Drug Interaction:
Tachycardia,,atrial flutter.
Summary-
Acecainde appears to be a potentially useful antiarrhythmic. The fact that it has little tendency
to induce the lupus -like syndrome frequently associated with procainamide is of interest,
but other alternatives to procainamide also exist.
Additional studies are necesary to compare the efficacy of this drug to currently available
agents and further define its place in therapy
Adverse Reaction:
Side effects-
Side effects are common app 45%. Discontinuation of therapy due to side effects , however, is only required in about 10% of patients. Gastrointestinal disturbances are the most common (nausea, vomiting,) followed by neurological symptoms such as dizziness, lightheadeness,blurred vision, numbness and tingling
Acecainde has little tendency to cause drug induced lupus-like syndrome which frequently
limits the usefulness of procainamide. The reaction appears to be caused by the parent
compound however a small amount of adminstered acecainide is converted back to
procainamide. Like all antiarrhythmics, acecainde may have a proarrhythmic effect.
Although not systematically studied in humans, reports of acecainide induced torsade
de points have been recorded.
Pharmacology/ Pharmacokinetics:
Pharmacology-
Acecainide (also known as N-acetylprocainamide , NAPA and acetyl procainamide)
ia an antiarrhyhmic agent which was first identified as the major active metabolite
produced by N-acetylation of procainamide(eg.Pronestyl, Procan SR ) . This drug has
distinct electrophysiologic effects which differ from the parent compound.
Acecainide is classified as a Type III (Vaughn-Williams classification) antiarrhythmic
agent along with amiadarone, (Cordarone) and bretylium (eg. Bretylon) because of
its ability to prolong arterial and ventricular action potential durations and refractory
periods. This occurs without significant depression of conduction velocity period and
conduction intervals.
Blood pressure and heart rate may be reduced but this effect is not consistently seen.
There is no significant effect on cardiac output or pulmonary artery wedge pressure .
Several studies have shown that acecainide increases myocardial contractility
Pharmacokinetcis-
Acecainide is well absorbed after oral admin, with bioavailability values ranging from
82% to 100% using capsule and tablet dosage formulations. Peak levels occur within
1 to 3 hours after oral administration. Protein binding averages 10% and is independent
of plasma concentration.
The half-life ranges from 4 to 13 hours in patients with normal renal function to as long
as 42 hours in functionlly anephric patients. Elderly patients show a reduction in acetainde
clearance which may reflect both age-related decrease in renal function and reduced
renal tubular secretion of the drug.
Hemodialysis and continuous arteriovenous hemofiltration enhance clearance
Clinical trials-
The fact that acecainide produces electrophysiologic effects which are distintly different
from procainide requires that the drug be evaluated separatley. A positive response to
procaininde is not necesarily predictive of a positive response to acecainde.
Acecainde has been used to supress premature ventricular complexes (PVCs) and
refractory ventricular arrhythmias. About 50% of patients with at least one PVC/minute
acheived 50% suppression of arrhythmias, 40% acheived 75% suppression at
plasma levels which averaged 22mcg/ml. In the only published long term trial of acecainde
in drug refractory arrhythmias 63% of patients were effectively controlled at 12 months
Animal studies suggest acecainde may be useful in converting artial flutter to sinus rhythm.
Manufacturer Details