A 67-Year-Old Man With Palpitations and Syncope

Nazem Akoum, MD, MS; Steven A. Lubitz, MD, MPH; Zachary D. Goldberger, MD, MSc, FACC


February 19, 2019

Editorial Collaboration

Medscape &

Management of sinus node dysfunction in the setting of tachy-brady syndrome can be challenging. Drugs used for rate control during periods of atrial fibrillation (eg, beta-blockers, calcium-channel blockers, digoxin) often exacerbate the bradycardia and pauses that are usually seen upon termination of the tachyarrhythmia. These drugs can also cause slow ventricular conduction during atrial fibrillation.

The use of Vaughan Williams Class III antiarrhythmic agents (eg, amiodarone, dronedarone, sotalol) or class IC agents (eg, flecainide or propafenone combined with an atrioventricular nodal blocking agent) may exacerbate the bradycardia and pauses, as seen with rate-control agents.

Of note, dofetilide is least likely to cause bradycardia. Like other Class III agents, dofetilide is a potassium-channel blocker but selectively targets the slow inward rectifier potassium current. It prolongs repolarization without affecting the rate of spontaneous depolarization in the sinus node cells. However, it requires a mandatory inpatient admission for initiation, given the potential for QT prolongation with risk for torsades de pointes, necessitating frequent ECG monitoring.

The implantation of a permanent pacemaker is often recommended in patients with tachy-brady syndrome.[1] The pacemaker is usually programmed in a demand mode and starts pacing whenever the heart rate drops below a certain threshold, thereby eliminating all pauses and periods of bradycardia that follow termination of atrial arrhythmias.

A question that commonly arises in patients with atrial fibrillation is whether suppression of the atrial tachyarrhythmia, using catheter ablation rather than antiarrhythmic drugs, could eliminate the termination pauses and bradycardia associated with the use of antiarrhythmic and rate-control agents and therefore avert the need for a permanent pacemaker. The answer is not straightforward, as the pathophysiology of sinus node dysfunction in the setting of atrial fibrillation is complex.

Anatomically, the sinus node is a compact structure located in the superior lateral region of the right atrium near the junction with the superior vena cava. The sinus node is made of specialized pacemaker cells that exhibit spontaneous electrical depolarization. These cells are shielded from neighboring atrial myocytes by connective tissue and transitional cells.[2,3] The sinus node receives parasympathetic and sympathetic autonomic nervous stimulation that determines the rate of firing or spontaneous depolarization.

In the setting of atrial arrhythmias including atrial fibrillation and atrial flutter, studies have demonstrated that the rapid electrical rhythm is associated with electrical remodeling that leads to longer sinus node recovery times.[4,5] Electrical remodeling in atrial fibrillation manifests with an increase in the dispersion of action potential durations. This electrical phenomenon is reversed with restoration and maintenance of sinus rhythm.[6,7] Some studies of patients with atrial fibrillation and sinus node disease have demonstrated that some patients who undergo successful catheter ablation demonstrate an improvement in sinus node dysfunction.[8] However, other studies have shown that some patients still require permanent pacing for bradycardia and pauses.[9] The discrepancy in the findings is likely related to fibrotic involvement of the sinus node, or structural remodeling, that leads to the clinical manifestations of sinus node disease. Excessive fibrosis involving the sinus node is not expected to be reversible; hence, for these patients, permanent pacing is unavoidable.


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