Atrial Fibrillation

Atrial Fibrillation is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

The medical management of AF requires careful consideration of three issues: rate control, rhythm control, and prevention of thromboembolic events.


  • Atrial tachyarrhythmia characterized by chaotic activation of the atria with loss of normal atrial mechanical function.
  • AF has a pattern on 12-lead ECG characterized by the absence of consistent P waves. Instead, rapid, low-amplitude oscillations or fibrillatory waves are noted in the baseline of leads that best demonstrate atrial activation (V1, II, III, aVF).
  • The ventricular response to AF is characteristically irregular and, often, rapid in the presence of intact AV conduction.
  • AF is the most common sustained cardiac arrhythmia encountered in clinical practice.


AF has been classified into four forms based on clinical presentation: first occurrence, paroxysmal, persistent, and permanent.

  • First occurrence may be symptomatic or asymptomatic. The spontaneous conversion rate is high, measured at >60% in hospitalized patients.
  • Paroxysmal AF describes a recurrent form of AF in which individual episodes are <7 days and usually <48 hours in duration.
  • Persistent AF describes a recurrent form of AF in which individual episodes are >7 days in duration and may require electrical or chemical cardioversion to terminate.
  • Longstanding persistent AF describes those patients with persistent AF for greater than 1 year who are still deemed candidates for treatment with cardioversion or radiofrequency ablation.
  • Permanent AF describes the form of AF that has failed attempts at electrical or pharmacologic cardioversion, has been present for more than 1 year, or has been accepted because of contraindications for cardioversion or lack of symptoms.


  • AF is the most common sustained tachyarrhythmia for which patients seek treatment and the most likely etiology for an irregularly irregular rhythm discovered on an inpatient ECG. AF is typically a disease of the elderly, affecting >10% of those >75 years old.
  • Independent risk factors for AF include advanced age, male gender, and the comorbid presence of diabetes mellitus and cardiovascular diseases such as CHF, valvular heart disease, hypertension (HTN), and previous myocardial infarction (MI).1 Age less than 65, obesity and obstructive sleep apnea (OSA) are important risk factors for new-onset AF.2
  • Following cardiothoracic surgery, AF occurs in 20%–50% of patients.3


  • The precise mechanisms giving rise to AF are not completely understood.
  • Initiation of AF is commonly because of rapid, repetitive firing of an ectopic focus within the pulmonary veins with fibrillatory conduction to the bodies of the atria.
  • Maintenance of persistent AF likely requires multiple reentrant circuits varying in location and timing to explain the self-perpetuating characteristic of AF.
  • Structural and electrical remodeling of the left atrium associated with cardiovascular disease promotes ectopic activity and heterogeneous conduction patterns that provide the substrate for AF. AF, when present, also promotes structural and electrical remodeling in the atria that stabilizes the rhythm.
  • Inflammation and fibrosis may play a major role in initiation and maintenance of AF. Inflammatory markers, such as interleukin-6 and C-reactive protein, are increased in AF and correlate with the duration of AF, success of cardioversion, and thrombogenesis.


  • Currently, there is a lack of prospective clinical trials that examine the value of primary prevention of non–postoperative AF through treatment of associated conditions or risk factor modification.
  • Some analysis suggests that statins may reduce recurrent AF by 61%, independent of their lipid-lowering effect.4
  • Angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) have been shown to prevent atrial remodeling in animals via suppression of the renin–angiotensin system. A metaanalysis of patients with CHF and HTN treated with either ACE-I or ARB demonstrated a reduction in new-onset AF by 20%–30%.5
  • A number of pharmacologic and nonpharmacologic strategies have been evaluated to prevent postoperative AF. Perioperative continuation of β-adrenergic antagonists has been shown to reduce postoperative AF rates. Amiodarone, sotalol, magnesium, and omega-3 fatty acids used in the perioperative period have also demonstrated a reduction in postoperative AF.6

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