Biomedical subjects
Publications and source records attributed to J Wynn.
Upper airway obstruction is a life-threatening emergency requiring prompt evaluation and careful intervention. The pathophysiology of upper airway obstruction is reviewed. Assessment techniques and stabilization are discussed with specific attention to intervention and stabilization prior to transport.
Discussions on the use of thrombolytic therapy include when is the best time for administration, where is the best place for administration, and who is the most appropriate to begin the administration. Rapid triage and intervention for patients with suspected acute myocardial infarction are special challenges in rural communities. To evaluate the possibility of instituting rapid, "golden hour" treatment for the patient with acute myocardial infarction, rural health care resources must be reviewed. Changes in the health care environment and access to emergent care for the patient with acute myocardial infarction directly affect any treatment. Timely interventions depend on available personnel, appropriate clinical protocols, and regional network systems.
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The acute antiarrhythmic properties of pirmenol were studied in 12 patients who failed clinical oral drug therapy with a history of a cardiac arrest or sustained ventricular tachycardia (VT). Programmed electrical stimulation studies were performed in ten men and two women with a mean age of 63 +/- 2 years. All patients had inducible ventricular tachycardia by programmed electrical stimulation when they were off all antiarrhythmic therapy. Patients were then tested on procainamide, 1000 mg, administered intravenously, and ventricular tachycardia could be provoked in nine of twelve patients. Pirmenol was given intravenously, 1.1 mg/kg bolus followed by 40 micrograms/kg/min over 40 minutes prior to drug testing. Pirmenol did not significantly change the baseline heart rate, blood pressure, or measured electrocardiographic values from control values. Ten of 12 patients were still inducible to ventricular tachycardia on pirmenol. Procainamide protected one of nine patients against VT induction. In patients still inducible on drug therapy, the VT rate was significantly slowed from 221 beats/min to 166 beats/min on pirmenol and to 200 beats/min on procainamide. The effects of this new antiarrhythmic agent were similar to procainamide in this drug-resistant study population.
The antiarrhythmic properties of indecainide were studied in 15 patients with a history of a cardiac arrest or ventricular tachycardia. Programmed electrical stimulation studies were performed in nine men and six women with a mean age of 68 +/- 2 years and a mean left ventricular ejection fraction of 41 +/- 4%. All patients had inducible ventricular tachycardia by programmed electrical stimulation while off all antiarrhythmic therapy. Patients were then tested on procainamide, 1000 mg, administered intravenously, and ventricular tachycardia could be provoked in 10 of 15 patients. Indecainide was given intravenously, 1 mg/kg. Indecainide did not significantly change the baseline heart rate, blood pressure, and QTc interval from control values. The PR and QRS intervals were significantly prolonged. Twelve of 15 patients were still inducible for ventricular tachycardia on indecainide. Procainamide protected 5 of 15 patients against ventricular tachycardia induction. In patients still inducible on indecainide therapy, the ventricular tachycardia rate was significantly slowed, from 281 bpm to 224 bpm on indecainide and to 215 bpm on procainamide. The effects of this new class IC antiarrhythmic agent appears similar to procainamide in patients with serious life-threatening tachyarrhythmias.
The antiarrhythmic properties of d-sotalol were studied in 38 patients undergoing electrophysiologic studies. Programmed electrical stimulation studies were performed in 28 men and in 10 women with a mean age of 67 years and a mean ejection fraction of 37 +/- 3%. All patients had inducible ventricular tachycardia while they were off all antiarrhythmic therapy. D-sotalol was given as a 2 mg/kg infusion over 15 minutes and did not significantly change the PR, QRS, or QTc intervals from baseline values in the group as a whole. In the group protected by d-sotalol, the percent change in the QTc interval as well as the percent change in refractoriness was significantly increased as compared to the group not protected. D-sotalol also significantly decreased heart rate. D-sotalol prevented the induction of ventricular tachycardia in 18 of the 38 patients, while significantly slowing the rate of the ventricular tachycardia in the group that could still have tachycardia provoked. Seventeen patients were tested on procainamide and only four were protected, while d-sotalol prevented the induction of ventricular tachycardia in 7 of these 17. Eleven patients were discharged on oral d-sotalol doses ranging from 100 to 400 mg twice daily. One patient died 1 month post discharge due to an acute myocardial infarction, and one patient had a cardiac arrest while on d-sotalol and survived and was switched to amiodarone therapy. The remaining nine patients are alive and well at 14 +/- 3 months. D-sotalol appears to be an effective antiarrhythmic drugs and appears to be well tolerated.
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The antiarrhythmic properties of ethmozine were studied in 27 patients with a history of a cardiac arrest or symptomatic ventricular tachycardia. Programmed electrical stimulation studies were performed in 20 men and seven women with a mean age of 62 years and a mean left ventricular ejection fraction of 43%. All patients had inducible ventricular tachycardia by programmed electrical stimulation while off all antiarrhythmic therapy. Patients were then tested on procainamide if their treatment with this drug orally had not previously failed. Procainamide, 1000 and 1500 mg, was administered intravenously, and ventricular tachycardia could be provoked in 14 of 18 patients. Ethmozine was given in an oral loading regimen starting 24 to 36 hours later. After 500 mg oral ethmozine, patients were given 15 mg/kg ethmozine every 8 hours for seven to nine doses prior to drug testing. Ethmozine did not significantly change the baseline heart rate, blood pressure, and QTc interval from the initial drug-free values. The PR and QRS intervals were significantly prolonged. Seven patients were protected on oral ethmozine; 14 patients still had ventricular tachycardia inducible at programmed electrical stimulation testing, and six patients developed ventricular tachycardia spontaneously on ethmozine and were not tested in the programmed electrical stimulation laboratory. One patient had gastrointestinal complaints and was not discharged on the drug. The five patients who tolerated the oral protocol without side effects and who were protected against programmed stimulation induction of ventricular tachycardia were discharged on oral therapy. One patient on long-term therapy appeared to develop an allergic reaction to the agent with unexplained fevers and was switched to amiodarone therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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Antiarrhythmic properties of N-acetylprocainamide, an active metabolite of procainamide, were studied in 15 patients who presented with a cardiac arrest or documented sustained ventricular tachycardia. Programmed electrical stimulation studies were performed. All patients tested had inducible ventricular tachycardia by programmed electrical stimulation techniques while off all antiarrhythmic therapy. Patients were then tested on procainamide 1000 mg administered intravenously, and ventricular tachycardia could be provoked in 8 of 10 patients. Twenty-four to 36 hours later, N-acetylprocainamide was administered, intravenously, and programmed stimulation was performed after 20 minutes. N-acetylprocainamide did not significantly change heart rate, mean arterial blood pressure, electrocardiographic intervals, A-H or H-V conduction times. N-acetylprocainamide prevented ventricular tachycardia induction in 6 of 15 patients. The mean serum N-acetylprocainamide levels in the group protected was 15.7 +/- 4 micrograms/ml and 16.2 +/- 4 micrograms/ml in the group not protected. These 6 patients were discharged on N-acetylprocainamide 1.5 grams orally every 8 hours. Three patients have been maintained on chronic N-acetylprocainamide every 8 hours. Three patients have been maintained on chronic N-acetylprocainamide therapy (6 +/- 2 months), two patients had breakthrough ventricular tachycardia on follow-up Holter monitoring and alternative therapy was given. N-acetylprocainamide has antiarrhythmic efficacy in preventing induction of ventricular tachycardia by programmed electrical stimulation in a high risk group of patients. On chronic oral therapy, N-acetylprocainamide appears to be well tolerated with antiarrhythmic efficacy that may be enhanced with further upward dose titration.
Antiarrhythmic properties of N-acetylprocainamide (NAPA), an active metabolite of procainamide, were studied in 12 patients with coronary artery disease who presented with cardiac arrest or documented sustained ventricular tachycardia (VT). Programmed electrical stimulation (PES) studies were performed in 10 men and 2 women, aged 52 to 80 years (mean 63), who had a left ventricular ejection fraction of 16 to 69% (mean 33). All patients tested had inducible VT provoked by PES without antiarrhythmic therapy. Patients were then tested with procainamide, 1,000 mg administered intravenously. VT could be provoked after procainamide treatment in 8 of 10 patients. Twenty-four to 36 hours later NAPA was administered, 18 mg/kg body weight intravenously, and PES was performed after 20 minutes. NAPA did not significantly change heart rate, mean arterial blood pressure, electrocardiographic intervals and AH or HV conduction times. The QT interval lengthened, but not significantly. The mean serum NAPA levels were 15.7 +/- 4 micrograms/ml in the group protected by NAPA and 16.2 +/- 4 micrograms/ml in the group not protected by NAPA. Five patients were discharged with NAPA therapy, 1.5 g orally every 8 hours. Two patients have been maintained with chronic NAPA therapy (10 +/- 3 months), and 2 patients had breakthrough VT on follow-up Holter monitoring and alternative therapy was given. One patient died while taking oral therapy. NAPA demonstrates antiarrhythmic efficacy in preventing induction of VT by PES in a high-risk group of patients. During chronic oral therapy in some patients, NAPA appears to be well tolerated, with antiarrhythmic efficacy that may be enhanced with further upward dose titration.
Reports of low pericardial-fluid complement levels in systemic lupus erythematosus and rheumatoid arthritis have been difficult to interpret, as few data are available to describe complement concentrations in patients without pericardial disease. The authors therefore determined normal values under standardized conditions of collection, storage, and assay. The normal ranges for pericardial-fluid C3, C4, and total hemolytic complement were 35-127 mg/dl, 6.3-23 mg/dl, and 1.9-9.1 CH50 units, respectively. Storage at -20 C resulted in a 50% reduction in values. Hence, storage at -70 C is recommended. As the level of pericardial-fluid total hemolytic complement is normally low, caution is needed in interpreting its apparent reduction in various immunologic diseases.
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The observation that thyroxine stimulated in vitro protein synthesis in the absence of mitochondria (Carter, W.J., Faas, F.H., and Wynn, J (1971) J. Biol. Chem. 246, 4973-4977) has been disputed on the basis that radioactivity incorporated into protein did not represent peptide synthesis but incorporation of labeled contaminants present in the L-(U-14C) valine precursor (Sokoloff, L., and Roberts, P.A. (1972 Fed. Proc. 31, 1525). The question of mitochondrial requirement is important in determining whether thyroxine has a direct action on the polysome or causes the release of stimulatory factors from mitochondria. In this paper, thyroxine stimulation of peptide synthesis in mitochondria-free systems has been confirmed. Peptide synthesis is required for the thyroxine effect since it is dependent on the presence of polysomes and an energy source in the reaction mixture and is abolished by puromycin. The thyroxine effect is not due to incorporation of labeled contaminants since hydrolysis of labeled protein recovered from control and thyroxine-treated reaction mixtures yields the labeled amino acid precursor as the only radioactive product. Thyroxine stimulates polyuridylic acid-directed polyphenylalanine synthesis, providing further evidence that thyroxine is stimulating peptide synthesis rather than incorporation of radioactive contaminants by mechanisms other than peptide synthesis. Although thyroxine stimulates polyphenylalanine synthesis, it does not influence polyuridylic acid hydrolysis measured in the same reaction. Therefore, thyroxine stimulation of peptide synthesis is not due to prevention of hydrolysis of nucleic acid components of the reaction mixture. Thyroxine does not influence the size or specific activity of the free valine pool in the reaction mixture, indicating that observed increases in valine incorporation reflect increased peptide synthesis rather than increased specific activity of the valine precursor. The fact that thyroxine stimulates peptide synthesis using (14C)aminoacyl-tRNA precursors strengthens this conclusion. Therefore, thyroxine stimulation of protein labeling is dependent on the presence of peptide synthesis and cannot be explained by incorporation of labeled contaminants, prevention of RNA hydrolysis, or change in the specific activity of the amino acid precursor. Thyroxine causes a genuine increase in peptide synthesis by a direct action at the polysomal level.