Electrophysiologic and hemodynamic effects of chronic oral therapy with the α2-agonists clonidine and tiamenidine in hypertensive volunteers

Abstract

Clonidine can produce symptomatic sinus bradycardia or atrioventricular (AV) block in some patients. Electrophysiologic studies have been performed after intravenous clonidine in patients showing such side effects; these have demonstrated variable depression of sinus and AV nodal function. We have evaluated the electrophysiologic and hemodynamic effects of chronic oral treatment with either clonidine (0.2 to 0.5 mg every 12 hours; n = 7) or another centrally active alpha 2-agonist, tiamenidine (0.5 to 1.5 mg every 12 hours; n = 7), in otherwise healthy hypertensive human volunteers. At dosages that modestly lowered diastolic blood pressure, both agents significantly slowed sinus rate and increased the atrial pacing rate producing AV nodal Wenckebach. Clonidine also significantly increased corrected sinus node recovery time and lowered cardiac output while similar (but statistically insignificant) trends were seen with tiamenidine. We conclude that chronic oral treatment with these alpha 2-agonists depresses sinus and AV nodal function in virtually all subjects, including those without manifest conduction system disease.