Beta2-agonist induced ventricular dysrhythmias secondary to hyperexcitable conduction system in the absence of a long QT syndrome.

BACKGROUND

The use of inhaled beta 2-agonists for bronchodilation in the treatment of lower airway obstruction is accepted worldwide. These agents are used for symptomatic relief of lower airway obstruction and, as well, can be employed prophylactically in exercise-induced bronchospasm. Cardiac dysrhythmias, specifically the long QT syndrome, have been associated with cardiac events precipitated by sympathomimetics. There are reports of documented long QT syndrome in association with syncope in children; however, there are no reports of beta 2-agonist-induced syncope in the absence of long QT syndrome.

OBJECTIVE

To determine predisposing cardiac factors resulting in syncope associated with inhaled beta 2-agonist use.

METHOD

Case report. The index case was evaluated for cardiac pathology through non-invasive techniques, cardiac catheterization, and electrophysiologic studies. Electrophysiologic studies included provocative challenge with parenteral adrenergic agents.

RESULTS

Non-invasive studies were unremarkable. There was no evidence of prolonged QT syndrome or support for vasopressor syncope. Electrophysiologic studies revealed reproducible polymorphic ventricular tachycardia. This predisposition required a ventricular stimulation program of higher intensity while on mexilitine.

CONCLUSIONS

This case of syncope associated with inhaled, short-acting beta 2-agonist resulted from a hyperexcitable conduction system rather than the presence of a long QT syndrome.