Tell me about atrial fibrillation (AF)?

Atrial Fibrillation: Overview

Atrial fibrillation is the most common sustained cardiac arrhythmia, affecting 1.5-2% of the general population, characterized by chaotic atrial electrical activity that causes loss of coordinated atrial contraction, increases stroke risk 5-fold, doubles mortality, and creates a bidirectional relationship with heart failure where each condition worsens the other. 1

Definition and Electrocardiographic Features

AF is a supraventricular tachyarrhythmia with uncoordinated atrial activation causing deterioration of atrial mechanical function. 1

On ECG, AF demonstrates:

• Absent distinct P waves, replaced by rapid oscillations (fibrillatory waves) that vary in amplitude, shape, and timing 2, 3
• Irregularly irregular R-R intervals with no discernible pattern 2
• Irregular ventricular response when AV conduction is intact, typically rapid 1
• Fibrillatory waves best visualized in leads II, III, aVF, and V1 2

The ventricular rate depends on AV node properties, autonomic tone, and medications. 1 Extremely rapid rates exceeding 200 bpm suggest an accessory pathway. 1

Epidemiology and Risk Profile

The lifetime risk of developing AF is 1 in 4 for individuals over age 55, with prevalence increasing from <1% before age 50 to 12% in those over 80 years. 1

The incidence is predicted to double over coming decades due to:

• Aging population 1
• Growing burden of cardiovascular comorbidities 1
• Increasing prevalence of risk factors including hypertension, diabetes, obesity, and sleep apnea 1

Clinical Significance and Complications

AF carries substantial morbidity and mortality through multiple mechanisms: 1

Thromboembolic Risk

• Increases stroke risk 5-fold 1
• Impaired atrial mechanical function promotes thrombus formation, particularly in the left atrial appendage 3

Hemodynamic Consequences

• Loss of atrial contraction reduces cardiac output by up to 20-30% 1
• Irregular ventricular rhythm itself decreases cardiac output 1
• Rapid ventricular rates can precipitate or worsen heart failure 1

Mortality Impact

• Doubles all-cause mortality, primarily from thromboembolic events and ventricular dysfunction 1
• Accounts for one-third of hospitalizations for cardiac rhythm disturbances 1

The AF-Heart Failure Connection

AF and heart failure create a vicious cycle where each condition promotes and worsens the other—"AF begets HF and HF begets AF." 1

Prevalence of Coexistence

• 10-57% of heart failure patients have AF, depending on age and HF severity 1
• 40-55% of patients with persistent or long-standing persistent AF develop heart failure 1
• The combination confers synergistically worse outcomes than either condition alone 1

Mechanisms Linking AF to Heart Failure

• Loss of atrial kick reduces ventricular filling 1
• Tachycardia-induced cardiomyopathy from prolonged rapid rates 1
• Irregular ventricular response impairs cardiac efficiency 1

How Heart Failure Promotes AF

• Elevated ventricular filling pressures cause atrial stretch 1
• Functional mitral regurgitation increases atrial volume load 1
• RAAS activation promotes atrial structural remodeling and fibrosis 1
• Neurohormonal changes alter atrial electrophysiology 1

Drug-Induced Atrial Fibrillation

An increasing number of cardiovascular, non-cardiovascular, and anticancer drugs can trigger AF, particularly in elderly patients with polypharmacy, though this entity receives insufficient attention in AF guidelines. 1, 4

High-Risk Medications

• Cardiovascular drugs: adenosine, dobutamine, dopamine 4
• Respiratory drugs: sympathomimetics, theophylline 4
• Anticancer agents: anthracyclines, taxanes, ibrutinib 4
• Antibiotics: fluoroquinolones 4
• Other agents: corticosteroids, ondansetron 4

Clinical Characteristics

• Most episodes are paroxysmal and may terminate spontaneously 1, 4
• Many cases are asymptomatic, making detection challenging 4
• Risk amplified by advanced age, pre-existing cardiovascular disease, and structural heart abnormalities 4

Distinguishing AF from Similar Arrhythmias

Atrial Flutter

• Regular "saw-tooth" pattern of flutter waves, most visible in leads II, III, aVF, and V1 2
• Regular atrial rate of 240-320 bpm 2
• Regular or regularly irregular ventricular response depending on AV conduction ratio 2
• Can alternate with AF or degenerate into AF 1

Multifocal Atrial Tachycardia

• At least 3 distinct P wave morphologies on a single ECG lead 2
• Irregular R-R intervals but visible P waves separated by isoelectric baseline 2
• Variable P-R intervals reflecting multiple atrial foci 2

Focal Atrial Tachycardia

• Distinct P waves with consistent morphology 2
• P waves separated by isoelectric baseline 2
• Regular or slightly irregular rhythm 2

Prognostic ECG Features

Fibrillatory wave amplitude provides prognostic information: 3

• Coarse-grained AF (amplitude ≥0.1 mV): higher cardioversion success rate, better left atrial appendage function, but higher incidence of previous cerebrovascular events 3
• Fine-grained AF (amplitude <0.1 mV): higher risk of heart failure events, poorer atrial function, increased thrombus formation 3

Management Principles

Treatment focuses on two main strategies beyond anticoagulation for thromboembolism prophylaxis: 5

Rate Control

• Uses AV nodal blocking medications (beta blockers, calcium channel blockers) to maintain goal heart rate 5
• Allows AF to persist while controlling ventricular response 5

Rhythm Control

• Uses antiarrhythmic drugs, cardioversion, and ablation to restore and maintain sinus rhythm 5
• Particularly important in patients with severe HF who gain rapid hemodynamic improvement with restoration of sinus rhythm 1

Critical Clinical Pitfalls

Wide-complex irregular tachycardia suggests AF with bundle branch block, AF with accessory pathway conduction, or polymorphic ventricular tachycardia—requires immediate expert evaluation. 2

AF with regular ventricular response may indicate coexisting complete AV block, ventricular tachycardia, or junctional tachycardia—examine atrial activity carefully in leads II, III, aVF, and V1. 2

When evaluating new-onset AF, always consider drug-induced AF in the differential, especially in patients with cancer history or polypharmacy. 4