Biomedical subjects

D Keefe

Publications and source records attributed to D Keefe.

49 records · Page 3Linked to original sources

PubMed1985

Long-term lorcainide therapy in patients with ventricular tachycardia.

One hundred patients inducible at electrophysiologic studies underwent serial drug testing with procainamide, lidocaine, and lorcainide to determine comparative efficacy. Acute intravenous administration was followed by repeat programmed electrical stimulation (PES) studies on separate days for each antiarrhythmic drug. Lorcainide prevented ventricular tachycardia (VT) induction in 69% of the 100 patients studied, procainamide was effective in 50% of the 75 patients studied, and lidocaine prevented VT induction in 30% of 53 patients. Following PES and serial drug testing, 46 patients were started on lorcainide, nine patients on procainamide, and 45 patients were started on other antiarrhythmic drug regimens. Seventy percent of the patients have remained on lorcainide therapy, while 47% have continued on other drug therapies started over a 20.5 +/- 3.2-month mean follow-up period. Despite sleep-wake disturbances and a need for sedation at night, lorcainide therapy was tolerated well in this population and remained an effective antiarrhythmic with prolonged administration.

Benzeneacetamides↗

PubMed1985

Digitalis: its place in therapy.

Since the initial introduction of digitalis 200 years ago by Withering, its low therapeutic ratio has limited the use of this agent. The utility of digitalis in patients with congestive heart failure and a recent myocardial infarction has been questioned recently. Findings of rigorously controlled clinical studies suggest a small but definite hemodynamic and clinical improvement in patients administered digitalis. Congestive heart failure can be effectively treated without cardiac glycosides. However, when used judiciously, digitalis provides an additional agent in our therapeutic armamentarium. The inotropic, dormotropic, and vagomimetic properties are uniquely suited for the patient with supraventricular arrhythmias and compromised left ventricular function.

Digitalis Glycosides↗

PubMed1984

Lorcainide therapy for the high-risk patient post myocardial infarction.

Nonsustained ventricular tachycardia (VT) in the late period (7 to 21 days) after myocardial infarction (MI) is reported to be a predictor of sudden death. Patients with 3-beat VT on Holter monitoring in the late infarction period would be suspected to demonstrate electrical instability on electrophysiologic studies. Forty-seven patients were identified as having at least 3-beat VT on Holter monitoring. Eighteen patients refused electrophysiologic studies or were not referred. Eight patients died; 3 were sudden deaths in 13 +/- 5 months, a 17% incidence. Twenty-nine patients underwent invasive electrophysiologic studies and 28 had inducible VT, 18 sustained and 10 nonsustained. Lorcainide prevented VT induction in 21 of the 28 patients, whereas 12 of the 22 patients studied on procainamide were protected. Lidocaine, tested in 21 patients, prevented VT induction in only 5. Lorcainide and procainamide prolonged refractoriness in those patients protected at programmed electrical stimulation (PES), whereas the QT interval was prolonged in patients in whom VT could still be induced. Twenty-seven of the 28 patients were placed on drugs predicted to be effective by PES studies, 19 on lorcainide. After a mean follow-up of 12.5 +/- 4 months the patient with noninducible arrhythmia is alive and 26 of the 28 patients with inducible arrhythmia are alive and well. Two patients died, 1 of stroke and 1 of pump failure after a second MI. No sudden deaths were observed in this group. Two patients had breakthrough arrhythmias and were treated by alternative antiarrhythmic therapy that was also effective on initial electrophysiologic studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1984

Evaluation of lorcainide in patients with symptomatic ventricular tachycardia.

One hundred patients with inducible ventricular tachycardia (VT) on electrophysiologic studies underwent serial drug testing with procainamide, lidocaine and lorcainide to determine comparative efficacy. Acute intravenous administration was followed by repeat programmed electrical stimulation (PES) studies on separate days for each antiarrhythmic agent. Lorcainide prevented VT induction in 69% of the 100 patients studied, procainamide in 50% of the 75 patients studied and lidocaine in 30% of 53 patients. After PES and serial drug testing, 46 patients were started on lorcainide, 9 on procainamide and 45 on other antiarrhythmic drug regimens. Eighty percent of the patients have remained on lorcainide therapy, whereas 47% have continued on other drug therapies started over 17.5-month mean follow-up period. Despite sleep-wake disturbances and a need for sedation at night, lorcainide therapy was well tolerated in this population and remained an effective antiarrhythmic agent with prolonged administration.

Anti-Arrhythmia Agents↗

PubMed1983

Evidence for neurotransmitter plasticity in vivo: developmental changes in properties of cholinergic sympathetic neurons.

We have examined the cholinergic sympathetic innervation of sweat glands in footpads of adult and developing rats. Acetylcholinesterase staining reveals a plexus of heavily stained fibers in the sweat glands of adult rats. Reaction product appears among and around bundles of axons that lie at a considerable distance from the cells of the secretory tubule. Each bundle contains 8-12 axons that possess numerous varicosities and contain small clear and large dense core vesicles. The glands of the hindpaws and their innervation develop during the first three weeks after birth. Catecholamine-containing axons were associated with the forming glands. At 7 and 10 days, intensely fluorescent fibers surrounded the tubules, and all of the axon profiles associated with the glands contained small granular vesicles (SGV) after permanganate fixation to reveal vesicular stores of norepinephrine. At 14 days the sweat gland plexus was less intensely fluorescent than at earlier ages and relatively few SGV were present. By 21 days, no endogenous catecholamine fluorescence and no SGV were detectable. However, following exposure to exogenous catecholamine, fluorescent fibers were present in the sweat glands of mature rats and they corresponded in position and density to the plexus localized with acetylcholinesterase staining. Catecholamine uptake was blocked by incubation in the cold and by desmethylimipramine and was not observed in cholinergic parasympathetic fibers in the iris or salivary glands. After intraperitoneal administration of 5-hydroxydopamine and permanganate fixation, all the axons in the sweat glands contained a few SGV. Thus, the developing sweat glands appear to be innervated by noradrenergic axons that lose their stores of endogenous catecholamines but not their capacity for uptake and storage as they elaborate an axonal plexus in the maturing glands. These observations support the hypothesis that cholinergic sympathetic neurons appear to undergo a transition from noradrenergic to cholinergic function during development in vivo similar to that previously described in cell culture.

Acetylcholinesterase↗

PubMed1982