Effects of cardiac glycosides on atrial contractile dysfunction after short-term atrial fibrillation.
BACKGROUND
Despite a long history of use in the treatment of paroxysmal atrial fibrillation (AF), the efficacy of cardiac glycosides has not been established. If such drugs are beneficial in this condition, the general view is that the benefit must be related to their inotropic actions.


RESULTS
To assess the effects of the rapid-acting cardiac glycoside, acetylstrophanthidin (AS), on AF and AF-induced right atrial (RA) "stunning," RA wall motion (with ultrasonic crystals), RA pressure, and peak first derivative of pressure (dp/dt) (with microtip transducers) were measured before and after 5 min of high-intensity rapid atrial stimulation (10 Hz; 10 mA; 1 ms) and after the cessation of poststimulation AF. Measurements were made in neurally intact and autonomically blockaded dogs both before and after the administration of AS (0.01 mg/kg IV bolus and 0.015 mg/kg/h IV infusion). AS prevented the post-AF reduction in RA peak dp/dt under neurally intact and autonomically blockaded conditions, and it prevented the post-AF increase in the RA end-systolic dimension and the decrease in the percentage of RA systolic shortening with autonomic blockade. AS was beneficial whether or not baseline inotropy was enhanced by AS. The duration of AF following atrial stimulation was the same before and after AS, but when compared to controls, AS treatment appeared to prolong AF.


CONCLUSIONS
Cardiac glycosides exert a favorable effect on AF-induced RA stunning, but this action is unrelated to its effects on the duration of AF.
Friedman
H S
HS
Department of Medicine, Long Island College Hospital and SUNY Health Science Center, Brooklyn, NY, USA. HSF2727@POL.NET
Win
M
M
Hussain
A
A
Sinha
A
A
D000818:Animals; D001281:Atrial Fibrillation / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D001340:Autonomic Nerve Block; D002301:Cardiac Glycosides / Q000008:administration & dosage*; D004285:Dogs; D004562:Electrocardiography / Q000187:drug effects; D006325:Heart Atria / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007262:Infusions, Intravenous; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D013327:Strophanthidin / Q000008:administration & dosage* / Q000031:analogs & derivatives*; D014630:Vagus Nerve; D018497:Ventricular Dysfunction, Right / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology
D002301:Cardiac Glycosides; D013327:Strophanthidin; C004681:acetylstrophanthidin