Jose L. Baez-Escudero, MD, FHRS and Miguel Valderrábano, MD

1. How common is atrial fibrillation (AF)?

    AF is the most commonly encountered arrhythmia in clinical practice, accounting for one-third of cardiac hospitalizations annually. Its incidence rises with increasing age for men and women, with an estimated prevalence of 5% at age 75 and 15% at age 85. As many as 2.3 million Americans and 4.5 million people in the European Union are estimated to have AF.

2. What cardiovascular diseases are likely to coexist in patients with AF?

    Hypertensive heart disease is the most common preexisting condition. However, systolic dysfunction, coronary artery disease (CAD), rheumatic valve disease, nonrheumatic valvular heart disease, chronic lung disease, and hyperthyroidism are common comorbidities. Patients without identifiable cardiovascular disease or other conditions associated with AF are said to have lone AF. These patients have a favorable prognosis with respect to thromboembolism and mortality.

3. What arrhythmias are related to AF?

    AF may occur in association with other arrhythmias, most commonly atrial flutter or atrial tachycardia. Atrial flutter may degenerate into AF and AF may organize to atrial flutter, particularly during treatment with antiarrhythmic agents prescribed to prevent recurrent AF. The electrocardiogram (ECG) pattern may fluctuate between atrial flutter and AF, reflecting changing activation of the atria. Focal atrial tachycardias, atrioventricular (AV) reentrant tachycardias, and AV nodal reentrant tachycardias may also trigger AF.

4. What are the main anatomic and physiologic substrates for the initiation of AF?

    Available data support both a focal triggering mechanism involving automaticity or multiple reentrant wavelets. The pulmonary veins (PVs) are the most common source of these rapid atrial impulses. Other known contributing factors in the genesis of AF include atrial electrical remodeling, sympathetic and parasympathetic stimuli, the renin-angiotensin-aldosterone system, and inflammation.

5. Which agents are effective in slowing the ventricular response in acute AF?

    In the absence of an accessory bypass tract and preexcitation syndrome (such as in patients with Wolff-Parkinson-White [WPW] syndrome), intravenous (IV) administration of beta-adrenergic blocking agents (β-blockers; esmolol, metoprolol, or propranolol) or nondihydropyridine calcium channel antagonists (verapamil, diltiazem) is recommended to slow the ventricular response to AF in the acute setting, exercising caution in patients with hypotension or systolic heart failure. In patients with AF and systolic dysfunction who do not have an accessory pathway, IV digoxin or amiodarone is recommended. However, digoxin should not be used as a sole agent.

6. How do you decide which antithrombotic therapy is most appropriate?

    Several schemes for stratification of stroke risk can identify patients who benefit most and least from anticoagulation. The most commonly used tool as outlined in the current guidelines is the CHADS₂ score for AF stroke risk scheme (Fig. 34-1), in which patients are stratified for risk according to the presence of moderate risk factors (1 point) and high risk factors (2 points). The use of appropriate anticoagulation is then decided according to the sum of points, as outlined in Table 34-1. A recently updated and modified CHA₂DS₂-VASc scoring system (Table 34-2) has been validated and used in patients who fall in the intermediate risk category. CHA₂DS₂-VASc assigns points for risk factors not included in the CHADS₂ score, such as female gender, age 65 to 75, and vascular disease.