How does prolonging atrioventricular (AV) node repolarization affect the treatment of atrial fibrillation?

From the Guidelines

Prolonging AV node repolarization helps manage atrial fibrillation by controlling ventricular rate rather than fixing the arrhythmia itself, as recommended by the 2024 ESC guidelines for the management of atrial fibrillation 1. This is achieved through AV nodal blocking agents like beta-blockers (metoprolol 25-100mg twice daily, carvedilol 3.125-25mg twice daily), calcium channel blockers (diltiazem 120-360mg daily, verapamil 120-360mg daily), and digoxin (0.125-0.25mg daily). These medications slow conduction through the AV node by extending its refractory period, which prevents many of the rapid, chaotic atrial impulses from reaching the ventricles. The mechanism involves blocking calcium or sodium channels or enhancing vagal tone, depending on the medication class. Some key points to consider when using these medications include:

• The doses of medications used may vary depending on the patient's condition and response to treatment.
• AV nodal blocking agents should be used with caution in patients with obstructive pulmonary disease or congestive heart failure, as they can worsen these conditions.
• The use of catheter ablation to modify AV nodal conduction has been reported to decrease the ventricular rate during AF and improve cardiac symptoms, but it has several limitations, including the risk of inducing complete AV block and a relatively high risk of increasing ventricular rate over the first 6 months after ablation 1. While these medications don't convert atrial fibrillation back to normal sinus rhythm, they make the arrhythmia more tolerable by preventing the rapid ventricular response that causes many symptoms and can lead to tachycardia-induced cardiomyopathy with prolonged rapid rates. It's also important to note that atrioventricular node ablation combined with cardiac resynchronization therapy should be considered in severely symptomatic patients with permanent AF and at least one hospitalization for HF to reduce symptoms, physical limitations, recurrent HF hospitalization, and mortality 1.

From the FDA Drug Label

The negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node. Amiodarone HCl Injection administration prolongs intranodal conduction (Atrial-His, AH) and refractoriness of the atrioventricular node (ERP AVN)

Prolonging AV node repolarization can help fix atrial fibrillation by slowing conduction and prolonging refractoriness in the AV node, which can help reduce the frequency of abnormal heart rhythms. This is achieved through the negative dromotropic effects of certain medications, such as amiodarone, on the AV node 2.

• Key effects: slowing of conduction and prolongation of refractoriness in the AV node
• Main benefit: reduction of abnormal heart rhythm frequency
• Medication example: amiodarone 2

From the Research

Prolonging AV Node Repolarization to Fix Atrial Fibrillation

• Prolonging AV node repolarization is a method to control the ventricular rate in patients with atrial fibrillation, as it slows down the impulse transmission within the AV node 3.
• This can be achieved through medications that depress the AV node, such as beta-blockers and calcium channel blockers, which have been shown to be effective in reducing the ventricular response in atrial fibrillation 4, 5, 6.
• The calcium channel blockers verapamil and diltiazem have been found to prolong the functional refractory periods of the slow and fast pathways in the AV node, leading to a reduction in ventricular rate 5.
• Beta-blockers, such as metoprolol and carvedilol, have also been shown to reduce the ventricular rate in atrial fibrillation by prolonging the AV node refractory period 5.
• The choice of medication depends on the individual patient's condition, such as the presence of congestive heart failure, and the desired level of rate control 4, 7, 6.
• Monotherapy with beta-blockers or calcium channel blockers may not always be optimal, and combination therapy with other medications, such as cardiac glycosides, may be necessary to achieve adequate rate control 7.