Atrial fibrillation

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Atrial Fibrillation

Based primarily on Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine

Definition & ECG Features

Atrial fibrillation (AF) is a supraventricular arrhythmia characterized by:
  • Fibrillatory (f) waves: low-amplitude baseline oscillations at 300–600 beats/min, variable in amplitude, shape, and timing
  • Irregularly irregular ventricular rhythm
In some patients, f waves are imperceptible and the diagnosis rests entirely on the irregularly irregular rhythm. The ventricular rate in untreated AF is typically 100–160 beats/min. In WPW syndrome, rates can exceed 250 beats/min via an accessory pathway.

Classification

TypeDefinition
ParoxysmalTerminates spontaneously within 7 days
PersistentContinuous >7 days
Long-standing persistentContinuous >1 year
PermanentPatient and clinician jointly decide to accept AF without further rhythm-control attempts
  • Vagotonic AF (~25% of paroxysmal): triggered by high vagal tone (evenings, sleep). Worsened by digoxin; helped by disopyramide.
  • Adrenergic AF (~10–15%): triggered by exertion/sympathetic activation; beta-blockers can help.

Epidemiology

AF is the most common sustained cardiac arrhythmia. Prevalence rises sharply with age (~12% in those ≥75 years, ~18% in those ≥85 years). Common associated conditions include hypertension, coronary artery disease, heart failure (HF), obesity, sleep apnea, and hyperlipidemia. AF affects men more than women. Lifetime risk is approximately 1 in 4 for middle-aged adults.

Mechanisms

AF is maintained by multiple reentrant wavelets within the atria, with atrial size and fibrosis (structural remodeling) providing the substrate. Key concepts:
  • Focal triggers: Ectopic foci in the pulmonary vein ostia are the predominant source of triggering ectopy — the basis for pulmonary vein isolation (PVI) catheter ablation
  • Electrical remodeling: AF itself shortens atrial refractory periods ("AF begets AF")
  • Structural remodeling: Atrial fibrosis, dilation, and inflammation impair conduction and promote reentry
  • Genetic factors: Multiple genetic loci have been identified; familial AF is recognized

Causes / Precipitants

CardiacNon-cardiac
HypertensionHyperthyroidism
Valvular heart disease (especially mitral)Pulmonary embolism
Coronary artery diseaseAlcohol ("holiday heart")
Heart failureObstructive sleep apnea
CardiomyopathyPost-surgical (especially cardiac/thoracic)
Congenital heart diseaseElectrolyte disturbances
PericarditisInfection/sepsis

Clinical Features

Symptoms include palpitations, dyspnea, fatigue, lightheadedness, and chest discomfort. Many patients are asymptomatic or have only subtle symptoms (especially older adults). Acute pulmonary edema may occur with abrupt loss of the atrial "kick" in a stiff left ventricle. Less commonly, AF presents as syncope, fall, or stroke.

Stroke Risk & Anticoagulation

Nonvalvular AF carries a fivefold increased stroke risk. Strokes are typically embolic from left atrial appendage (LAA) thrombus formation.

CHA₂DS₂-VASc Score (stroke risk)

Risk FactorPoints
Congestive HF1
Hypertension1
Age ≥75 years2
Diabetes mellitus1
Stroke/TIA history2
Vascular disease1
Age 65–74 years1
Sex category (Female)1
  • Score ≥2 (men) or ≥3 (women): anticoagulation recommended
  • All patients ≥75 years have a score of ≥2 regardless of other factors

Anticoagulation Options

AgentNotes
DOACs (dabigatran, rivaroxaban, apixaban, edoxaban)Preferred over warfarin in nonvalvular AF; no INR monitoring needed; similar or better efficacy with less bleeding in most trials
WarfarinTarget INR 2.0–3.0 (2.0–2.5 in elderly); still used in valvular AF (e.g., mechanical valves, rheumatic mitral stenosis)
LAA occlusion (Watchman device)For patients with high stroke risk who cannot tolerate long-term anticoagulation
AspirinNot recommended as primary stroke prevention in AF
Bleeding risk is assessed with the HAS-BLED score. A high bleeding score should prompt correction of reversible risk factors, not automatic withholding of anticoagulation.

Acute Management

  1. Hemodynamic instability → immediate DC cardioversion
  2. Rate control: IV beta-blockers (metoprolol, esmolol) or non-dihydropyridine calcium channel blockers (diltiazem, verapamil) for rapid ventricular rate; digoxin or amiodarone in decompensated HF
  3. Rhythm control / cardioversion:
    • If AF duration <48 hours (or adequately anticoagulated for ≥3 weeks): electrical or pharmacologic cardioversion safe
    • If duration unknown or ≥48 hours: transesophageal echocardiography (TEE) to exclude LAA thrombus before cardioversion, followed by ≥4 weeks of anticoagulation post-cardioversion
  4. Anticoagulation: Initiate unless contraindicated regardless of rhythm strategy

Long-Term Management: Rate vs. Rhythm Control

Rate Control

  • Target resting heart rate ≤80 beats/min (lenient: ≤110 beats/min acceptable in asymptomatic patients)
  • Agents: beta-blockers, diltiazem/verapamil; digoxin as add-on; amiodarone for refractory cases
  • The RACE and AFFIRM trials showed rate control is not inferior to rhythm control for mortality in most patients

Rhythm Control

  • Preferred in: symptomatic patients, younger patients, AF with hemodynamic compromise, tachycardia-induced cardiomyopathy
  • EAST-AFNET 4 trial demonstrated early rhythm control reduces cardiovascular outcomes when initiated soon after diagnosis
  • Pharmacologic options: flecainide, propafenone (structurally normal hearts); sotalol; amiodarone (most effective but significant side-effect profile); dofetilide; dronedarone
  • "Pill-in-the-pocket" approach: patient self-administers flecainide or propafenone at onset of AF episode

Nonpharmacologic Management

Catheter Ablation

  • Pulmonary vein isolation (PVI) is the cornerstone — eliminates the main triggering foci
  • Indicated for symptomatic paroxysmal or persistent AF failing or intolerant of AADs; increasingly considered first-line for selected patients
  • Success rates: ~70–80% for paroxysmal AF at 1 year (single procedure); lower for persistent AF
  • Complications: phrenic nerve injury, pulmonary vein stenosis, esophageal injury (rare but serious), cardiac tamponade, stroke

Risk Factor Modification

  • Weight loss, treatment of sleep apnea, blood pressure control, and exercise reduce AF burden and improve ablation outcomes
  • The LEGACY and ARREST-AF studies showed intensive risk factor management meaningfully reduces AF recurrence

AV Node Ablation + Pacemaker

  • Reserved for symptomatic AF with failed rate/rhythm control; creates complete AV block requiring permanent pacing ("ablate and pace" strategy)

Surgical Maze Procedure

  • Used when cardiac surgery is performed for another indication; creates lesion lines interrupting reentrant circuits

Special Clinical Situations

SituationKey Considerations
Postoperative AFCommon after cardiac/thoracic surgery; often self-terminates; beta-blockers and amiodarone for prevention
WPW + AFMedical emergency — AV nodal blockers (digoxin, verapamil, adenosine) are contraindicated (can accelerate conduction via accessory pathway → VF); treat with procainamide IV or DC cardioversion
Heart failure + AFRate control with beta-blockers or amiodarone; catheter ablation reduces HF hospitalizations
Hypertrophic cardiomyopathyAF poorly tolerated; aggressive rhythm control; anticoagulate all patients regardless of CHA₂DS₂-VASc score
PregnancyElectrical cardioversion is safe; pharmacologic options limited; anticoagulation management complex

Key Takeaways

  • AF is an irregularly irregular arrhythmia driven by disorganized atrial electrical activity, most commonly triggered from pulmonary vein foci
  • The primary dangers are stroke (from LAA thrombus) and tachycardia-induced cardiomyopathy
  • Anticoagulation based on CHA₂DS₂-VASc is the single most important intervention to reduce morbidity
  • DOACs are preferred over warfarin in nonvalvular AF
  • Rate vs. rhythm control both have roles; early rhythm control may improve outcomes
  • Catheter ablation (PVI) is increasingly first-line for symptomatic AF
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, Chapter 66
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