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Biomedical subjects

J L Anderson

Publications and source records attributed to J L Anderson.

At least 217 records · Page 12Linked to original sources
PubMed1989

Evidence for regulation of sodium transport from airspace to vascular space by cAMP.

Evidence has been accumulating that regulation of the rate of solute and fluid removal from the alveolar spaces may play an important role in the prevention and/or resolution of alveolar pulmonary edema. In this study, the isolated perfused rat lung was used to investigate the effects of an adenosine 3',5'-cyclic monophosphate (cAMP) analogue or a phosphodiesterase inhibitor on active sodium transport from airspace to vascular space. Three tracers were instilled into the airways of isolated Krebs-Ringer bicarbonate solution (KRB)-perfused rat lungs. The appearance of tracers in the single-pass perfusate was measured, and the apparent permeability-surface area products (PS) were calculated for each tracer at each sample time based on Fick's first law of diffusion. After steady-state PS values had been reached, a cAMP analogue or phosphodiesterase inhibitor was added to the perfusate. Both agents caused significant increases in the PS for 22Na. In another group of experiments, a cAMP analogue was added to the perfusate, followed by the subsequent addition of a sodium transport inhibitor and the resultant large decrease in the PS for 22Na. These data are consistent with the regulation of active sodium transport across the intact mammalian alveolar epithelium by a cAMP-mediated process leading to removal of sodium from the alveolar spaces, with anions and water following passively.

Animals↗
PubMed1989

Relation of baseline characteristics to suppression of ventricular arrhythmias during placebo and active antiarrhythmic therapy in patients after myocardial infarction.

In the Cardiac Arrhythmia Pilot Study (CAPS), patients early (6-60 days) after acute myocardial infarction (MI) with ventricular premature complexes (VPCs) of over 10 per hour were randomized to receive, unaware, therapy with one of four antiarrhythmic drugs (n = 402) or placebo (n = 100). Treatment success was defined as 70% or more decrease in VPC rate and 90% or more decrease in VPC runs. If the first active drug was ineffective, a second drug was given. If placebo was ineffective, a second placebo was given. To determine whether or not baseline clinical characteristics predict the response to antiarrhythmic therapy, 10 baseline variables were selected for investigation: age, prior MI, time from CAPS MI to randomization, ejection fraction, baseline VPC frequency, presence of runs (greater than or equal to 3 consecutive VPCs, greater than or equal to 100 beats/min), beta-blocker therapy, digitalis therapy, MI transmurality, and MI location. At the end of the first drug treatment, apparent treatment success in patients receiving placebo was associated on univariate analysis with absence of prior MI, with trends for younger age and Q wave MI, whereas in patients receiving active therapies, higher ejection fraction and younger age were associated with better suppression. In the encainide and flecainide treatments, where the greatest response was observed, absence of prior MI, higher ejection fraction, and younger age were associated with more successful treatment. In a multivariate analysis with these variables, ejection fraction and age remained significant for all active therapies, absence of prior MI and ejection fraction remained significant in the encainide and flecainide treatments, and absence of prior MI in the placebo treatment. Few variables except ejection fraction were associated with VPC suppression during the 1-year follow-up, and only lower ejection fraction and older age related to loss of long-term suppression. Thus, there are only a few independent baseline clinical variables (notably, ejection fraction) that substantially affect antiarrhythmic drug efficacy in suppressing VPCs in patients early after MI. Some variables, however, may be associated with spontaneous arrhythmia variability, leading to an apparent (placebo) response. These findings will be helpful in designing and interpreting treatment studies in patients after MI.

Anilides↗
PubMed1989

Prevention of symptomatic recurrences of paroxysmal atrial fibrillation in patients initially tolerating antiarrhythmic therapy. A multicenter, double-blind, crossover study of flecainide and placebo with transtelephonic monitoring. Flecainide Supraventricular Tachycardia Study Group.

Paroxysmal atrial fibrillation (PAF) is a problematic clinical arrhythmia that is usually symptomatic. Unfortunately, few adequate trials and trial methods are available for assessment of the value of therapy, and traditional treatment has often been ineffective or associated with unacceptable side effects. Transtelephonic monitoring is a new method that allows evaluation of paroxysmal arrhythmias and arrhythmia-related symptoms in outpatients. We used a patient-initiated transtelephonic monitor system to evaluate the potential of flecainide, a class 1C antiarrhythmic, in prevention of symptomatic recurrences of PAF. Sixty-four patients qualified for the study (two or more PAF attacks documented within a 4-week baseline period) and entered a dose-finding phase to determine drug tolerance. Dose was incremented at weekly intervals from 200-300 and finally to 400 mg/day. The largest dose that was well tolerated was selected for the 4-month, double-blind, randomized, crossover comparison with placebo. Fifty-five patients entered and 53 received both treatments in the double-blind phase; 48 of these patients without protocol violations were evaluable for efficacy comparisons. Evaluable patients had undergone an average of 3.8 previous drug trials (range, 1-8); 30 were men, 18 had hypertension, and 14 had ischemic heart disease. The study demonstrated a highly significant correlation (p less than 0.0001) between perceived symptoms and documented PAF by transtelephonic monitoring. The rate of symptoms and PAF attacks was also significantly reduced by therapy (median dose, 300 mg/day). The first PAF attack occurred after a median of 3 days on placebo versus 14.5 days on flecainide (p less than 0.001) therapy. Similarly, the time interval between attacks was lengthened, from a median of 6.2 days on placebo to 27.0 days on flecainide (p less than 0.001) therapy. PAF was prevented in 15 patients (31%) during flecainide and four (9%) during placebo therapy (p = 0.013). However, during the study, 13 patients dropped out, seven because of adverse effects (five cardiac), five for other reasons, and one because of cardiac arrest/death. Adverse cardiac events occurred in a total of seven patients (11%) during flecainide therapy. Thus, transtelephonic monitoring is a useful method for documentation of the occurrence of paroxysmal arrhythmias such as PAF and its related symptoms during daily living and for assessment of new therapies in an outpatient setting.

Atrial Fibrillation↗
PubMed1989

The nurse's role in cancer rehabilitation. Review of the literature.

Rehabilitative nursing is an integral part of all phases of patient-centered care. The role of the nurse in addressing rehabilitation issues for cancer patients is one of teaching, counseling, and coordination. Nurses have made significant contributions to educational programs available to cancer patients and their families. The program structure, content, and setting are as varied as the potential patient. Site-specific support programs, as well as programs that identify and support positive coping behaviors, have been developed by nurses. In their efforts to maximize resource allocation in a variety of settings, nurses have developed roles and programs that promote the process of rehabilitation. This review of nursing literature provides a source for nurses wishing to continue designing programs that enhance rehabilitation.

Adaptation, Psychological↗
PubMed1988

Dependence of assessment of coronary artery reperfusion during acute myocardial infarction on angiographic criteria and interobserver variability.

The angiographic films of 240 patients with acute myocardial infarction were studied in a randomized trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) versus intracoronary streptokinase therapies. The interobserver variability of grading coronary artery perfusion by the Thrombolysis in Myocardial Infarction Study Group (TIMI) criteria was measured as well as the effect of different definitions of reperfusion on the determination of reperfusion rate. There was good agreement in the reading of infarct artery flow grades between 2 blinded observers for each grade considered separately (k = 0.726 +/- 0.014) and for grades 0 or 1 (no perfusion) versus grades 2 or 3 (perfusion) (k = 0.905 +/- 0.011). Discordance between grades 0 or 1 versus 2 or 3 occurred in 74 (5%) of the 1,615 angiographic readings. Discrepancies of clinical significance which affected qualification for study entry, reperfusion or reocclusion status occurred in only 15 patients (6%). Grade 1 flow was found to have the most variable interpretation. Reperfusion rates for APSAC and streptokinase differed significantly when reperfusion was defined by 3 different criteria. The reperfusion rate ranged from 51 to 72% for APSAC and from 60 to 75% for streptokinase depending upon criteria selected. For comparison of the results of different thrombolytic studies, a standard semiquantitative system for grading infarct artery perfusion should be used, readings should be blinded and the criteria used for the definition of reperfusion should be clearly specified.

Aged↗
PubMed1988

Summary of efficacy and safety of flecainide for supraventricular arrhythmias.

This report provides an overview of the safety and efficacy of flecainide for supraventricular tachyarrhythmias (SVT) based on a review of the world literature. This review provided 107 entries, but 5 were review articles and 22 were articles not translated into English. The remaining 80 articles or published abstracts form the basis for this report. A total of 1,371 courses of therapy with intravenous or oral flecainide, or both, were represented. Efficacy was defined by each investigator. Intravenous flecainide was successful in terminating ongoing tachycardias in 81% of reported cases of atrioventricular (AV) nodal reentrant tachycardias, 88% of AV reentrant tachycardias and 100% of atrial tachycardias. Atrial fibrillation or flutter was terminated by intravenous flecainide in 62% of cases and arrhythmias associated with Wolff-Parkinson-White syndrome in 73%. Oral flecainide was successful in longer-term management of arrhythmia in 74 and 81% of patients with AV nodal and AV reentrant tachycardia, respectively, and in 83% with atrial tachycardia. Atrial flutter or fibrillation responded to oral drug in 61% of cases and arrhythmias related to Wolff-Parkinson-White syndrome in 61%. Adverse experiences were reported in studies totaling 695 patients (designated "at-risk patients"). They were not commented on in studies with the remaining 594 patients. Overall, a total of 6.9% of at-risk patients (3.7% of total patients) reported cardiac adverse experiences; 19% of at-risk patients (10% of total patients) reported at least 1 noncardiac adverse effect. Cardiac adverse events included worsened arrhythmias in 28, conduction disturbances in 15 and congestive heart failure in 5. The most frequent noncardiac adverse experiences were paresthesia and visual disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1988

Treatment of cardiac myopathies with beta blockers. What do we know, where do we go from here?

The increase in sympathetic nervous system activity noted in heart failure of several etiologies has beneficial effects in the short term; in the long term, though, it may be detrimental. This provides a rationale for use of beta-blocker therapy in patients with cardiac myopathies of various etiologies. Postinfarction trials in patients with ischemic heart disease have suggested that beta blockade provides a substantial mortality benefit, and beta blockers are accepted as first-line therapy for hypertrophic cardiomyopathy. The use of beta-blocking drugs for dilated cardiomyopathy (DCM), however, is currently investigational. Early trials reporting benefits in functional class, exercise capacity, and myocardial function stimulated further interest in this application of beta blockade. Recent studies comparing metoprolol with placebo or standard treatment have shown promising improvements in functional class and exercise capacity. The patients who will benefit most from beta-blocker therapy in DCM may be those with a high resting heart rate and a short duration of symptoms and, perhaps, feminine gender. Marked structural abnormality on cardiac biopsy (eg, fibrosis) may suggest a poor response to treatment. A multicenter controlled study of metoprolol in dilated cardiomyopathy is in progress. If the outcome is favorable, beta-blocker therapy in DCM may become an accepted, rather than an experimental, treatment.

Adrenergic beta-Antagonists↗
PubMed1988

Worsening of ventricular tachycardia by amiodarone.

The details of worsening of ventricular tachycardia in 8 (4.1%) of 194 patients receiving treatment with amiodarone are reported. Two forms of amiodarone-induced tachycardia were recognized: first, the development of new tachycardias (three patients) and second, a change in the pattern of recurrence of clinical tachycardia (five patients). In retrospect, the time from the initiation of amiodarone to the initial documentation of worsening ranged from 1 to 23 days (mean +/- SD, 9.4 +/- 8.2 days) and the time from the initiation of therapy to the recognition of worsening ranged from 6 to 26 days (14.6 +/- 10.1 days). Seven patients survived the worsening of tachycardia and one died. The total dose of amiodarone received and the duration of administration did not correlate with time to manifestation or time to resolution of worsening. This report emphasizes that worsening of ventricular tachycardia as a result of amiodarone is often difficult to differentiate from inadequate drug loading or early recurrence of 2 patient's clinical tachycardia. Further, because of the pharmacokinetics of the drug, the manifestations of worsening may be prolonged. In the cases reported, it ranged from 2 to 26 days (7.9 +/- 8.3 days), which is longer than previously reported. Because of the potential for amiodarone to cause life-threatening worsening of ventricular tachycardia and in accordance with current results, a period of in-hospital monitoring of at least 10 days at the start of therapy with amiodarone is recommended.

Aged↗
PubMed1988

Effect of reperfusion on electrocardiographic and enzymatic infarct size: results of a randomized multicenter study of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) versus intracoronary streptokinase in acute myocardial infarction.

The effect of early coronary artery reperfusion on ECG and enzymatic parameters was examined in 240 patients with acute myocardial infarction. These patients had participated in a randomized trial comparing intravenous anisoylated plasminogen streptokinase activator complex (APSAC) (n = 123) and intracoronary streptokinase (n = 117) therapy. Reperfusion occurred in 59 of 115 (51%) patients receiving APSAC and 67 of 111 (60%) patients receiving streptokinase (p = NS). There was greater early resolution of ST segment elevation in the reperfused than in the nonreperfused patients (p less than or equal to 0.003) and more rapid Q wave evolution (p less than or equal to 0.03). Sigma Q was lower in reperfused than in nonreperfused patients at 8 hours (1.41 +/- 1.18 versus 2.11 +/- 2.10 mV; p less than or equal to 0.05) and at 24 hours (1.43 +/- 1.25 mV versus 2.08 +/- 1.88 mV; p less than or equal to 0.02). Time to peak level was shorter in the reperfused patients for creatine kinase (CK) (10.7 +/- 5.5 hours versus 14.9 +/- 5.9 hours; p less than 0.0001) and lactic acid dehydrogenase (LDH) (29.6 +/- 13.6 hours versus 34.4 +/- 10.5 hours; less than or equal to 0.03) enzymes. Peak LDH-1 was lower in the reperfused group (274 +/- 149 U/L versus 341 +/- 173 U/L; p less than or equal to 0.04). Reperfusion at a mean of 3.9 hours after the onset of infarction was associated with more rapid resolution of ST segment elevation, faster Q wave evolution, smaller ECG infarct size, earlier cardiac enzyme release, and smaller enzymatic infarct size than later or no reperfusion.

Anistreplase↗
PubMed1988

Protective effect of dietary brussels sprouts against mammary carcinogenesis in Sprague-Dawley rats.

The effect of dietary brussels sprouts (Brassica oleracea, L.) on mammary carcinogenesis induced by 7,12-dimethylbenz[a]anthracene (DMBA) was studied in Sprague-Dawley female rats. Rats fed a 20% brussels sprouts diet only during the initiation period of carcinogenesis had a palpable mammary tumor incidence of 13%, while those fed a casein-cornstarch semi-purified diet during this initiation period had a tumor incidence of 77% after 15 weeks post DMBA dose. When the rats were switched from the semi-purified diet to the 20% brussels sprouts diet at this time, there appeared to be a regression of small mammary tumors after 6 weeks on this dietary treatment. This regression was transitory since during the final 10 weeks of this 1 year study, 100% of this group of rats developed tumors. The rats fed the 20% brussels sprouts diet during tumor initiation exhibited a 67% incidence of fibroadenomas. The rats fed the semi-purified diet during initiation, but switched later to the brussels sprouts diet, showed over a 90% incidence of adenocarcinomas.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Multicenter reperfusion trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: controlled comparison with intracoronary streptokinase.

The recent establishment of a firm therapeutic role for reperfusion in acute myocardial infarction has stimulated interest in the development of more ideal thrombolytic agents. Anisoylated plasminogen streptokinase activator complex (APSAC) is a new plasminogen activator possessing properties that are promising for intravenous thrombolytic application in acute myocardial infarction. To assess the reperfusion potential of intravenous APSAC, a multi-center, angiographically controlled reperfusion trial was performed. An approved thrombolytic regimen of intracoronary streptokinase served as a control. Consenting patients with clinical and electrocardiographic signs of acute myocardial infarction were studied angiographically and 240 qualifying patients with documented coronary occlusion (flow grade 0 or 1) were randomized to treatment in less than 6 h of symptom onset (mean 3.4 h, range 0.4 to 6.0) with either intravenous APSAC (30 U in 2 to 4 min) or intracoronary streptokinase (160,000 U over 60 min). Both groups also received heparin for greater than or equal to 24 h. Reperfusion was evaluated angiographically over 90 min and success was defined as advancement of grade 0 or 1 to grade 2 or 3 flow. Rates of reperfusion for the two treatment regimens were 51% (59 of 115) at 90 min after intravenous APSAC and 60% (67 of 111) after 60 min of intracoronary streptokinase (p less than or equal to 0.18). Reperfusion at any time within the 90 min was observed in 55 and 64%, respectively (p less than or equal to 0.16). Time to reperfusion occurred at 43 +/- 23 min after intravenous and 31 +/- 17 min after intracoronary therapy. The success of intravenous therapy was dependent on the time to treatment: 60% of APSAC patients treated within 4 h exhibited reperfusion compared with 33% of those treated after 4 h (p less than or equal to 0.01). Reperfusion rates were also dependent on initial flow grade (p less than or equal to 0.0001): 48% (81 of 168) for grade 0 (APSAC = 43%, streptokinase = 54%), but 78% for grade 1 (APSAC = 78%, streptokinase = 77%). APSAC given as a rapid injection was generally well tolerated, although the median change in blood pressure at 2 to 4 min was greater after APSAC than after streptokinase (-10 versus -5 mm Hg). Mean plasma fibrogen levels fell more at 90 min after the sixfold higher dose of APSAC than after streptokinase (to 32 versus 64% of control). Reported bleeding events were more frequent after APSAC but occurred primarily at the site of catheter insertion and no event was intracranial.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Vancomycin pharmacokinetics, renal handling, and nonrenal clearances in normal human subjects.

The renal handling of vancomycin is unknown. Previously reported studies have not achieved steady-state conditions with constant vancomycin concentrations. We measured systemic vancomycin clearance simultaneously with the renal clearances of vancomycin, creatinine, inulin, and para-aminohippurate in nine healthy subjects at steady-state serum vancomycin concentrations of 7 and 14 mg/L. For all steady-state observations the renal clearance of vancomycin was 89 +/- 11 ml/min (mean +/- SE), the clearance of inulin 105 +/- 9 ml/min, the clearance of creatinine 117 +/- 9 ml/min, and the clearance of para-aminohippuric acid 496 +/- 41 ml/min. The systemic clearance of vancomycin was 131 +/- 7 ml/min. The clearances of creatinine, inulin, and para-aminohippuric acid and the renal clearance of vancomycin were not statistically different at both steady-state vancomycin concentrations. The ratio of the renal clearance of vancomycin to the clearance of inulin was 0.89 +/- 0.06 and to creatinine clearance 0.79 +/- 0.05. Both ratios were independent of vancomycin concentration, urine flow rate, and filtration fraction. The systemic clearance of vancomycin was 10% greater at serum vancomycin concentrations of 14 mg/L than at 7 mg/L (p less than 0.05) because of an increase in the nonrenal clearance. Therefore in healthy subjects, 30% of the systemic vancomycin clearance is by nonrenal mechanisms and this nonrenal clearance is concentration dependent. Assuming protein binding to be between 10% and 20%, renal vancomycin excretion is predominantly by glomerular filtration. Small amounts of tubular vancomycin transport cannot be excluded by these techniques.

Adult↗
PubMed1988

An analysis of commitments made by student clinicians in speech-language pathology and audiology.

This study identified and classified commitments made by student clinicians in speech-language pathology and audiology supervisory conferences and provides a methodology for documenting change in supervisees' behavior as a result of supervisory interaction. Five different types of commitments were isolated and served as the basis of the Commitment Classification System. They included clinical procedures, clinical process administration, supervisory procedures, supervisory process administration, and academic information/teaching function. The independent variables were condition (written agreement or no written agreement between supervisee and supervisor), order of conditions, experience level of supervisee, week number within each condition, and type of commitments. Frequency data were collected for 6 consecutive weeks. The resulting 1,389 commitments made by 64 student clinicians in 384 individual conferences at 12 universities were analyzed within a multiple analysis of variance. Significant findings (p less than .05) indicated that the greatest number of commitments made involved planning, analysis, and evaluation of the clinical process with particular attention on client behavior; and the number of commitments made was a function of written accountability and order of conditions.

Audiology↗
PubMed1988

The new antiarrhythmic drugs. How to put them to the best use.

Treatment of cardiac arrhythmia should be specifically aimed at symptom control or reduction in the risk of sudden cardiac death. Until recently, a limited number of antiarrhythmic drugs were available to the practicing physician, but during the last four years, seven new ones were approved. However, these drugs are complex and have different mechanisms of action and potential for adverse effects, so the safety of therapy with them continues to be debated. Although there is little doubt that many of the new drugs (particularly flecainide [Tambocor] and encainide [Enkaid]) are highly effective in suppressing ventricular premature complexes, they should be used with caution, since they also carry a potential for worsening arrhythmia (proarrhythmic effect) and congestive heart failure. Since suppression of arrhythmia has not yet been proven to reduce mortality, care must be taken in evaluating the risk-benefit ratio when prescribing therapy, particularly for patients with less malignant arrhythmias. Careful evaluation of the effects of treatment in individual patients is indicated whenever antiarrhythmic drugs are used. Until important mortality trials have been completed (eg, the Cardiac Arrhythmia Suppression Trial), therapy should be conservative and reserved for patients with severely symptomatic or malignant arrhythmias.

Anti-Arrhythmia Agents↗
PubMed1988

Changes in spontaneous variability of ventricular ectopic activity as a function of time in patients with chronic arrhythmias.

Previous determinations of spontaneous variability in ventricular arrhythmia have often been based on measurements from consecutive days in small patient populations, whereas clinical determinations of drug efficacy typically compare measurements at intervals of 1 week and longer to baseline. We, therefore, sought to determine whether spontaneous arrhythmia variability changes as a function of time during periods ranging from 1 day to 1 year or longer. The percent reduction in the frequency of total premature ventricular complexes (PVCs) and repetitive ventricular beats required to show true drug effect rather than spontaneous variability in PVCs was determined in 47 consecutive patients with chronic ventricular arrhythmias who underwent multiple ambulatory monitor recordings while off active drug treatment (during placebo therapy). The variability in PVC rate was determined during the intervals of 1 day, 1 week, 2 weeks, 3 weeks, 4 weeks, and 1 year or longer. The percent reductions in total PVCs required to exceed the 95% confidence limits of spontaneous variability at these intervals were 55%, 85%, 86%, 93%, 96%, and 96%, respectively. Corresponding values for repetitive beats were 75%, 95%, 92%, 95%, 94%, and 98%, respectively. The percent increase in total PVCs and repetitive beats required to establish "arrhythmia aggravation" caused by an antiarrhythmic drug with a 95% confidence limit also was calculated for this study population and was 124% and 303%, respectively, at 1-day intervals and 2,269% and 4,091%, respectively, at 1-year (or longer) intervals for the 24-hour monitor recordings. Variability was not substantially affected by underlying heart disease or ejection fraction. PVC rate showed a modest negative correlation with variability (r = 0.3). Thus, variability is substantially greater at 1 week, the usual time for clinical assessment of antiarrhythmic drug efficacy, than at 1 day (p less than 0.01). Suppression of more than 85% of total PVCs and more than 95% of repetitive beats appears to be necessary after 1-2 weeks to be confident of a true drug effect. Even greater variability is observed after 1 month and up to 1 year so that reductions of up to 95% in total PVCs and 98% in repetitive beats may represent spontaneous change.(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Arrhythmia Agents↗