Atrial Fibrillation

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

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General Principles

Definition

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

Classification

Five forms based on clinical presentation: first occurrence, paroxysmal, persistent, long-standing persistent, and permanent.

  • First occurrence may be symptomatic or asymptomatic. Spontaneous conversion rate is high, measured at >60% in hospitalized patients.
  • Paroxysmal—recurrent form of AF in which individual episodes are <7 days and usually <48 hours in duration.
  • Persistent—recurrent form of AF in which individual episodes are >7 days in duration and may require electrical or chemical cardioversion to terminate.
  • Long-standing persistent—AF for >1 year, still deemed manageable with cardioversion or RFA.
  • Permanent—AF after failed attempts at electrical or chemical cardioversion, has been present for more than 1 year, or has been accepted due to contraindications for cardioversion or lack of symptoms.

Epidemiology

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

Pathophysiology

  • Precise mechanisms giving rise to AF are not completely understood.
  • Initiation due to rapid, repetitive firing of ectopic focus within the pulmonary veins with fibrillatory conduction to bodies of the atria.
  • Maintenance 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 major role in initiation and maintenance. Inflammatory markers, such as interleukin 6 and C-reactive protein (CRP), are increased in and correlate with duration of AF, success of cardioversion, and thrombogenesis.

Prevention

  • Lack of prospective clinical data examining the value of risk factor modification in the prevention of non–postoperative AF.
  • Some data suggest statins may reduce recurrent AF by 61%, independent of lipid-lowering effect.4
  • Angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARBs) shown to prevent atrial remodeling in animals via suppression of the renin–angiotensin system. A meta-analysis of patients with CHF and HTN treated with either ACE-I or ARB has demonstrated 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 (β-blockers) has shown to reduce postoperative AF rates. Amiodarone, sotalol, magnesium, and omega-3 fatty acids used in perioperative period also demonstrated reduction in postoperative AF.6

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General Principles

Definition

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

Classification

Five forms based on clinical presentation: first occurrence, paroxysmal, persistent, long-standing persistent, and permanent.

  • First occurrence may be symptomatic or asymptomatic. Spontaneous conversion rate is high, measured at >60% in hospitalized patients.
  • Paroxysmal—recurrent form of AF in which individual episodes are <7 days and usually <48 hours in duration.
  • Persistent—recurrent form of AF in which individual episodes are >7 days in duration and may require electrical or chemical cardioversion to terminate.
  • Long-standing persistent—AF for >1 year, still deemed manageable with cardioversion or RFA.
  • Permanent—AF after failed attempts at electrical or chemical cardioversion, has been present for more than 1 year, or has been accepted due to contraindications for cardioversion or lack of symptoms.

Epidemiology

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

Pathophysiology

  • Precise mechanisms giving rise to AF are not completely understood.
  • Initiation due to rapid, repetitive firing of ectopic focus within the pulmonary veins with fibrillatory conduction to bodies of the atria.
  • Maintenance 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 major role in initiation and maintenance. Inflammatory markers, such as interleukin 6 and C-reactive protein (CRP), are increased in and correlate with duration of AF, success of cardioversion, and thrombogenesis.

Prevention

  • Lack of prospective clinical data examining the value of risk factor modification in the prevention of non–postoperative AF.
  • Some data suggest statins may reduce recurrent AF by 61%, independent of lipid-lowering effect.4
  • Angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARBs) shown to prevent atrial remodeling in animals via suppression of the renin–angiotensin system. A meta-analysis of patients with CHF and HTN treated with either ACE-I or ARB has demonstrated 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 (β-blockers) has shown to reduce postoperative AF rates. Amiodarone, sotalol, magnesium, and omega-3 fatty acids used in perioperative period also demonstrated reduction in postoperative AF.6

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