Athletes and Vagal Atrial Fibrillation

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The vagus nerve innervates the following cardiac structures and causes:

• SA node: negative chronotropic effect (slows heart rate)
• AV node: negative dromotropic effect (slows conduction)
• Atrial myocardium: shortens action potential (AP) and effective refractory period (ERP)

The vagus nerve innervates the atria unevenly. Upon stimulation, uneven shortening of AP and ERP occurs, resulting in atrial dispersion (difference in duration) of AP and ERP, which creates a substrate for micro-reentry. This establishes a substrate for atrial fibrillation (AF).

Bradycardia prolongs atrial diastole, providing more time for the development of ectopic impulses and micro-reentry.

Vagal AF occurs due to parasympathetic (vagus nerve) stimulation.

• Vagal AF occurs mainly at night.

The trigger of vagal AF is bradycardia.

Vagal atrial fibrillation – most common triggers
Sleep
Postprandial state (after a large meal)
Relaxation after stress or after exercise
Alcohol (especially beer)
Nausea
Vomiting, swallowing

AF may occur during sleep due to sleep apnoea syndrome (this does not have to be vagus-mediated).

• During sleep, transient airway obstruction occurs, leading to organ and atrial ischaemia.
• Transient atrial ischaemia is a trigger for AF.

Adrenergic AF

• Occurs due to sympathetic stimulation:
• Exercise, physical exertion, stress, infection, caffeine, energy drinks
• Adrenergic stimulation triggers 15% of paroxysmal AF
• Occurs mainly during the day

Vagal AF

• Occurs due to parasympathetic (vagus nerve) stimulation:
• Sleep, postprandial state, relaxation, alcohol, nausea, vomiting, swallowing
• Vagal stimulation triggers 6% of paroxysmal AF
• Occurs mainly at night
• It is usually paroxysmal
• Annual risk of progression to persistent AF is 5–14%

Athletes and vagal AF

• Trained athletes have increased vagal (parasympathetic) tone
• due to adaptation of the autonomic nervous system to chronic exercise.
• The athlete’s heart has an increased stroke volume,
• therefore bradycardia (<50/min.) is sufficient to maintain adequate cardiac output.

Vagal vs Adrenergic Atrial Fibrillation
Vagal AF	Adrenergic AF
More common in younger patients (25–60 years)	More common in older patients (>60 years)
More common in men than women (4:1)	More common in men than women (2:1)
Without structural heart disease	Structural heart disease
Induced by parasympathetic stimulation: Sleep Postprandial state Relaxation Alcohol Nausea Vomiting	Induced by sympathetic stimulation: Exercise Physical exertion Stress Caffeine Infection Energy drinks
Occurs mainly at night	Occurs mainly during the day
Preceded by bradycardia	Preceded by tachycardia
Slow ventricular response (<100/min.)	Rapid ventricular response (>100/min.)
Worsens after beta-blocker administration	Improves after beta-blocker administration
Less frequently progresses to persistent AF	More frequently progresses to persistent AF

For chronic treatment of vagal AF, the following is recommended:

• Disopyramide (Class IA)
• It has a strong vagolytic effect.
• It blocks cardiac M2 muscarinic receptors, thereby reducing the effect of the vagus nerve on the heart.

For acute treatment of vagal AF (if the patient is not taking disopyramide), the following is recommended:

• Flecainide (Class IC)
• as a “pill-in-the-pocket” strategy together with an AV node–slowing drug.
• Through sodium channel blockade, it slows conduction and reduces atrial excitability.
• Flecainide is administered as a “pill-in-the-pocket” when the patient develops a symptomatic AF episode. Procedure:
• 30 minutes before flecainide 300 mg oral as a single dose, it is recommended to administer a small oral dose of an AV node–slowing drug:
• Diltiazem 30 mg oral as a single dose
• Verapamil 40 mg oral as a single dose
• Metoprolol 12.5 mg oral as a single dose
• This prevents 1:1 atrial flutter conduction.

In vagal AF, bradycardia-inducing drugs should not be administered long-term:

• Beta-blockers
• Verapamil
• Diltiazem
• Amiodarone
• Sotalol
• Propafenone (Class IC, but with additional weak beta-blocking effect)

In vagal AF, the primary issue is not AV nodal conduction itself, but marked vagal predominance in the atria, which triggers AF:

• Bradycardia prolongs atrial diastole, allowing more time for ectopic impulses to develop.
• Uneven shortening of the atrial action potential and effective refractory period occurs, leading to micro-reentry.

A single low dose of a beta-blocker or verapamil/diltiazem before flecainide in vagal AF:

• does not worsen the AF episode,
• but reliably prevents 1:1 atrial flutter conduction.

Vagal atrial fibrillation	Class
For long-term treatment of vagal atrial fibrillation, disopyramide is recommended.	I
For acute treatment of vagal AF (if the patient is not taking disopyramide), the “pill-in-the-pocket” strategy with flecainide is recommended. 30 minutes before flecainide, an AV node–slowing drug (beta-blocker, verapamil, diltiazem) is recommended as prevention of 1:1 atrial flutter conduction.	I
In the treatment of vagal atrial fibrillation, the following antiarrhythmic drugs may be considered: Beta-blockers Verapamil Diltiazem Amiodarone Sotalol Propafenone	IIb

These guidelines are unofficial and do not represent formal guidelines issued by any professional cardiology society. They are intended for educational and informational purposes only.