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Biomedical subjects

T Aarsland

Publications and source records attributed to T Aarsland.

At least 19 recordsLinked to original sources
PubMed1995

Plasma proatrial natriuretic factor is predictive of clinical status in patients with congestive heart failure.

Atrial stretch results in myocyte release of the prohormone atrial natriuretic factor (1-126). The N-terminal (1-98) fragment, proatrial natriuretic factor (proANF) is released on an equimolar basis with the C-terminal (99-126) active hormone and may be assayed simply due to in vitro stability. This study was undertaken to evaluate the relation between proANF and routinely available measures of clinical status. ProANF was sampled from 202 patients (median age 68 years [range 15 to 85], 77% men) recruited from an active outpatient heart failure clinic. Patients were subgrouped according to New York Heart Association functional class, radionuclide ejection fraction (EF), echocardiographic left ventricular (LV) end-diastolic diameter, and Doppler-determined systolic pulmonary arterial pressure. The median proANF (pmol/L) values for patients in New York Heart Association classes I, II, III, IV were 725, 1,527, 1,750, and 5,172, respectively. The proANF value for the group with EF > 40% was 1,534 versus 1,993 for EF < or = 40% (p < 0.05). The value for the group with LV diameter < 60 mm ws 838 versus 1,751 for LV diameter > or = 60 mm (p < 0.01). The value for the group with systolic pulmonary artery pressure < 45 mm Hg was 1,241 versus 2,660 for systolic pulmonary artery pressure > or = 45 mm Hg (p < 0.01). ProANF correlated better than the other variables with New York Heart Association functional class and was more closely associated with noninvasive measurements than New York Heart Association functional class.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Improvement of serum lipids and blood pressure during intervention with n-3 fatty acids was not associated with changes in insulin levels in subjects with combined hyperlipidaemia.

OBJECTIVES: To investigate the effect of an omega-3 fatty acid concentrate K85 on serum lipids, lipoproteins, insulin metabolism and blood pressure in subjects with combined hyperlipidaemia. DESIGN: After a run-in dietary period of 10 weeks, subjects were randomly allocated to receive either encapsulated K85 (n = 28) or corn oil (n = 29). The intervention was double-blind. SETTING: An outpatient centre in Stavanger, Norway. SUBJECTS: Fifty-seven of 141 individuals, who, after the run-in period continued to meet the inclusion criteria: serum triglycerides of > or = 2.0 mmol L-1 and total serum cholesterol of > or = 6.0 mmol L-1. INTERVENTION: Encapsulated K85, containing 85% eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA), or corn oil, both administered in a daily dose of 4 g for 12 weeks. MAIN OUTCOME MEASURES: Change in metabolic and haemodynamic parameters related to intervention. RESULTS: Serum EPA and DHA increased significantly in the K85 group during the treatment period. The body-mass index remained unchanged. A 28% reduction in serum triglycerides was noted in the K85 group from the first 4 weeks. Total serum cholesterol was significantly reduced with both regimens. Serum high-density lipoprotein cholesterol increased significantly during the first 8 weeks in the K85 group. Significant reductions in systolic and diastolic blood pressures were noted in subjects on K85. The treatment did not affect serum glucose, plasma insulin and proinsulin levels. Insulin:glucose and proinsulin:glucose ratios remained unchanged. CONCLUSIONS: The atherogenic risk profile was improved with K85 in subjects with combined hyperlipidaemia, but n-3 fatty acids supplementation did not affect glucose/insulin homeostasis.

Adult↗
PubMed1994

Plasma endothelin determination as a prognostic indicator of 1-year mortality after acute myocardial infarction.

BACKGROUND: Plasma endothelin concentrations are increased in the acute phase of myocardial infarction and in chronic heart failure. Since endothelin may contribute to hemodynamic deterioration by potent vasoconstrictory and cardiotoxic actions, increased plasma levels may be associated with an unfavorable prognosis after myocardial infarction. METHODS AND RESULTS: We tested the hypothesis that plasma endothelin determination in the subacute phase of myocardial infarction is related to subsequent survival and assessed whether plasma endothelin measurements provide additional prognostic information to that obtained from clinical and biochemical variables previously known to be associated with high mortality. Plasma endothelin determination was obtained from 142 patients (average age +/- SD, 67.8 +/- 10.1 years) on day 3 after documented myocardial infarction and was related to 1-year mortality. Sixteen patients died during the follow-up period. In a univariate Cox proportional-hazards model, day 3 plasma endothelin concentrations were significantly related to mortality (P < .0001). Patient age, previous treatment for systemic hypertension, presence of clinical heart failure, and plasma atrial natriuretic factor levels were all related to mortality in univariate analysis but provided no additional prognostic information to that obtained from endothelin determination in a multivariate model. CONCLUSIONS: Plasma endothelin concentrations are strongly related to outcome after myocardial infarction and provide prognostic information independent of clinical and biochemical variables previously associated with a poor prognosis.

Aged↗
PubMed1994

Comparison of the efficacy of three dose levels of moexipril versus placebo as add-on therapy to hydrochlorothiazide in patients with moderate hypertension.

This parallel, double-blind trial was designed to evaluate the efficacy of three dose levels of moexipril versus placebo as add-on therapy to hydrochlorothiazide (HCTZ) in patients with uncomplicated moderate to severe hypertension. Two hundred patients (aged 25-74 years) with sitting diastolic blood pressure (DBP) between 95 and 114 mm Hg after 4 week treatment with HCTZ 25 mg once daily were randomized to placebo, or moexipril 3.75, 7.5 mg, or 15 mg. BP was measured at 22-26 h postdose at biweekly visits and at 1, 2, 3, and 4 h postdose after the first dose of double-blind medication. At endpoint, adjusted mean reductions from baseline sitting DBP were 8.4, 8.8, and 8.9 mm Hg in the moexipril 3.75-, 7.5-, and 15-mg groups, respectively, as compared with a reduction of 4.6 mm Hg in the placebo group (p = 0.003). The differences in systolic BP (SBP) reductions were statistically significant in favor of each of the moexipril groups over the placebo group at all trough time-points. Adjusted mean changes in sitting SBP were 10.9, 12.0, and 11.7 mm Hg, respectively, as compared with a reduction of 0.6 mm Hg in the placebo group (p < 0.001). Our results indicate that moexipril and HCTZ constitute a clinically valuable combination in treatment of patients with moderate to severe hypertension.

Adult↗
PubMed1993

Prognostic value of plasma atrial natriuretic factor, norepinephrine and epinephrine in acute myocardial infarction.

Neurohumoral activation in acute myocardial infarction (AMI) may reflect the degree of hemodynamic compromise, contribute to the progression of heart failure and augment to the risk of serious ventricular arrhythmias. Consequently, assessment of neurohumoral variables may provide an index of prognostic value in AMI. Plasma levels of atrial natriuretic factor (ANF), norepinephrine and epinephrine were determined in 145 patients on day 3 after AMI. During the 360-day follow-up period 17 patients died. In univariate analysis, all 3 neurohormones were significantly related to 1-year mortality rates (ANF, p < 0.001; norepinephrine, p = 0.009; epinephrine, p = 0.048). After correction for age, sex, anamnestic, biochemical and clinical variables including signs of clinical heart failure in a multivariate model, ANF remained independently related to mortality. The association between plasma norepinephrine and survival failed to reach statistical significance after introduction of clinical heart failure in the model. Comparison of patients subdivided according to median hormone levels (ANF, 30.3 pmol/liter; norepinephrine, 2.29 nmol/liter) demonstrated a significantly increased mortality rate in patients with elevated ANF (p < 0.001), but not elevated norepinephrine levels. These results suggest that early plasma ANF levels are related to survival in patients with AMI, independently of signs of clinical heart failure.

Aged↗
PubMed1993

The effect of early converting enzyme inhibition on neurohumoral activation in acute myocardial infarction.

The effect of early converting enzyme inhibition with enalapril on the extent of neurohumoral activation in acute myocardial infarction was evaluated in a randomized, placebo-controlled double blind fashion. Plasma levels of atrial natriuretic factor and noradrenaline on day 1, i.e. prior to randomization (n = 99), and on days 3 (n = 145) and 30 (n = 69) following myocardial infarction were determined. Enalapril did not significantly affect neurohumoral activation on day 3 (enalapril vs. placebo (mean (S.E.M.); atrial natriuretic factor: 35.3 (3.0) vs. 37.2 (2.9) pmol/l; noradrenaline: 2.82 (0.20) vs. 3.70 (1.02) nmol/l) or at 1 month (atrial natriuretic factor: 33.1 (3.0) vs. 32.4 (3.9) pmol/l; noradrenaline: 2.77 (0.25) vs. 2.82 (0.28) nmol/l). However, in myocardial infarction patients developing heart failure, a significant attenuation of the day 3 atrial natriuretic factor, but not of the noradrenaline response, was seen (atrial natriuretic factor: 47.0 (7.7) vs. 59.0 (6.4) pmol/l, P < 0.05; noradrenaline: 3.37 (0.42) vs. 6.59 (3.26) nmol/l, P = ns). In conclusion, enalapril did not significantly reduce neurohumoral activation in acute myocardial infarction, possibly because the activation in most patients is modest and confined to the early convalescent phase. However, in patients with myocardial infarction and heart failure enalapril therapy was associated with a reduction in early plasma atrial natriuretic factor levels, compatible with decreased cardiac filling pressures.

Aged↗
PubMed1993

Rate responsive cardiac pacing using a minute ventilation sensor.

A minute ventilation sensing rate responsive pacemaker was implanted in 15 patients (8 males and 7 females) with bradycardia. The mean age was 72.8 +/- 8.7 years. The single chamber system measures transthoracic impedance between the tip electrode of a standard bipolar lead and the pulse generator case. In the adaptive mode the pulse generator calculates a rate responsive factor or slope during maximal exercise but functions as in the VVI mode. The patients exercised maximally on an upright cycle ergometer with the pacemaker programmed to VVI mode, adaptive mode, and rate responsive mode. Exercise and gas exchange data were collected continuously and analyzed using an automated breath-by-breath system. The slope, heart rate, and ventilation were measured every 20 seconds. Heart rate in pacemaker dependent patients correlated well to minute ventilation (correlation coefficient ranging from 0.72-0.95, P < 0.0001). This study demonstrates that minute ventilation is a good metabolic sensor in rate responsive pacing.

Aged↗
PubMed1992

Effect of timolol on cardiopulmonary exercise performance in men after myocardial infarction.

The effect of the nonselective beta blocker timolol on maximal cardiopulmonary exercise performance was evaluated in 28 men with previous myocardial infarction without effort angina (mean age 63 +/- 8 years). Patients were randomized to placebo or timolol (10 mg twice daily) for 4 weeks and then crossed over to the alternative therapy in a double-blind manner. At the completion of each treatment period, patients underwent symptom-limited maximal cardiopulmonary exercise on a cycle ergometer. Exercise time, heart rate, oxygen consumption (VO2), oxygen (O2) pulse and respiratory exchange ratio were measured at peak exercise and at a submaximal exercise level defined at a respiratory exchange ratio of 1.00. Timolol treatment reduced peak heart rate from 153 +/- 11 to 102 +/- 14 beats/min (-33%, p less than 0.001). Exercise time decreased from 680 +/- 91 to 633 +/- 78 seconds (-7%, p less than 0.001). Peak VO2 decreased from 25.3 +/- 4.7 to 21.4 +/- 3.5 ml/min/kg (-15%, p less than 0.001). O2 pulse increased from 12.9 +/- 1.9 to 16.7 +/- 2.3 ml/beat (+29%, p less than 0.001). Peak respiratory exchange ratio did not change significantly, indicating comparable effort. At submaximal exercise, defined at a respiratory exchange ratio of 1.00, there was no difference in exercise time between placebo and timolol. Heart rate decreased with timolol compared with placebo, from 126 +/- 16 beats/min by 31% (p less than 0.001), VO2 decreased from 18.5 +/- 4.3 ml/min/kg by 10% (p less than 0.001), O2 pulse increased from 11.5 +/- 2.0 ml/beat by 30% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Effect of long-term enalapril therapy on cardiopulmonary exercise performance in men with mild heart failure and previous myocardial infarction.

Forty-one men with documented myocardial infarction greater than 6 months previously were randomized to long-term (48 weeks) therapy with placebo or enalapril on a double-blind basis. All patients were receiving concurrent therapy with digitalis and a diuretic drug for symptomatic heart failure (functional class II or III). The mean age was 64 +/- 7.3 years and no patient suffered from exertional chest pain. Patients underwent maximal cardiopulmonary exertional chest pain. Patients underwent maximal cardiopulmonary exercise testing to exhaustion on an ergometer cycle nine times over the course of 48 weeks. Gas exchange data were collected on a breath by breath basis with use of a continuous ramp protocol. In the placebo group (n = 21), the mean (+/- SD) peak oxygen consumption (VO2) at baseline was 18.8 +/- 5.2 versus 18.5 +/- 5.5 ml/kg per min at 48 weeks (-1.4%, p = NS). In the enalapril group (n = 20), the corresponding values were 18.1 +/- 3.1 versus 18.3 +/- 2.6 ml/kg per min (+2.8%, p = NS). The mean VO2 at the anaerobic threshold for the placebo group at baseline study was 13.1 +/- 3.5 versus 12.8 +/- 2.1 ml/kg per min at 48 weeks (-2.2%, p = NS). The corresponding values for the enalapril group were 11.8 +/- 2.3 versus 11.8 +/- 2.4 ml/kg per min (+1.4%, p = NS). The mean total exercise duration in the placebo group at baseline study was 589 +/- 153 versus 620 +/- 181 s at 48 weeks (+5.4%, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Anaerobic Threshold↗
PubMed1991

Effects of long-term enalapril therapy on cardiopulmonary exercise performance after myocardial infarction.

BACKGROUND: The Enalapril Postinfarction Exercise (EPIE) trial was designed to study the effect of enalapril treatment on peak and submaximal cardiopulmonary exercise performance over the course of 1 year in men after myocardial infarction with mild exercise intolerance. METHODS AND RESULTS: One hundred sixty men with a peak VO2 less than 25 ml/kg/min and without effort angina were randomized to receive enalapril 20 mg qd or placebo on a double-blind basis. The mean age was 60.3 +/- 7.6 years. All patients received concurrent beta-blocker therapy for secondary prophylaxis. Treatment began at 21 days (group 1, n = 100) or more than 6 months after infarction (group 2, n = 60). Patients underwent exercise with real-time gas-exchange analysis nine times over the course of 48 weeks. In group 1, improvement in exercise performance occurred during the course of the trial in both groups of patients receiving placebo or enalapril. The mean peak VO2 for the placebo-treated patients in group 1 increased from 18.3 +/- 3.4 ml/kg/min by 4.9% at 48 weeks (p less than 0.05). The corresponding values for enalapril-treated patients were 18.9 +/- 3.8 ml/kg/min with a 3.7% increase (p = 0.07). Total exercise time increased in the placebo-treated patients from 645 +/- 96 seconds by 7.3% (p less than 0.01). Corresponding values for enalapril-treated patients were 674 +/- 103 seconds with a 5.4% increase (p less than 0.01). In group 2, the mean peak VO2 at baseline for the placebo-treated patients of 20.3 +/- 3.8 ml/kg/min increased by 4.4% at 48 weeks (p = NS). The corresponding values for enalapril-treated patients were 19.2 +/- 3.6 ml/kg/min with a 2.6% increase (p = NS). Total exercise time increased in the placebo-treated patients from 677 +/- 114 seconds by 0.7% (p = NS). Corresponding values for enalapril-treated patients were 659 +/- 99 seconds with a 1.1% increase (p = NS). There were no significant differences between the placebo and enalapril subgroups at any time with regard to peak VO2, exercise duration, or the VO2 at the anaerobic threshold. CONCLUSIONS: This trial demonstrates that long-term converting enzyme inhibition with enalapril had no significant effect on the peak or submaximal cardiopulmonary exercise performance over the course of 1 year in men after myocardial infarction with only mildly reduced exercise capacity.

Aged↗
PubMed1990

Validation of a computerized technique for detection of the gas exchange anaerobic threshold in cardiac disease.

Respiratory gas exchange data were collected from 77 men greater than 6 months after acute myocardial infarction. Maximal exercise was performed on an ergometer cycle programmed for a ramp protocol of 15 W/min. The gas exchange anaerobic threshold (ATge) was determined by analysis of the carbon dioxide elimination (VCO2) vs oxygen consumption (VO2) curve below a respiratory exchange ratio of 1.00 using a computerized algorithm. This value was estimated at the inflection of VCO2 from a line with a slope of 1 which intersects the VCO2 vs VO2 curve. The relation of the ATge to the lactate acidosis threshold was studied in 29 patients. The reproducibility of the ATge method was studied in 77 patients. Mean (+/- standard deviation) VO2 for the ATge was 905 +/- 220 vs 866 +/- 299 ml/min for the lactate acidosis threshold (r = 0.86, p less than 0.001). Mean VO2 at the ATge for test 1 was 968 +/- 225 vs 952 +/- 217 ml/min for test 2 (r = 0.71, p less than 0.001). Mean peak VO2 was 1,392 +/- 379 vs 912 +/- 202 ml/min at the ATge (r = 0.76, p less than 0.001). Results demonstrate that this ATge method correlates well with the lactate acidosis threshold, is reproducible, and should be useful as an objective measure of submaximal exercise performance.

Aged↗
PubMed1990

Plasma atrial natriuretic factor concentration during maximal cardiopulmonary exercise in men with mild heart failure.

The response in terms of production of atrial natriuretic factor to maximal cardiopulmonary exercise was investigated in 13 patients with mild heart failure (New York Heart Association function class II) secondary to previous myocardial infarction. Exercise induced a rapid and gradually increasing production of atrial natriuretic factor. The concentration at the termination of the test was statistically higher than at rest (64.5 +/- 9.7 versus 119.4 +/- 18.3 pmol/l. P = 0.001). Resting levels of the natriuretic factor correlated well to levels at peak exercise (r = 0.797, P = 0.001). The increase in concentration from rest to peak exercise (atrial natriuretic factor delta) was inversely correlated to the peak consumption of oxygen (r = -0.584, P = 0.036), indicating that the response to exercise is not attenuated in the patients with most marked functional impairment. The relationship between resting levels of atrial natriuretic factor and peak consumption of oxygen did not reach statistical significance (r = -0.421, P = 0.152), but a significant inverse relationship was observed between concentration at peak exercise and peak consumption of oxygen (r = -0.671, P = 0.012). Levels of atrial natriuretic factor during peak exercise are related to functional impairment in mild heart failure and may discriminate between the functional capacity of patients belonging in the same class of clinical function.

Aged↗
PubMed1990

A comparison of methodologies in detection of the anaerobic threshold.

Peak cardiopulmonary exercise performance is readily evaluated. The most appropriate methodology for assessment of submaximal exercise performance, however, is a subject of controversy. Therefore, we assessed the difference between conventional methodologies using standard criteria to estimate the onset of anaerobiosis and compared them with known gas exchange and blood lactate [( La]) concentrations. Oxygen uptake (VO2) was determined at both the gas exchange anaerobic threshold (ATge) and the lactate threshold (LaT) using the following three types of commonly used methodologies in a blinded fashion: 1) conventional techniques based on manual inspection of plots of gas exchange indexes and [La] versus time, 2) computerized linear regression analysis of two-segment model plots for VCO2 versus VO2 and log [La] versus log VO2, and 3) fixed values determining the VO2 at a respiratory exchange ratio (VCO2/VO2) of 1.00 and at an [La] of 2 mmol/l. Respiratory exchange data were collected on a breath-by-breath basis in 30 men with documented myocardial infarction. Simultaneously, arterial blood was sampled for [La] every 20 seconds during maximal exercise on an upright bicycle ergometer programmed for a continuous ramp protocol of 15 W/min. The mean (+/- SD) peak VO2 was 1,463 (+/- 312) ml/min. The mean (+/- SD) VO2 values for each method were as follows: (table; see text) These results indicate that a good positive correlation exists between the gas exchange and lactate data by all three approaches. The chosen fixed values yield the highest threshold detection for both ATge and LaT. Detection was lowest using regression analysis for LaT.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

The pharmacokinetics of lisinopril in hospitalized patients with congestive heart failure.

1. The pharmacokinetics of the angiotensin converting enzyme inhibitor, lisinopril, were studied in an open, randomized, balanced, two-period, crossover design in 12 in-patients with stable, chronic congestive heart failure (CHF). 2. To evaluate the pharmacokinetics of lisinopril in CHF, lisinopril was administered orally (10 mg) and intravenously (5 mg) in each patient. Each dose was followed by a 72 h period with frequent blood sampling and fractional urine collections for radioimmunoassay of lisinopril. 3. Mean urinary recovery of lisinopril was 15 and 88% following oral and intravenous administration, respectively; absorption/bioavailability of lisinopril based on urinary recovery ratios was 16%, less than that found in normal subjects. 4. Serum concentrations of lisinopril following intravenous administration were higher in this study than those previously observed in normal subjects. 5. The results of this study suggest a reduced absorption of lisinopril in CHF and altered disposition, possibly associated with age as well as the disease state.

Administration, Oral↗
PubMed1988

Reproducibility of cardiopulmonary exercise testing in men following myocardial infarction.

Peak oxygen consumption during progressive exercise is of clinical relevance in the functional evaluation of the cardiac patient. The use of cardiopulmonary exercise testing for the evaluation of the efficacy of therapeutic intervention requires that the methods used yield reproducible results. This study compared the results of two consecutive, symptom-limited, maximal exercise tests in 170 men following confirmed myocardial infarction. On-line, real-time respiratory gas exchange was measured on a breath-by-breath basis. The data were processed by the system using a 9 s moving average filter and the peak values were determined as averaged over a representative 20-s interval during the final 1 min of the test. The mean (+/- SD) total exercise times for the two tests were 635 (+/- 109) vs. 652 (+/- 112) (r = 0.946). The mean (+/- SD) peak VO2 values were 1480 (+/- 337) vs. 1495 (+/- 350) ml min-1 (r = 0.923). Performance could not be predicted by routine assessment of infarct type or size. This study demonstrates that maximal cardiopulmonary exercise testing in men following myocardial infarction yields highly reproducible results.

Adult↗
PubMed1988

Comparison of topical timolol vs betaxolol on cardiopulmonary exercise performance in healthy volunteers.

The effects of topical timolol vs betaxolol on cardiopulmonary exercise performance were studied in a randomised double-masked fashion in 12 healthy male volunteers. Cardiopulmonary parameters were evaluated at the anaerobic threshold and at peak exercise. Intraocular pressure was determined before and after treatment by applanation tonometry. No differences were found in aerobic or peak exercise capacity. Maximal heart rate was slightly lower (P less than 0.05) following treatment with timolol compared with betaxolol. However, a correspondingly higher oxygen pulse (oxygen uptake/heart rate) compensated for this reduction and resulted in no difference in peak performance. At physiological work levels, it was not possible to demonstrate any influence of topical, selective or non-selective, beta-adrenergic blockade on cardiopulmonary exercise performance in these healthy volunteers.

Adrenergic beta-Antagonists↗