Causes of Atrial Fibrillation
Atrial fibrillation is primarily caused by structural heart disease, cardiovascular risk factors, and acute temporary triggers that create an arrhythmogenic substrate through atrial remodeling, fibrosis, and electrophysiological changes. 1
Cardiovascular Conditions Associated with AF
Structural Heart Disease (70% of AF cases)
- Valvular heart disease (especially mitral valve disease)
- Coronary artery disease (CAD)
- Hypertension (particularly with left ventricular hypertrophy)
- Heart failure (both with reduced and preserved ejection fraction)
- Cardiomyopathies:
- Hypertrophic cardiomyopathy
- Dilated cardiomyopathy
- Restrictive cardiomyopathies (amyloidosis, hemochromatosis, endomyocardial fibrosis)
- Congenital heart disease (especially atrial septal defect in adults)
- Other cardiac conditions:
- Sinus node disease
- Ventricular pre-excitation (WPW syndrome)
- Cardiac tumors
- Constrictive pericarditis
- Mitral valve prolapse
- Calcification of the mitral annulus
- Cor pulmonale
- Idiopathic dilation of the right atrium 1
Acute Temporary Causes
- Alcohol intake ("holiday heart syndrome")
- Surgery
- Electrocution
- Myocardial infarction
- Pericarditis
- Myocarditis
- Pulmonary embolism
- Other pulmonary conditions 1
Non-Cardiac Conditions
- Hyperthyroidism
- Metabolic disorders
- Sleep apnea
- Obesity
- Diabetes mellitus
- Chronic kidney disease
- Drug-induced AF (various cardiovascular, non-cardiovascular, and anticancer drugs) 1
Pathophysiological Mechanisms
Structural Abnormalities
- Atrial fibrosis - a common feature in both experimental and human AF
- Inflammation - inflammatory infiltrates consistent with myocarditis found even in patients with paroxysmal AF without recognized structural heart disease
- Hypertrophy - often associated with hypertension and other heart diseases
- Atrial dilation - increases wall stress and promotes arrhythmogenesis
- Myocyte loss - from glycogen deposits, mitochondrial disturbances, and gap-junction abnormalities 1
Electrophysiological Mechanisms
AF requires both a trigger for initiation and an appropriate anatomic substrate for maintenance:
Triggers of AF:
- Ectopic focal discharges (most commonly from pulmonary vein myocardial sleeves)
- Abnormal automaticity and triggered activity in pulmonary vein myocytes
- Reentry due to conduction abnormalities 1
Autonomic Nervous System Influence:
- Vagal AF: Occurs at night, during rest, after eating, or alcohol ingestion; preceded by bradycardia
- Adrenergic AF: Occurs during daytime, provoked by exercise or emotional stress 1
Lone AF (AF without Associated Heart Disease)
- Approximately 30-45% of paroxysmal cases and 20-25% of persistent cases occur in younger patients without demonstrable underlying disease
- May present as isolated or familial arrhythmia
- Underlying disease may appear over time 1
Risk Factors for AF Development
Well-Established Risk Factors
- Aging - multifactorial effect including LA enlargement, reduced LAA flow velocity, and prothrombotic diathesis
- Male sex
- Hypertension - causes ventricular diastolic abnormalities and atrial remodeling
- Obesity - BMI ≥27 significantly increases risk 2
Lifestyle Factors
- Alcohol consumption
- Cigarette smoking
- Sedentary lifestyle
- High-level physical training (paradoxically) 3, 2
Clinical Implications
Understanding the cause of AF is crucial for:
- Determining appropriate treatment strategies
- Potentially eliminating AF by treating the underlying condition
- Assessing stroke risk (CHA₂DS₂-VASc score)
- Preventing progression from paroxysmal to persistent or permanent AF
The complex interplay of structural abnormalities, electrophysiological changes, and systemic factors underscores the importance of comprehensive evaluation of patients with AF to identify potentially reversible causes and optimize management strategies.
AI: I notice I didn't fully address the neurogenic forms of AF. Should I add more detail about vagal and adrenergic forms of AF?