Enhancement of the antiarrhythmic action of disopyramide by digoxin.
Acute antiarrhythmic testing with 200 mg of disopyramide p.o. was performed in two groups of 15 patients each, with a prevalence of ventricular premature depolarization (VPD) exceeding one per minute. Patients in the first group were not receiving cardiac glycosides; those in the second group were on maintenance therapy with oral digoxin. Systolic time intervals (STI) were recorded throughout the test in order to evaluate left ventricular performance. Plasma levels of disopyramide were measured at peak ECG changes and digoxin levels before and 2 h following administration of disopyramide. Only five patients in the first group responded with an 80% or greater reduction in VPD rate and abolition of repetitive forms. In contrast, 13 digitalized patients responded to disopyramide. Mean plasma levels of disopyramide did not differ in the two groups (1.68 and 1.78 microgram/ml, respectively). Digoxin plasma levels in no case exceeded 3 ng/ml and did not change significantly after disopyramide. Significant increases in STI and in the QTC interval were recorded only in patients of the first group. The PR interval was prolonged in both groups, but to a greater extent in patients receiving digoxin. We conclude that digitalization may prevent myocardial functional depression caused by disopyramide and enhance its antiarrhythmic action.
D000328:Adult; D001145:Arrhythmias, Cardiac / Q000188:drug therapy; D004077:Digoxin / Q000494:pharmacology*; D004206:Disopyramide / Q000009:adverse effects / Q000494:pharmacology*; D004357:Drug Synergism; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011725:Pyridines / Q000494:pharmacology*; D013599:Systole / Q000187:drug effects
D011725:Pyridines; D004077:Digoxin; D004206:Disopyramide