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Biomedical subjects

U Berglund

Publications and source records attributed to U Berglund.

At least 19 recordsLinked to original sources
PubMed2000

[Significant undertreatment of high cholesterol level in ischemic heart disease].

Lipid and lipoprotein analysis was performed in 127 consecutive patients with stable incapaciting angina referred by cardiologists for coronary angiography (mean waiting time, 121 days). Ninety-four per cent of the patients manifested evidence of myocardial ischaemia at exercise testing, or had had earlier myocardial infarction or earlier revascularisation with angioplasty or bypass surgery. Despite the well-known results of the large statin trials in secondary prevention (4S and CARE), only a third of the patients had LDL cholesterol levels in accordance with Swedish and European guidelines, i.e., below 3.0 mmol/L.

Adult↗
PubMed1998

Enhanced onset of platelet inhibition with a loading dose of ticlopidine in ASA-treated stable coronary patients.

Antiplatelet therapy reduces the rate of complications of coronary angioplasty. Ticlopidine, in addition to acetyl salicytic acid (ASA), improves the results after coronary stenting, but early complications still occur. Ticlopidine given in the standard way has a slow onset of action. Eighteen ASA-treated stable coronary patients were randomized to standard ticlopidine treatment (250 mg twice daily) or to a loading dose of 1500 mg followed by 250 mg twice daily. After one day, standard treatment had a very modest antiplatelet effect, as assessed by ADP-induced platelet fibrinogen binding, whereas the loading dose resulted in a considerably better platelet inhibition; relative inhibition, 5.6-10.6 vs. 24.9-35.3% (p<0.005) with final ADP concentrations 3 and 0.6 microM, respectively. It is possible that a loading dose of ticlopidine, given the day before the procedure, might reduce the complications related to angioplasty and stenting.

Angina Pectoris↗
PubMed1997

[Large arterial thrombosis. Rapid recanalization with a new thrombocyte inhibitor].

A 56-year-old male cigarette smoker, without other risk factors for arterial disease and no history of heart disease or thrombotic events, was admitted as an emergency case because of chest pain shortly after a fall. He had a right coronary artery occlusion, which was managed with angioplasty and stenting. A large thrombotic occlusion in the distal aorta probably occurred simultaneously with the coronary occlusion, became symptomatically manifest and was diagnosed when the chest pain subsided after stenting. This thrombus was successfully treated with the new platelet inhibitor abciximab.

Abciximab↗
PubMed1997

Pharmacokinetics and effect of ticlopidine on platelet aggregation in subjects with normal and impaired renal function.

The pharmacokinetics and the effect of ticlopidine on platelet aggregation were determined in patients with chronic renal failure (n = 6), who were not on dialysis and had glomerular filtration of 16.9 +/- 4.4 mL/min, and were matched with the pharmacokinetics and effects in healthy volunteers (n = 7). Participants were studied after acute oral administration of ticlopidine at the beginning of the study and after 36 days of treatment with 250 mg twice daily. For unchanged ticlopidine there were no significant differences between the concentration profiles for the two study groups. By day 36 the minimum concentrations in plasma were identical (0.35 +/- 0.22 mg/L and 0.36 +/- 0.21 mg/L, respectively). Using 14C-labeled ticlopidine, the concentration profiles of radioactivity on day 1 were similar to those on day 36 for both groups. However, maximum concentrations and area under the concentration-time curve at 72 hours were both higher in patients with renal failure than in healthy volunteers. Treatment with ticlopidine progressively decreased sensitivity to adenosine diphosphate-induced platelet aggregation. At day 36, the concentration of adenosine diphosphate required to achieve 50% platelet aggregation was approximately 2.5 times greater than before treatment. Both patients and healthy volunteers exhibited closely comparable changes. The response to collagen-induced platelet aggregation was not changed in patients by treatment with ticlopidine. In contrast, volunteers required a three- to fourfold increase in collagen concentration to achieve 50% platelet aggregation after 36 days of therapy. Although some differences in both pharmacokinetics and pharmacodynamics of ticlopidine have been demonstrated between patients and and healthy volunteers, results in this study demonstrated that a change of dosage is not required in renal failure.

Adult↗
PubMed1992

Thrombolysis with recombinant human tissue-type plasminogen activator during instability in coronary artery disease: effect on myocardial ischemia and need for coronary revascularization. TRIC Study Group.

Two hundred five men, 40 to 70 years of age, admitted to the coronary care unit with unstable coronary artery disease (unstable angina or non-Q wave myocardial infarction), were randomized to double-blind placebo-controlled treatment with an intravenous infusion of recombinant tissue-type plasminogen activator (rTPA), 1 mg/kg body weight (maximum 100 mg) during 4 hours, in addition to aspirin, heparin, and beta-blockade. No severe complications occurred. Myocardial ischemia, defined as myocardial infarction, incapacitating angina despite medication, or signs of ischemia at the exercise test, was reduced by treatment with rTPA compared with placebo both at discharge, 53% compared with 70% (p = 0.02), and at 1 month, 61% compared with 80% (p = 0.005). Signs of myocardial ischemia during the exercise test were reduced at discharge 51.0% compared with 68% (p = 0.03) and at 1 month 48% compared with 62% (p = 0.09). Coronary angiography after 1 month showed no difference in major coronary lesions between the groups, nor was there any reduction in the number of performed coronary revascularization procedures. In conclusion, treatment with rTPA in unstable coronary artery disease in men reduced myocardial ischemia but did not significantly reduce the need for revascularization in long-term follow-up.

Adult↗
PubMed1991

Influence on platelet function by heparin in men with unstable coronary artery disease.

Ninety-seven men with unstable coronary artery disease (CAD), i.e. unstable angina or a non Q-wave myocardial infarction, entered a double-blind placebo-controlled study with heparin intravenously 30,000-40,000 U daily. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP and as the platelet inhibitory effect of prostacyclin, before and after 5 days of treatment. Heparin increased aggregation induced by ADP 1 microM from 39.6 +/- 3.1% to 52.1 +/- 4.1% (p = 0.014) and reduced the inhibition of aggregation by prostacyclin 1.0 ng/ml from 59.6 +/- 3.7% to 39.3 +/- 5.6% (p less than 0.001). No changes occurred in the placebo group. Thus, treatment with heparin enhances the platelet sensitivity to ADP and decreases the platelet inhibitory effect of prostacyclin in men with unstable CAD. Concomitant treatment with acetylsalicylic acid abolishes the increased response to ADP, but does not seem to influence the interaction between heparin and prostacyclin.

Analysis of Variance↗
PubMed1991

Persistent inhibition of platelet function during long-term treatment with 75 mg acetylsalicylic acid daily in men with unstable coronary artery disease.

One-hundred-and-ninety-three men with unstable coronary artery disease (CAD) (i.e. unstable angina or a non-Q wave myocardial infarction) were randomized in a double-blind fashion to acetylsalicylic acid (ASA) 75 mg daily (n = 100) or placebo (n = 93) within 72 h of admission to the Coronary Care Unit. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP before and after 5 days, 1, 12, 18 and 24 months of treatment. ASA decreased aggregation by collagen 1 mg l-1 from 81.3 +/- 1.7% before to 34.0 +/- 1.7% after 1 month (P less than 0.001), while no change was observed in the placebo group. Aggregation by ADP 1 microM after 1 month was 42.1 +/- 1.1% and 51.0 +/- 2.0% in the ASA and placebo groups respectively (P less than 0.001). The platelet inhibition by ASA was maintained during 24 months. All ASA patients had reduced aggregation during treatment. A cumulative dose of 300 mg (4 doses of 75 mg) was not enough for maximal inhibition at the second aggregation test. Thus, ASA 75 mg daily causes platelet inhibition in all patients without attenuation during long-term treatment. If low dose ASA is started in unstable coronary artery disease a loading dose exceeding 300 mg is suggested.

Adult↗
PubMed1991

Stimulus sequence and the exponent of the power function for loudness.

In two experiments, 15 and 13 subjects estimated the loudness of 12 sound-pressure levels (38-104 dB; 6-dB intervals) of a 1000-Hz tone by the method of magnitude estimation with a modulus assigned to the first stimulus presented. The tone duration was 1 sec. and the interstimulus interval was 6 sec. The presentation order was systematically ascending-descending in one experiment and balanced-irregular in the other. The results indicate that (1) loudness is a power function of sound pressure with an exponent of 0.60 for the systematic order and 0.29 for the irregular order. (2) For both the irregular and systematic orders, a large step-size (12 or 18 dB) between the stimulus on Trial n and on Trial n-1 (or n-3) results in a slight assimilation effect. This also occurs for the small step-size (6 dB) in the irregular order. (3) The size of momentary exponents (based on two points, Trials n and n-1 or n-3) depends on the sound pressures of successive stimuli, whether the steps are positive or negative, and whether the stimuli have been presented in systematic or irregular order. For positive steps, the momentary exponent is lower for a soft tone (Trial n) than for a loud tone, whereas for negative steps the momentary exponent is lower for a loud tone than for a soft tone. These effects ar more pronounced when these stimuli are presented in an irregular order. A relative judgment model is offered for magnitude estimation. It assumes that subjects judge the loudness of a stimulus in terms of three reference markers: the minimum and maximum sound pressures as well as the sound pressure of the previous stimulus.

Adult↗
PubMed1990

Serum lipoproteins in day and shift workers: a prospective study.

This study was designed to assess changes in diet and serum lipoproteins in shift workers. Twelve shift workers and 13 day workers were examined before employment and after six months at work. Total cholesterol and serum triglycerides did not change significantly. In both groups a decrease in systolic blood pressure was observed. The ratio between apoB and apoA-1 lipoproteins increased by 18% in shift workers compared with 5% in day workers. The change in the ratio between apoB and apoA-1 lipoproteins showed a significant inverse correlation with the change in intake of dietary fibres.

Adult↗
PubMed1988

Platelet function and plasma fibrinogen and their relations to gender, smoking habits, obesity and beta-blocker treatment in young survivors of myocardial infarction.

Seventy-three (58 men and 15 women) survivors of myocardial infarction below 45 years of age and 73 healthy matched controls were investigated regarding in vitro platelet aggregability to ADP and collagen, platelet sensitivity to prostacyclin and plasma levels of beta-thromboglobulin, platelet factor 4 and fibrinogen. The patients, studied 3-6 months after the acute event, had a reduced platelet sensitivity to prostacyclin. They did not differ from the controls regarding the other platelet function tests. Females had higher platelet reactivity than men. Smoking, obesity or beta-blocker treatment did not influence platelet function. The patients had higher fibrinogen levels than the controls. Gender did not influence, while smoking and obesity increased plasma fibrinogen. Patients on beta-blockade had lower fibrinogen levels than patients without this therapy. The high fibrinogen level and the low platelet sensitivity to prostacyclin might indicate an increased thrombotic liability in young myocardial infarction patients.

Adrenergic beta-Antagonists↗
PubMed1987

Predictive importance of clinical findings and a predischarge exercise test in patients with suspected unstable coronary artery disease.

The prognostic information of clinical variables and a predischarge exercise test was studied in 400 patients (282 men, 118 women) admitted to the coronary care unit with suspected unstable coronary artery disease, that is, recurring chest pain of new onset, increasing anginal pain in formerly stable angina pectoris or suspected nontransmural acute myocardial infarction. Forty-nine coronary events occurred in the 276 men who performed the exercise test during the following year, whereas only 5 coronary events occurred among the 118 women. The only variable of prognostic importance in women was nontransmural myocardial infarction. In men, the clinical variables increasing age, duration of angina, ST- or T-segment changes on the rest electrocardiogram and increasing angina or nontransmural myocardial infarction as inclusion criteria were associated with increased occurrence of coronary artery bypass surgery, transmural myocardial infarction or cardiac death. Findings of ST-segment depression, limiting chest pain or low rate-pressure product during the exercise test were of greater value than any clinical variable in prediction of coronary artery bypass surgery, transmural myocardial infarction or cardiac death. Within all clinical subgroups of men, the results of the exercise test had an additive predictive value for future coronary events. Combinations of clinical data and exercise test results enabled the best identification of patients with high or low risk for coronary events.

Adult↗
PubMed1987

Effects of the platelet inhibitor ticlopidine on exercise tolerance in stable angina pectoris.

Coronary blood flow might be reduced by platelet aggregates or by vasospasm induced by platelet-produced thromboxane A2. Therefore the effects of the platelet inhibitor ticlopidine (500 mg daily) on platelet function and on exercise tolerance were investigated in a double-blind placebo-controlled study in 38 middle-aged men with stable incapacitating angina pectoris. Before and after 4 and 8 weeks of treatment, exercise tests were performed in warm and cold environments. The in vitro platelet reactivity to ADP was determined at rest and the plasma levels of beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were measured before and immediately after exercise. There were no signs of increased platelet activity at rest or after exercise as judged by the levels of BTG and PF4. Despite a potent inhibition of platelet reactivity to ADP in vitro during ticlopidine treatment, the exercise tolerance was reduced in exercise tests in both warm and cold environments and in daily life. Therefore platelet activity does not seem to play any significant role in exercise tolerance in the stable phase of angina pectoris.

Adult↗