PubMed Health⌕ Search

Biomedical subjects

N Gustafson

Publications and source records attributed to N Gustafson.

14 recordsLinked to original sources
PubMed2000

Randomized trial of paclitaxel plus supportive care versus supportive care for patients with advanced non-small-cell lung cancer.

BACKGROUND: In phase II trials, paclitaxel has been shown to have antitumor activity in patients with advanced non-small-cell lung cancer (NSCLC). However, the survival and quality-of-life (QOL) benefits of paclitaxel used as a single agent compared with supportive care alone have not been assessed in a randomized clinical trial. METHODS: A total of 157 patients with stage IIIB or IV NSCLC who had received no prior chemotherapy were randomly assigned to receive either best supportive care alone (78 patients) or paclitaxel plus supportive care (79 patients). Paclitaxel was administered as a 3-hour intravenous infusion every 3 weeks. Supportive care included palliative radiotherapy and supportive therapy with corticosteroids, antibiotics, analgesics, antiemetics, transfusions, and other symptomatic therapy as required. The primary end point of the study was survival. Time to disease progression, response rate, adverse events, and QOL were secondary end points. RESULTS: Pretreatment characteristics were evenly distributed between the two arms. Survival was statistically significantly better in the paclitaxel plus supportive care arm than in the supportive care alone arm (two-sided P =.037) (median survival = 6.8 months versus 4.8 months). Cox multivariate analysis showed paclitaxel plus supportive care to be statistically significantly associated with improved survival (two-sided P =.048). QOL was similar for both treatment arms, except for the functional activity score of the Rotterdam Symptom Checklist, where QOL data statistically significantly favored the paclitaxel plus supportive care arm (two-sided P =.043). CONCLUSION: The addition of paclitaxel to best supportive care significantly improved survival and time to disease progression compared with best supportive care in patients with advanced NSCLC and may improve some aspects of QOL.

Adult↗
PubMed2000

Impact of dietary fat and fiber intake on nutrient intake of adolescents.

OBJECTIVE: To evaluate the impact of fat and fiber intake on energy and nutrient intake of 15-year-old adolescents. STUDY DESIGN: Twenty-four-hour dietary recalls were collected on a random sample of 15-year-olds. Subjects were then categorized into groups based on fat and fiber intake, with 319 students meeting criteria for 1 of 4 dietary intake quadrants: low fat, low fiber; low fat, high fiber; high fat, low fiber; and high fat, high fiber. Students with medium fat or fiber intakes were excluded from the study. Low-fat and high-fat intake were defined as <30% and >40% of total energy intake, respectively. Low- and high-fiber intake were defined as <15 g/day and >20 g/day, respectively. RESULTS: Low-fat and high-fiber intake had a minimal impact on energy intake and did not adversely affect nutrient intake. High-fiber intake was associated with greater likelihood of adequate intake of vitamins A, B6, B12, and C; niacin; thiamin; riboflavin; folacin; magnesium; iron; zinc; phosphorus; and calcium. High-fat intake was associated with greater likelihood of adequate vitamin B12 intake. Significant differences in fat and fiber intake distributions were found for ethnic background and gender, with more non-white than white students in the high-fat groups and more males than females in the high-fiber groups. CONCLUSIONS: A low-fat and high-fiber diet meeting current nutrition recommendations does not adversely affect energy or nutrient intake, increases nutrient density of the diet, and increases the likelihood of adequate intake for several key nutrients.

Adolescent↗
PubMed1994

Recombinant human superoxide dismutase (h-SOD) fails to improve recovery of ventricular function in patients undergoing coronary angioplasty for acute myocardial infarction.

BACKGROUND: Animal studies have demonstrated a burst of oxygen free radical generation after reperfusion of ischemic myocardium that could be blocked by administration of the free radical scavenger recombinant human superoxide dismutase (h-SOD). A multicenter, randomized, placebo-controlled clinical trial was designed to test the hypothesis that free radical-mediated reperfusion injury could be reduced by intravenous administration of h-SOD begun before percutaneous transluminal coronary angioplasty (PTCA) in patients with acute transmural myocardial infarction. METHODS AND RESULTS: One hundred twenty patients were randomized to receive placebo (n = 59) or h-SOD (n = 61) given as a 10-mg/kg intravenous bolus followed by a 60-minute infusion of 0.2 mg.kg-1.min-1. Left ventricular function was analyzed via paired contrast left ventriculograms performed before PTCA and after 6 to 10 days and paired radionuclide ventriculograms performed within 24 hours of PTCA and after 4 to 6 weeks. Both h-SOD- and placebo-treated patients showed improvement in global and regional left ventricular function after successful reperfusion. Compared with the placebo group, no additional improvement was observed in the patients treated with h-SOD. CONCLUSIONS: The results of this clinical trial failed to demonstrate a beneficial effect of h-SOD on global or regional left ventricular function in patients who underwent successful PTCA for treatment of acute myocardial infarction.

Angioplasty, Balloon, Coronary↗
PubMed1993

Relation between plasma concentrations of didanosine and markers of antiviral efficacy in adults with AIDS or AIDS-related complex.

The relation between the average steady-state plasma concentration (Cpss) of didanosine and selected measures of efficacy, such as CD4 cell count, p24 antigenemia, and weight gain, was evaluated in patients participating in a phase 1 safety and pharmacokinetics study. All patients were diagnosed as having AIDS or severe AIDS-related complex. These individuals first received intravenous didanosine for 2 weeks at doses of 0.8-33 mg/(kg.d) and then took the drug orally at twice the intravenous dose. Cpss values were calculated on the basis of apparent oral clearance after 4 weeks of oral administration and average daily dose over the first 12 weeks of the study. These data were available for 61 patients enrolled at three clinical sites. High values for Cpss were strongly correlated with an increase in CD4 count (P = .006), a decrease in serum levels of p24 antigen (P = .006), and weight gain (P = .0001) at week 12. Logistic regression analysis was used to assess the influence of Cpss on response (as judged by the three criteria just mentioned) after adjustment for other potential factors related to infection with human immunodeficiency virus. The baseline CD4 cell count and the status with regard to prior zidovudine therapy were related to the CD4 response. However, the odds that a response would include all three parameters were nearly twice as high when the Cpss value increased by twofold.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Complex↗
PubMed1991

Lack of effect of peroral acyclovir for the treatment of acute infectious mononucleosis.

Perorally administered acyclovir was evaluated in the therapy of acute infectious mononucleosis in a multicentered, randomized, double-blind, placebo-controlled trial. A total of 120 patients received 600 mg of acyclovir or placebo five times daily for 10 days. All patients were entered into the study within 7 days of symptom onset and had a positive Monospot test. Analysis of mean values and time to resolution of fever, lymphadenopathy, weight change, hepatomegaly, splenomegaly, liver function tests, atypical lymphocytes, hours of bed rest, sense of well-being, and return to normal activities revealed no significant differences. There was a trend toward suppression of Epstein-Barr virus excretion in the oropharynx in acyclovir recipients. No toxicity was detected in patients treated with acyclovir. Under the conditions of the study, there was no evidence that treatment with perorally administered acyclovir affected the course of infectious mononucleosis.

Acyclovir↗
PubMed1989

Lecithin:sphingomyelin ratio in the amniotic fluid of male and female fetuses.

The effect of fetal sex on the amniotic fluid lecithin:sphingomyelin (L:S) ratio was determined with a prospective, randomized, double-blind study designed to evaluate the effect of antenatal steroid administration on the incidence of neonatal respiratory distress syndrome. The immature L:S ratios of 183 single births to nondiabetic women were analyzed. L:S ratios increased with increasing gestational age. Regression lines of L:S versus gestational age suggested that male infants' L:S ratios were lower than females', although the differences were not statistically significant.

Amniotic Fluid↗
PubMed1988

Rate of disappearance of creatine kinase-MB after acute myocardial infarction: clinical determinants of variability.

The apparent rate of disappearance (Kd) of creatine kinase (CK)-MB is used in the calculation of the size of acute myocardial infarction (AMI), but little is known about the determinants of variability of this parameter. We therefore evaluated the relationship between clinical characteristics and apparent Kd in 328 patients with AMI without evidence of recurrent infarction. Patients with a history of cigarette smoking within 6 months had higher rates of disappearance of CK-MB, but no relationship was found between renal function and apparent Kd. Slower rates of disappearance of CK-MB were correlated with longer times from the onset of symptoms to peak CK-MB value (p less than 0.001), while higher peak CK-MB levels were not correlated with apparent rates of enzyme clearance. Decreased rates of disappearance of CK-MB were found in patients who had congestive heart failure during or after the hospitalization (both p less than 0.05), and who died during the hospitalization or during study follow-up (both p less than 0.05). Slower rates of disappearance were also significantly correlated with lower ejection fractions on radionuclide ventriculography at 10 days (p less than 0.001) and at 3 months (p less than 0.05) after AMI. These data suggest that patients with slower rates of disappearance of CK-MB may have poorer prognoses, perhaps reflecting continuing necrosis and enzyme release from jeopardized myocardium.

Creatine Kinase↗
PubMed1988

Prognostic significance of location and type of myocardial infarction: independent adverse outcome associated with anterior location.

To determine the relative prognostic significance of location (anterior or inferior) and type (Q wave or non-Q wave) of infarction, the hospital course and follow-up outcome (mean duration 30.8 months) of 471 patients with a first infarction were analyzed. Analyses were performed grouping the patients according to infarct location (anterior, n = 253; inferior, n = 218), infarct type (Q wave, n = 323; non-Q wave, n = 148), and both location and type (inferior non-Q wave, n = 85; inferior Q wave, n = 133; anterior non-Q wave, n = 63; and anterior Q wave, n = 190). Patients with anterior infarction had a substantially worse in-hospital and follow-up clinical course compared with those with inferior infarction, evidenced by a larger infarct size (21.2 versus 14.9 g Eq/m2 creatine kinase, MB fraction [MB CK], p less than 0.001), lower admission left ventricular ejection fraction (38.1 versus 55.3%, p less than 0.001) and higher incidence of heart failure (40.7 versus 14.7%, p less than 0.001), serious ventricular ectopic activity (70.2 versus 58.9%, p less than 0.05), in-hospital death (11.9 versus 2.8%, p less than 0.001) and total cumulative cardiac mortality (27 versus 11%, p less than 0.001). Patients with Q wave infarction similarly experienced a worse in-hospital course compared with patients with non-Q wave infarction, evidenced by a larger infarct size (20.7 versus 12.7 MB CK g Eq/m2, p less than 0.001), lower admission left ventricular ejection fraction (43.7 versus 50.6%, p less than 0.001), and a higher incidence of heart failure (31.9 versus 21.6%, p less than 0.05) and in-hospital death (9.3 versus 4.1% p less than 0.05). However, there was no increased rate of reinfarction or mortality in hospital survivors with non-Q wave infarction compared with those with Q wave infarction, and total cardiac mortality was similar (16 versus 21%, p = NS). To evaluate the role of infarct location and type independent of infarct size, patients were grouped according to quartile of infarct size, and outcome was reanalyzed within each group. Patients with anterior infarction demonstrated a lower left ventricular ejection fraction on admission and after 10 days than did patients with inferior infarction, even after adjustment for infarct size, as well as a higher incidence of congestive heart failure and cumulative cardiac mortality.(ABSTRACT TRUNCATED AT 400 WORDS)

Actuarial Analysis↗
PubMed1986

Sudden death and its relation to QT-interval prolongation after acute myocardial infarction: two-year follow-up.

Risk of sudden death was assessed in 533 patients who survived 10 days after acute myocardial infarction (AMI) and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of clinical and laboratory variables measured before hospital discharge revealed that the QT interval, either corrected (QTc) or uncorrected for heart rate, did not contribute significantly to prediction of subsequent sudden death or total mortality. In this population, frequent ventricular premature complexes (more than 10 per hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction of 0.40 or less) identify patients at high risk of sudden death. In patients with these adverse clinical findings, the QTc was 0.468 +/- 0.044 second among those who died suddenly and 0.446 +/- 0.032 second in survivors, and was not statistically significant as an additional predictor of sudden death. Consideration of the use of type I antiarrhythmic agents, digoxin, presence of U waves and correction for intraventricular conduction delay did not alter these findings. Although QT-interval prolongation occurs in some patients after acute myocardial infarction, reduced LV ejection fraction and frequent ventricular premature complexes are the most important factors for predicting subsequent sudden death in this patient population.

Adrenergic beta-Antagonists↗
PubMed1986

Digoxin therapy and mortality after myocardial infarction. Experience in the MILIS Study.

Recent studies have led to controversy about whether long-term digoxin therapy after confirmed or suspected myocardial infarction increases mortality. We analyzed the mortality experience in 903 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size (MILIS). As in previous studies, the decision to treat or not to treat with digoxin was made by the patient's personal physician on the basis of the usual clinical indications. Cumulative mortality was 28 percent for the 281 digoxin-treated patients as compared with 11 percent for the 622 patients who did not receive digoxin (P less than 0.001; follow-up interval, six days to 36 months; mean, 25.1 months). However, patients treated with digoxin had more base-line characteristics predictive of mortality than did their counterparts. Adjustment for these differences with two separate applications of the Cox method yielded P values of 0.14 and 0.34 for tests of difference in mortality, providing no evidence for a significant excess mortality associated with digoxin. Thus, the findings in the MILIS population do not support the assertion that digoxin therapy is excessively hazardous after infarction, but the existence of an undetected harmful effect can only be excluded with a randomized study. Until the results of such a study are available, we recommend careful consideration of whether any treatment of ventricular dysfunction is actually needed, consideration of alternatives to digoxin therapy, and restriction of digoxin use to the subgroup of patients (with severe chronic congestive failure and a dilated left ventricle) previously shown to have a beneficial clinical response.

Clinical Trials as Topic↗
PubMed1986

Abrupt withdrawal of beta-blockade therapy in patients with myocardial infarction: effects on infarct size, left ventricular function, and hospital course.

The effects of abrupt withdrawal or continuation of beta-blockade therapy during acute myocardial infarction were evaluated in 326 patients participating in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Thirty-nine patients previously receiving a beta-blocker and randomly selected for withdrawal of beta-blockers and placebo treatment during infarction (group 1) were compared with 272 patients previously untreated with beta-blockers who were also randomly assigned to placebo therapy (group 2). There were no significant differences between the two groups in MB creatine kinase isoenzyme (15.8 +/- 10.9 vs 18.2 +/- 14.4 g-eq/m2, respectively) estimates of infarct size, radionuclide-determined left ventricular ejection fractions within 18 hr of infarction (0.44 +/- 0.15 vs 0.47 +/- 0.16) or 10 days later (0.42 +/- 0.14 vs 0.47 +/- 0.16), creatine kinase-determined incidence of infarct extension (13% vs 6%), congestive heart failure (43% vs 37%), nonfatal ventricular fibrillation (5% vs 7%), or in-hospital mortality (13% vs 9%). Patients in group 1 had more recurrent ischemic chest pain (p = .002) within the first 24 hr after infarction, but not thereafter. However, this did not appear to be related to a rebound increase in systolic blood pressure, heart rate, or double product. In a separate analysis, 20 propranolol-eligible group 1 patients randomly selected for withdrawal of beta-blockade (group 3) were compared with 15 patients randomly selected for continuation of prior beta-blockade therapy (group 4). This comparison yielded similar results. These data indicate that the beta-blockade withdrawal phenomenon is not a major clinical problem in patients with acute myocardial infarction. beta-Blockade therapy can be discontinued abruptly during acute myocardial infarction if clinically indicated.

Aged↗
PubMed1984

Risk factors for sudden death after acute myocardial infarction: two-year follow-up.

The risk of sudden coronary death after myocardial infarction (MI) was assessed in 533 patients who survived 10 days after MI and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of multiple clinical and laboratory variables determined before hospital discharge revealed that frequent ventricular premature beats (VPBs) (greater than or equal to 10/hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction less than or equal to 0.40) were independently significant markers of risk for subsequent sudden death believed to be the result of a primary ventricular arrhythmia. The incidence of sudden death was 18% in patients with both LV dysfunction and frequent VPBs (11 times that of patients with neither of these findings). Seventy-nine percent of all sudden deaths occurred within 7 months after the index MI. In 280 survivors reclassified 6 months after MI with regard to the presence or absence of frequent VPBs and LV dysfunction, these risk factors could not be associated with sudden coronary death over a further follow-up period of up to 18 months; the overall incidence of sudden cardiac death was low (1.4%) after 6 months. Thus, the presence of frequent VPBs in association with LV dysfunction early after MI identifies patients at high risk for sudden death over the next 7 months.

Aged↗