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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
| Type | Definition |
|---|
| Paroxysmal | Terminates spontaneously within 7 days |
| Persistent | Continuous >7 days |
| Long-standing persistent | Continuous >1 year |
| Permanent | Patient 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
| Cardiac | Non-cardiac |
|---|
| Hypertension | Hyperthyroidism |
| Valvular heart disease (especially mitral) | Pulmonary embolism |
| Coronary artery disease | Alcohol ("holiday heart") |
| Heart failure | Obstructive sleep apnea |
| Cardiomyopathy | Post-surgical (especially cardiac/thoracic) |
| Congenital heart disease | Electrolyte disturbances |
| Pericarditis | Infection/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 Factor | Points |
|---|
| Congestive HF | 1 |
| Hypertension | 1 |
| Age ≥75 years | 2 |
| Diabetes mellitus | 1 |
| Stroke/TIA history | 2 |
| Vascular disease | 1 |
| Age 65–74 years | 1 |
| 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
| Agent | Notes |
|---|
| 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 |
| Warfarin | Target 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 |
| Aspirin | Not 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
- Hemodynamic instability → immediate DC cardioversion
- 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
- 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
- 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
| Situation | Key Considerations |
|---|
| Postoperative AF | Common after cardiac/thoracic surgery; often self-terminates; beta-blockers and amiodarone for prevention |
| WPW + AF | Medical 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 + AF | Rate control with beta-blockers or amiodarone; catheter ablation reduces HF hospitalizations |
| Hypertrophic cardiomyopathy | AF poorly tolerated; aggressive rhythm control; anticoagulate all patients regardless of CHA₂DS₂-VASc score |
| Pregnancy | Electrical 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