From the Guidelines
Syncope in atrial fibrillation occurs through several key mechanisms, primarily due to rapid ventricular response, pauses following termination of atrial fibrillation, and underlying structural heart disease. The mechanisms of syncope in atrial fibrillation (AF) are multifactorial, involving both haemodynamic and neurally-mediated reflex effects 1.
Key Mechanisms
- Rapid ventricular response, where the irregular and fast heart rate reduces cardiac output and cerebral perfusion, leading to loss of consciousness
- Pauses that can follow termination of atrial fibrillation, especially in patients with sick sinus syndrome, causing a temporary cessation of cardiac output
- Bradycardia-related syncope can occur in atrial fibrillation patients taking rate-controlling medications like beta-blockers, calcium channel blockers, or digoxin
- Underlying structural heart disease such as aortic stenosis or hypertrophic cardiomyopathy, which can independently cause syncope through outflow obstruction
Clinical Considerations
In clinical practice, it is essential to consider the potential mechanisms of syncope in atrial fibrillation and address any underlying structural heart disease, as well as optimize rate control and rhythm control strategies 1.
Management
Management of syncope in atrial fibrillation focuses on rate control with medications, rhythm control strategies, anticoagulation to prevent thromboembolism, and addressing any underlying structural heart disease. The primary goal is to prevent symptom recurrence and reduce mortality risk, which can be achieved through a comprehensive treatment approach 1.
From the Research
Mechanisms of Syncope in Atrial Fibrillation (AF)
The mechanisms of syncope in atrial fibrillation (AF) are complex and multifactorial. Some of the possible mechanisms include:
- Autonomic reflexes: Studies have shown that autonomic reflexes, such as vasovagal syncope, can play a role in the genesis of syncope associated with paroxysmal AF 2.
- Suppression of intrinsic cardiac pacemakers: Suppression of intrinsic cardiac pacemakers during tachycardia can lead to asystole and syncope 3.
- Proarrhythmic effects of antiarrhythmic drugs: Antiarrhythmic drugs can have proarrhythmic effects, such as inducing torsades de pointes, which can cause syncope 4.
- Sympatho-vagal imbalance: Sympatho-vagal imbalance can contribute to the development of AF and syncope 5, 6.
- Abnormal neural response: Patients with syncope associated with paroxysmal AF may have an abnormal neural response during both sinus rhythm and arrhythmia 2.
Role of Autonomic Nervous System
The autonomic nervous system (ANS) plays a crucial role in the genesis and maintenance of AF. Studies have shown that ANS imbalance can contribute to the development of AF and syncope 5, 6. The ANS can be modulated through various techniques, such as catheter ablation of ganglionated plexi, renal sympathetic denervation, and vagal nerve stimulation 5, 6.
Clinical Implications
Understanding the mechanisms of syncope in AF is important for clinical management. Patients with syncope associated with paroxysmal AF may require different treatment strategies, such as antiarrhythmic drugs, catheter ablation, or pacing 4, 5, 6. Additionally, identifying and addressing underlying conditions, such as sympatho-vagal imbalance, can help prevent syncope and improve outcomes 5, 6.