Abstract

Fifteen patients without sinoatrial (SA) or atrioventricular (AV) node dysfunction underwent electrophysiologic study (EPS) before and after intravenous diltiazem: 0.20 mg/kg bolus followed by 0.0007 mg/kg/min infusion (seven patients) or 0.25 mg/kg bolus followed by 0.0012 mg/kg/min infusion (eight patients). In six patients intravenous digoxin (0.018 mg/kg) was given and 45 minutes later EPS was repeated while the diltiazem infusion continued. Diltiazem prolonged sinus cycle length (+7%, p less than 0.01), lengthened AH conduction time (+22% in constant rate atrial paced rhythm, p less than 0.001), prolonged AV node functional and effective refractory periods (+6%, p less than 0.01 and +16%, p less than 0.05, respectively), lengthened AV node Wenckebach cycle length (+13%, p less than 0.001), shortened atrial functional refractory period (-3%, p less than 0.05), and reduced mean arterial pressure (-8%, p less than 0.005 in constant rate atrial paced rhythm). Subsequently, intravenous digoxin further prolonged sinus cycle length (+12%, p less than 0.05), AH conduction time (+17%, p less than 0.05), AV node Wenckebach cycle length (+9%, p less than 0.05), and AV node functional refractory period (+7%, p less than 0.05), shortened atrial effective refractory period (-7%, p less than 0.05) and ventricular effective refractory period (-6%, p less than 0.05), and increased systolic arterial pressure (+6%, p less than 0.05). Diltiazem and digoxin have additive depressant effects on SA and AV node function without significant adverse effects.

View details for Web of Science ID A1982MX22600009

View details for PubMedID 7055046