Electrophysiologic effects of disopyramide in patients with atrioventricular nodal dysfunction.
Seventeen patients with first-degree or Mobitz I atrioventricular (AV) block and narrow QRS complexes underwent electrophysiologic drug testing before and after i.v. administration of disopyramide. Disopyramide did not significantly change the mean sinus cycle length (895 +/- 131 vs 877 +/- 119 msec), mean maximal sinus node recovery time (1134 +/- 160 vs 1133 +/- 13 msec), mean atrial effective refractory period (314 +/- 72 vs 307 +/- 54 msec), mean AV nodal conduction time (187 +/- 79 vs 180 +/- 73 msec) or the mean paced cycle length at which AV nodal Wenckebach conduction occurred (545 +/- 144 vs 497 +/- 130 msec) after disopyramide. The mean AV nodal effective refractory period decreased significantly (from 535 +/- 137 to 521 +/- 122 msec), and both infranodal conduction time and the paced ventricular cycle length producing ventriculoatrial block increased significantly (from 56 +/- 12 to 63 +/- 13 msec and from 625 +/- 158 to 655 +/- 157 msec, respectively). We conclude that i.v. disopyramide administered in a dose resulting in therapeutic blood levels showed no adverse effects on AV nodal conduction in patients with AV nodal dysfunction. In contrast, i.v. disopyramide depressed retrograde AV conduction.
D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000097:blood / Q000627:therapeutic use; D002304:Cardiac Pacing, Artificial; D004206:Disopyramide / Q000097:blood / Q000627:therapeutic use*; D004562:Electrocardiography; D004594:Electrophysiology; D006327:Heart Block / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D008875:Middle Aged; D011725:Pyridines / Q000627:therapeutic use*
D000889:Anti-Arrhythmia Agents; D011725:Pyridines; D004206:Disopyramide