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Biomedical subjects

W Kushner

Publications and source records attributed to W Kushner.

9 recordsLinked to original sources
PubMed1984

Torsade de pointes induced by N-acetylprocainamide.

N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide. Initial evaluation with an intravenous infusion of NAPA indicated a favorable antiarrhythmic response. The QTC interval was prolonged, but the 2.4 ms/microgram per ml incremental QTC interval lengthening caused by NAPA was not greater than usual. During subsequent oral therapy with NAPA, torsade de pointes developed at plasma levels of this drug that appeared to be well tolerated during the initial evaluation.

Acecainide↗
PubMed1983

Efficacy and safety of N-acetylprocainamide in long-term treatment of ventricular arrhythmias.

Four patients with chronic ventricular arrhythmias, shown to respond over the short term to N-acetylprocainamide (NAPA), were treated for between 3 and 4 yr with NAPA, and 24-hr ambulatory ECGs were obtained monthly to monitor their responses. When the patients were ambulatory and receiving NAPA, the mean frequency of premature ventricular complexes averaged 70% (range 60% to 82%) below that recorded at 6-mo intervals when the patients were hospitalized and receiving placebo. Analysis of variance showed that NAPA exerted an antiarrhythmic effect in these patients and that tolerance to this effect did not develop with long-term therapy. Plasma NAPA concentrations required to achieve this level of response averaged 21 micrograms/ml (12 to 35 micrograms/ml) and were roughly twice as high as those which appeared to be maximally effective when the patients were hospitalized for their initial evaluation. NAPA therapy was associated with positive antibody titers in only one patient and seems less prone to cause drug-induced lupus erythematosus than procainamide, but NAPA shares the gastrointestinal and other side effects of procainamide.

Acecainide↗
PubMed1979

Long-term antiarrhythmic therapy with N-acetylprocainamide.

The effects of long-term NAPA therapy were evaluated in 6 patients with chronic PVCs known to respond to this drug during a previous placebo-controlled, dose-ranging trial. Underlying cardiac status was evaluated every six months by switching each patient from NAPA to placebo. Placebo period PVC frequency after one year of NAPA therapy was reduced, compared to baseline placebo values. Mean PEP/LVET, measured while the patients received placebo, was elevated at the beginning of the study but was normal after one year of NAPA therapy. Comparison of NAPA and placebo period observations indicated a reduction in PEP/LVET when NAPA therapy was begun. This effect, however, could not be demonstrated one year later when mean placebo period PEP/LVET was normal. The apparent dependence of this effect on underlying status of left ventricular function suggests that the initial reduction in PEP/LVET represents an an indirect effect of NAPA rather than a direct inotropic action. NAPA therapy was well tolerated by the 6 patients and ANA titers became abnormal in only one, in marked contrast to reported experience with procainamide.

Aged↗
PubMed1977

Dose-ranging trial of N-acetylprocainamide in patients with premature ventricular contractions.

Ten patients with chronic premature ventricular contractions (PVCs) received short-term oral therapy with N-acetylprocainamide (NAPA) to determine its antiarrhythmic efficacy and side effects under the conditions of a placebo-controlled, dose-ranging trial. NAPA was effective in suppressing PVCs in 8 patients but caused a paradoxical increase in PVC frequency in one. Results were equivocal in the remaining patient because PVCs did not recur when NAPA therapy was withdrawn. Mean NAPA plasma levels as high as 41.1 microng/ml did not have untoward hypotensive or myocardial depressant effects, as judged by electrocardiographic and systolic time intervals. There was, in fact, a consistent reduction in PEP/LVET ratio, indicating that NAPA increases the force of myocardial contraction. The mean NAPA elimination half-life of 10.9 hr was longer than the 6.2 hr half-life reported for normal subjects, but its prolongation was predictably correlated with reductions in creatinine clearance. Gastrointestinal side effects experienced by 3 patients and insomnia noted by 2 patients are similar to known adverse reactions to procainamide.

Aged↗
PubMedDate not supplied

Kinetic analysis of the vasodilator and ganglionic blocking actions of N-acetylprocainamide.

The hypotensive effects of N-acetylprocainamide (NAPA) were studied in anesthetized dogs and in a normal subject. In dogs, intravenous NAPA infusions reduced mean arterial pressure and the pressor response of the isolated, perfused gracilis muscle vascular bed to preganglionic, but not postganglionic, sympathetic stimulation. The kinetics of these effects were correlated with NAPA pharmacokinetics. The time course of NAPA concentrations in a hypothetical biophase was characterized, and the relationship between NAPA biophase concentrations and the intensity of the effects was determined. From these results, it was estimated that peak effects would occur in dogs 6.6 min after intravenous bolus injection of NAPA, and that biophase NAPA concentration would lower mean arterial pressure 0.39 mm Hg/microgram/ml and would attenuate by 0.224 mm Hg/microgram/ml the gracilis muscle vascular bed pressor response to preganglionic stimulation. In the normal subject, a similar analysis indicated that maximal hypotension would occur 8.0 min after intravenous NAPA injection, and that blood pressure would fall 0.40 mm Hg/microgram/ml relative to biophase NAPA concentrations. These results suggest that blood pressure should be monitored for at least 10 min after patients receive and intravenous NAPA injection, and that repeated NAPA doses probably should not be administered more frequently.

Acecainide↗