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Biomedical subjects

U Abildgaard

Publications and source records attributed to U Abildgaard.

At least 19 recordsLinked to original sources
PubMed2001

Subcutaneous enoxaparin once or twice daily compared with intravenous unfractionated heparin for treatment of venous thromboembolic disease.

BACKGROUND: Low-molecular-weight heparins administered subcutaneously once or twice daily have been reported to be as safe and efficacious as intravenous unfractionated heparin in the treatment of acute venous thromboembolic disease. OBJECTIVE: To determine whether subcutaneous enoxaparin administered once or twice daily is as effective as continuously infused unfractionated heparin in acute symptomatic venous thromboembolic disease. DESIGN: Randomized, controlled, partially blinded equivalence trial. SETTING: 74 hospitals in 16 countries. PATIENTS: 900 patients with symptomatic lower-extremity deep venous thrombosis, including 287 (32%) with confirmed pulmonary embolism. INTERVENTIONS: Initial therapy with dose-adjusted intravenous unfractionated heparin compared with subcutaneous enoxaparin at fixed dosages of 1.0 mg/kg of body weight twice daily or 1.5 mg/kg once daily. Long-term oral anticoagulation was started in all patients within 72 hours of randomization. MEASUREMENTS: Clinical end points assessed during a 3-month follow-up period. RESULTS: Equivalent efficacy was seen in the heparin group and both enoxaparin groups. Symptomatic venous thromboembolism recurred in 12 of 290 patients receiving unfractionated heparin (4.1%), 13 of 298 patients receiving once-daily enoxaparin (4.4%), and 9 of 312 patients receiving twice-daily enoxaparin (2.9%). Compared with unfractionated heparin, the treatment difference was 0.2% (95% CI, -3.04% to 3.49%) for once-daily enoxaparin and -1.2% (CI, -4.2% to 1.7%) for twice-daily enoxaparin. Incidence of major hemorrhage did not differ among the three treatment groups. Major hemorrhage occurred in 6 of 290 patients (2.1%) in the unfractionated heparin group, 5 of 298 patients (1.7%) in the once-daily enoxaparin group, and 4 of 312 patients (1.3%) in the twice-daily enoxaparin group. CONCLUSIONS: Subcutaneous enoxaparin once or twice daily is as effective and safe as dose-adjusted, continuously infused unfractionated heparin in the prevention of recurrent symptomatic venous thromboembolic disease.

Administration, Cutaneous↗
PubMed2000

[Contrast echocardiography. Basic principles and clinical applications].

Recent advances in ultrasound technology and intravenous contrast agents have made it possible for contrast echocardiography to move from bench to bedside. Ultrasound contrast agents enhance endocardial border delineation and the Doppler signal, which may improve the diagnostic accuracy of echocardiography in selected patients. The most exciting feature of contrast echocardiography is its capability to achieve a quantitative assessment of myocardial perfusion, and the method may thus provide a range of clinical applications in patients with ischaemic heart disease.

Contrast Media↗
PubMed2000

Tissue factor pathway inhibitor (TFPI) in disseminated intravascular coagulation: low levels of the activated factor X-TFPI complex.

Tissue factor pathway inhibitor (TFPI) fractions and coagulation markers were determined in 26 patients with disseminated intravascular coagulation (DIC). Thrombin-antithrombin complex and fibrin monomer values were markedly elevated in all patients (P < 0.01). The median TFPI activity level (2.1 nmol/l) was lower than in normal controls (2.6 nmol/l; P < 0.01). The median free TFPI level was within the normal reference range, but seven patients had levels above and nine patients had levels below normal range. The median activated factor X (FXa)-TFPI complex level in patients (0.13 nmol/l) was lower than in controls (0.18 nmol/l; P < 0.01). Only one patient had a FXa-TFPI complex level above the normal range, while eight patients had levels below. In conclusion, TFPI activity, free TFPI antigen and FXa-TFPI complex levels vary considerably in DIC. Activation of coagulation may increase TFPI levels, as reported by other workers and supported by a positive correlation between tissue factor and free TFPI in the present material. A negative correlation between fibrin monomer and free TFPI (r = -0.46, P = 0.019) might indicate that hyperactive coagulation leads to consumption of TFPI. Subnormal FXa-TFPI levels in DIC, possibly caused by consumption, may imply a reduced capacity to inactivate the triggering factor VIIa-tissue factor complex.

Adult↗
PubMed1999

[Low molecular heparin in a pregnant women with heart valve prosthesis].

Women with a prosthetic heart valve who wish to bear a child face a difficult choice. Continued medication with warfarin during pregnancy will offer her a reasonable good protection against thrombosis, but carries a considerable risk of teratogenic effects. Subcutaneously administered heparin is an alternative to warfarin. Standard (unfractionated) heparin has not offered sufficient protection against valve thrombosis, which may be a life-threatening complication. We were contacted by a woman who wished to become pregnant and who did not want to use warfarin if this implied a risk for the foetus. We followed a protocol using low molecular weight heparin in rather high doses. The dose was adjusted according to the results of blood test controls, which confirmed increased need for anticoagulation as the pregnancy evolved. Serial eccocardiography excluded valve thrombosis. The woman needed psychological support from her general practitioner. No complications occurred, and she gave birth to a normal child. We describe the various alternatives for anticoagulant treatment in pregnant women with mechanical heart valves. The choice of anticoagulant regimen and their consequences must be thoroughly discussed with the woman.

Adult↗
PubMed1999

Fibrin monomer antigen: a novel marker of mortality in acute myocardial infarction.

AIMS: A novel sensitive method for analyses of soluble fibrin monomer antigen was used to assess the predictive value of fibrin monomer when estimating mortality after acute myocardial infarction. METHODS AND RESULTS: Fibrin monomer was measured in plasma samples from 293 patients enrolled in a randomized clinical trial of low molecular weight heparin (dalteparin) in acute myocardial infarction (the FRAMI trial). Samples taken on days 2 and 7 were analysed using the Enzymun-Test FM(R)(Boehringer Mannheim, Germany). Non-survivors had significantly higher fibrin monomer levels relative to survivors (day 2, median (min-max): 1.8 mg. l-1(<0.01-73.1) vs 0.4 mg. l-1(<0. 01-103.5), P<0.0001). Fibrin monomer levels were significantly associated with congestive heart failure (P<0.001), enzymatic infarct size (P<0.0001), dalteparin treatment (P<0.001), and thrombolytic therapy (P=0.016). The relationship between fibrin monomer and mortality remained statistically significant after adjustment for these variables. In logistic regression analyses, fibrin monomer levels, age and congestive heart failure were all independent predictors of fatal outcome. CONCLUSIONS: Increased fibrin monomer level is an independent predictor of mortality in patients with myocardial infarction. It allows further risk stratification when combined with known risk factors such as age and presence of congestive heart failure.

Aged↗
PubMed1999

Recurrent endocarditis in silver-coated heart valve prosthesis.

BACKGROUND AND AIM OF THE STUDY: In order to prevent prosthetic valve endocarditis (PVE), the implantation of a new silver-coated sewing ring has been introduced to provide peri- and postoperative protection against microbial infection. METHODS: A 56-year-old woman with aortic stenosis had elective replacement with a St. Jude Medical mechanical valve fitted with a silver-coated sewing ring (Silzone). The patient developed early PVE, which necessitated reoperation after one month. Despite a second Silzone prosthesis being implanted, the endocarditis recurred. During a third operation an aortic homograft was implanted, and after six months a fourth operation was performed for a pseudoaneurysm at the base of the homograft, in proximity to the anterior mitral valve leaflet. RESULTS: The diagnosis of PVE was confirmed by the presence of continuous fever, transesophageal echocardiography and growth of penicillin-resistant Staphylococcus epidermidis from the valve prosthesis. CONCLUSION: The implantation of all prosthetic valves is encumbered with a risk of endocarditis. Although silver has bacteriostatic actions, the advantages of silver-coated prostheses in the treatment of this condition have yet to be assessed in clinical trials.

Anti-Bacterial Agents↗
PubMed1999

Predictive value of coagulation markers concerning clinical outcome 90 days after anterior myocardial infarction.

To study the predictive value of coagulation markers concerning clinical outcome, prothrombin fragment F1.2 (F1.2), fibrin monomer antigen (FM), D-Dimer (DD), and fibrinogen were measured in plasma samples drawn 2 and 7 days after acute myocardial infarction (AMI) in 314 consecutive patients randomized in a clinical trial of low molecular weight heparin (Dalteparin) (the FRAMI trial). Placebo-treated patients suffering death or new AMI within 90 days had significantly higher levels at day 2 of FM (Enzymun-Test FM), and DD (TINAquant D-dimer) (p = 0.001 and 0.02, respectively), but not F1.2 (Enzygnost F1.2 micro), relative to those without serious clinical events. At day 7 all three coagulation activation markers were significantly higher in patients with subsequent adverse clinical outcome. The Dalteparin group had significantly lower levels of these markers as compared to the placebo group. Left ventricular (LV) thrombus formation was not associated with changes in coagulation activation. However, patients with thrombus had significantly higher fibrinogen levels than those without thrombus (p = 0.004 day 2), independent of treatment group. Thus, markers of coagulation activation may be useful in stratification of patients when estimating risk for adverse clinical outcome after AMI. Furthermore, elevated fibrinogen levels are associated with increased risk of LV thrombus formation.

Anticoagulants↗
PubMed1998

[Venous thromboembolism--incidence and risk factors in Oslo].

Over a period of three years, 378 patients with objectively verified venous thromboembolism were treated at Aker University Hospital. Below the age of 60, men and women had about the same incidence of venous thromboembolism, but that age the incidence was significantly higher among men than among women. Incidence increased exponentially with age, from about 1:10,000 at age 20 to about 1:1,000 at age 50. The incidence found here is lower than in earlier Nordic studies. The great majority of the patients (93%) had deep venous thrombosis in the lower extremities, 11% had symptomatic and verified pulmonary embolism, and 1% had their thrombus in an inner organ vein. 23% of patients were previously treated for venous thromboembolism, and 22% had cancer. Seven women were on oral contraception, and 22 used postmenopausal hormone substitution. An obvious temporary precipitating factor was present in 42% of the patients, while 36% had a spontaneous venous thromboembolism. Hereditary thrombophilic disorder was found in 32% of patients below the age of 60.

Adolescent↗
PubMed1998

[Prevention of thrombosis in medical patients--documentation is missing].

A questionnaire regarding current routines for thromboprophylaxis was distributed to all 63 medical departments in Norwegian hospitals; 58 (92%) responded. All departments declared that they practiced prophylaxis against venous thromboembolism, and in most departments the decision (as to whether to practice prophylaxis) was left to the physicians. Written guidelines were used in only 12 departments, 21% of those who responded. The indications listed were those associated with a particular risk of thrombosis. Previous thrombosis and malignancy were listed less frequently than expected. There is a need for specific evidence regarding the efficacy and safety of thromboprophylaxis in medical patients. In our opinion this requires that further placebo-controlled studies be carried out.

Documentation↗
PubMed1998

Elevated TFPI in malignant disease: relation to cancer type and hypercoagulation.

We have previously reported high levels of the coagulation inhibitor TFPI in the blood of patients with gastrointestinal cancer. TFPI is not an acute-phase reactant, but high levels have also been reported in patients with septicaemia and disseminated intravascular coagulation (DIC). To study its relationship with other types of malignancy, TFPI activity was first determined in plasma samples from 214 patients with various malignancies. In a second cohort of 83 patients, total and free TFPI antigen, protein C, antithrombin, fibrin monomer and D-dimer were also measured. Elevated TFPI activity and antigens were found in about half of the patients with solid tumours. In contrast, elevated TFPI was rare in haematological malignancies (12%). In the 18 patients with acute nonlymphocytic leukaemia (ANLL), elevated free TFPI was found only in patients who also had DIC. No correlation was found between TFPI levels and fibrin monomer or D-dimer levels. Only four out of 20 patients with solid tumours had normal levels of fibrin monomer and D-dimer, yet three out of these four had elevated TFPI. In conclusion, elevated TFPI in ANLL is related to the coexistence of DIC. In solid tumour disease increased TFPI may reduce protective fibrin formation, but the pathogenic mechanism is as yet unknown.

Adult↗
PubMed1998

Low-molecular weight heparin reduces the generation and activity of thrombin in unstable coronary artery disease.

Unstable coronary artery disease (UCAD) is associated with an increased risk of further coronary events. In the FRISC study, the risk was decreased during treatment with a high, twice-daily, dose of dalteparin, a low-molecular-weight heparin. However, lowering the dose resulted in raised risk of recurrences. To investigate the underlying pathophysiology, the thrombin generation and activity in patients with UCAD randomized to a 6-week placebo-controlled treatment with dalteparin were evaluated. Plasma prothrombin fragment 1+2 (F1+2) (n = 342), thrombin-antithrombin complex (TAT) (n = 186) and soluble fibrin (SF) (n = 298) were analyzed before and during treatment with dalteparin/placebo administered subcutaneously, 120 IU/kg bw twice daily for 5-8 days and 7.500 IU once daily the following 35-40 days. High-dose treatment with dalteparin resulted in significantly reduced levels of all coagulation markers, demonstrating diminished thrombin generation and activity. When reducing the dalteparin dose, plasma TAT and SF remained low, indicating minimal fibrin formation. However, F1+2 increased during this period. though the level at day 45 was still lower than in the placebo group. In the placebo group elevated thrombin generation and activity persisted during the entire period. In conclusion, high-dose treatment with dalteparin twice daily resulted in significantly reduced thrombin generation and activity. However, after changing to a lower, once-daily dose, the treatment was not sufficient in preventing a return to a procoagulable state. These changes of the coagulation activity might explain the changes in event rate observed during dalteparin treatment.

Aged↗
PubMed1997

Randomized trial of low molecular weight heparin (dalteparin) in prevention of left ventricular thrombus formation and arterial embolism after acute anterior myocardial infarction: the Fragmin in Acute Myocardial Infarction (FRAMI) Study.

OBJECTIVES: The present trial investigated the efficacy and safety of dalteparin in the prevention of arterial thromboembolism after an acute anterior myocardial infarction (MI). BACKGROUND: Left ventricular (LV) thrombus formation is associated with increased risk of arterial embolism in patients with an acute MI. Thrombolytic and antiplatelet therapy do not prevent thrombus formation. METHODS: A total of 776 patients were enrolled in a multicenter, randomized, double-blind, placebo-controlled trial of subcutaneous dalteparin (150 IU/kg body weight every 12 h during the hospital period). Thrombolytic therapy and aspirin were administered in 91.5% and 97.6% of patients, respectively. The primary study end point was the composite of thrombus formation diagnosed by echocardiography and arterial embolism on day 9 +/- 2. RESULTS: Of 517 patients with echocardiographic recordings available for end point analysis, thrombus formation or embolism, or both, was found in 59 (21.9%) of 270 patients (59 with thrombus, none with embolism) in the placebo group and 35 (14.2%) of 247 patients (34 with thrombus, 1 with embolism) in the dalteparin group (p = 0.03). The risk reduction of thrombus formation associated with dalteparin treatment was 0.63 (95% confidence interval 0.43 to 0.92, p = 0.02). Analyses of all randomized patients (388 in each group) revealed no significant difference between the placebo and dalteparin groups with respect to arterial embolism (6 vs. 5 patients), reinfarction (8 vs. 6 patients) and mortality rates (23 vs. 23 patients, p = NS for all). Dalteparin was associated with an increased risk of hemorrhage: major in 11 dalteparin group patients (2.9%) verus 1 placebo group patient (0.3%, p = 0.006); minor in 52 dalteparin group patients (14.8%) versus 8 placebo group patients (1.8%, p < 0.001). CONCLUSIONS: Dalteparin treatment significantly reduces LV thrombus formation in acute anterior MI but is associated with increased hemorrhagic risk.

Aged↗
PubMed1997

Effect of alveolar hypoxia on segmental pulmonary vascular resistance and lung fluid balance in dogs.

In a biventricular bypass preparation with constant-flow perfusion, pulmonary arterial pressure (Ppa), average pulmonary capillary pressure (Ppc), venous pressure (Pv), extravascular lung water volume (EVWd) and capillary permeability-surface area product for urea (PS) were determined in control animals and in animals subjected to alveolar hypoxia. During hypoxia, Ppa increased in a biphasic manner, the site of hypoxic pulmonary vasoconstriction being located in the arterial upstream segment. At baseline, Ppc values were identical in control and experimental animals (3.4 +/- 0.4 vs. 3.6 +/- 0.2 mmHg). During 150 min of airway hypoxia, the rise in Ppc (5.1 +/- 0.3 mmHg) did not exceed the rise in Ppc (4.9 +/- 0.5 mmHg) recorded in control animals at same time interval during normoxic ventilation. EVWd increased during hypoxia to values significantly higher than those obtained in control animals (0.559 +/- 0.036 vs. 0.466 +/- 0.027 mL water g-1 lung). PS remained unchanged at baseline level throughout experiments in both groups of animals. Present data suggest that lung oedema formation during alveolar hypoxia may be caused by increased transcapillary fluid loss preferentially through transcellular hydraulic pathways in capillary endothelial cells.

Animals↗