Features and Evaluation
Patients most commonly complain of palpitations, lightheadedness, fatigue, chest pain, or dyspnea. However, many episodes of Afib are asymptomatic. The physical examination may reveal an irregularly irregular pulse, varying intensity of the first heart sound, or murmurs associated with valvular disease.
The ACC/AHA/ESC Practice Guidelines present a coherent plan for the evaluation of the patient with Afib, described in the following text:
History and Physical Examination
The history should attempt to determine:
Particular attention should be placed on determining if any of the risk factors or potential causes described in the prior section apply to the patient.
Laboratory and Other Tests
A 12-lead electrocardiogram (EKG) should be obtained to ascertain the diagnosis of Afib. An EKG may also reveal evidence of cardiac ischemia, prior myocardial infarction, presence of other arrhythmias, and left ventricular hypertrophy.
A chest x-ray should be obtained to evaluate the pulmonary parenchyma, vasculature, and cardiac silhouette.
Transthoracic echocardiography (TTE) should be performed. TTE can assess atrial size, ventricular size and function, and evaluate for valvular heart disease, pulmonary hypertension, and pericardial disease. Although TTE may show left atrial thrombus formation, it is not the diagnostic test of choice. A transesophageal echocardiogram (TEE) should be performed to definitively assess for the presence of left atrial thrombi.
Thyroid function tests should be obtained to assess for hyperthyroidism.
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