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Biomedical subjects

U T Seyfert

Publications and source records attributed to U T Seyfert.

At least 19 recordsLinked to original sources
PubMed2005

Haemocompatibility of polymer-coated stainless steel stents as compared to uncoated stents.

Acute and subacute stent thrombosis still represent an unsolved problem in connection with endovascular stents. For this reason coatings are tested now with the intention to reduce thrombogenicity of stainless steel surfaces. This comparative study examined whether a polymeric stent coating affected the haemocompatibility of a stainless steel stent. For compatibility testing, coated and non-coated stents were implanted in a low-grade thrombogenic closed-loop system perfused with platelet rich plasma at shear rates far below the threshold value at which shear-rate-induced activation of thrombocytes occurs. After 21 circulations of the filling volume (exposure time: 6.2 min), the number of single circulating platelets in the perfusion system with uncoated stainless steel stents decreased almost twice as much as was the case with polymer-coated stents. This is thought to indicate that more thrombocytes had adhered to the uncoated stainless steel stent, or that the thrombocytes were clustered in circulating aggregates. Parallel to the platelet aggregation/adherence, a release reaction took place, as was evident from the TAT complexes indicating the generation of thrombin. In the case of the implantation of uncoated stainless steel stents, both the number of activated circulating thrombocytes and the level of platelet reactivity (number of thrombocytes circulating in the plasma as aggregates) were notably higher than in the system with polymer-coated stents. At the same time it should be noted that the activation or aggregation is almost wholly attributable to the exogenic surface of the implanted stent, since activation due to the tube system or to shear rate can be excluded (as shown by measurements of the system without a stent). In addition to activation of the thrombocytes, a notable increase in the number of receptors per platelet (significant only in the system with the uncoated stent) took place. This supports both the adherence of the thrombocytes and their readiness to aggregate, since more receptors (docking places for ligands) are available. The better haemocompatibility of the polymer-coated stents, as verified in the laboratory, was also evident under microscopic examination of the explanted stents following the perfusion tests.

Blood Platelets↗
PubMed2003

[Haemostatic disorders in ENT patients. Part 2: Pathophysiology, diagnostics, clinical feature and therapy].

In the first part of the medical education article on haemostatic disorders in ENT patients the basic physiology of haemostasis and main diagnostic tools were presented and discussed. The second part presents disorders of the coagulation system,thrombocyte function and blood vessels with special emphasis on clinical practice in ENT surgery. In this context, haemophilia A and B, von Willebrand disease and different forms of thrombocytopenia are of main clinical importance. Some underlying diseases such as malignomas, renal and hepatic insufficiency in combination with drug therapy (e.g.anticoagulants and thrombocyte function inhibitors) play an important role in clinical practice as well. Sepsis and haemorrhage may lead to disseminated intravascular coagulation (DIC). Beside a systematic review, important haemostatic disorders are illustrated with case reports.

Adolescent↗
PubMed2003

Influence of the direct NO-donor SIN-1 on the interaction between platelets and stainless steel stents under dynamic conditions.

It was investigated whether the NO-donor SIN-1, the active metabolite of molsidomine, influenced the activation of platelets, the formation of circulating platelet aggregates, the spontaneous aggregation of platelets and the activation of the clotting system triggered by a body foreign surface in an in vitro closed-loop perfusion model. With human platelet-rich plasma at micromolar concentrations SIN-1 exerted pronounced effects on the interaction between platelets and an exogenous surface. In the absence of SIN-1, the number of circulating single platelets decreased significantly, which could be due either to the formation of circulating platelet aggregates or to the adhesion of platelets to the stent. Both these processes were blocked by the addition of SIN-1. Moreover, the platelets exhibited hyperaggregability in the absence of SIN-1 whereas the NO-donor was able to completely inhibit spontaneous platelet aggregation. Similar results were obtained in flow cytometry experiments. Without SIN-1, high platelet surface densities of both the GPIb/IX and GPIIb/IIIa receptors were observed. In addition, the density of the fibrinogen receptor increased significantly with the number of perfusion cycles. SIN-1 was able to suppress the augmented GPIIb/IIIa receptor expression significantly. Molsidomine seemed to have the potential to reduce the incidence of thrombotic processes triggered by the exogenous surface of the stent.

Adult↗
PubMed2002

[Perioperative therapy of von Willebrand disease. Demonstration of pathophysiology, clinical problems and therapy options using two case reports].

Von Willebrand disease (vWD) is the most widespread inherited bleeding disorder caused by quantitative or qualitative abnormalities of von Willebrand factor (vWF), an adhesive glycoprotein found in blood plasma and platelets and participating in primary and secondary/endothelium haemostasis as well. Although bleeding symptoms are often mild or moderate, patients with vWD represent a very heterogenous group with different phenotypes and a wide variability of the clinical pattern. In accordance with different defects of vWF, vWD is classified into various types and subtypes. This is illustrated by two case reports of patients with different types of vWD. Two main therapeutic options are available for the prevention and treatment of bleeding: desmopressin (DDAVP) and replacement therapy with plasma concentrates containing both factor VIII and vWF. DDAVP is the treatment of choice for most patients with type 1, representing about 80% of all patients with vWD. In patients with most types of type 2 and in all patients of type 3, DDAVP alone is ineffective or even contraindicated, and it is usually necessary to switch to plasma concentrates. Although treatment of vWD seems to be relatively simple in most cases, the exact diagnosis and phenotype characterization requires specialized or expert laboratory facilities. Furthermore, no reliable screening method for the diagnosis of vWD exists. Acquired vWD has similar clinical features and laboratory findings to the congenital forms and is mostly associated with lymphoproliferative or autoimmune disorders or neoplasia.

Adolescent↗
PubMed2002

Evaluation of the haemocompatibility of titanium based biomaterials.

The increased use of metallic biomaterials in contact with blood e.g. for the application as coronary stents leads to the development of new biomaterials. The main requirements for stents are high flexibility, high cold deformability and sufficient mechanical strength (static and dynamic), which can be obtained by strain hardening, radio-opacity and haemocompatibility. In order to investigate the properties of the metallic biomaterials in contact with blood, a comparison of the haemocompatibility of newly developed materials with established materials has been performed. To evaluate haemocompatibility without the influence of the geometry of the material, spherical powders produced by rotating electrode process (REP) were used in a dynamic test system with full human blood under two different stress conditions. The high shear stress simulates the arterial and the low shear stress simulates the venous situation. The use of a dimensionless score point (SP) system where the parameters of the haemocompatibility are determined with and without a material exposition allows an objective comparison of the materials used.

Alloys↗
PubMed2000

[The effect of aprotinin and tranexamic acid on fibrinolysis and thrombin generation during cardiopulmonary bypass].

OBJECTIVE: Antifibrinolytic drug therapy has proved to be effective in reducing blood loss associated with cardiac surgery and cardiopulmonary bypass (CPB). Concerns remain regarding the risk of enhancing thrombosis. In the present study we investigated the effect of aprotinin (AP) and tranexamic acid (TA) on fibrinolysis and thrombin generation during CPB. METHODS: 60 patients undergoing coronary artery bypass graft surgery were randomised in 3 groups. They received either aprotinin ("high-dose-scheme"), tranexamic acid (2 g/h) or no antifibrinolytic therapy (control group). Collection of blood was performed at 7 pre-, intra- and postoperatively predetermined intervals. Fibrinolytic activity was determined by measuring concentrations of D-dimer, thrombin generation by the measurement of thrombin-antithrombin III complex (TAT). RESULTS: There was no significant increase of D-dimers in the AP or TA group. D-dimer concentration in the control group increased significantly after starting CPB. Comparing with the control group, thrombin generation in the AP group was significant less, while TA group produced significantly higher values. CONCLUSION: After the administration of AP for cardiac surgery we observed reductions in both intraoperative fibrinolysis and thrombin generation. In case of TA suppression of fibrinolytic activity in the absence of concomitant reduction in thrombin generation occurred. These results suggest that TA could potentiate a hypercoagulable state with the risk of thrombosis in the perioperative setting.

Aged↗
PubMed2000

The polysaccharide fucoidan inhibits microvascular thrombus formation independently from P- and L-selectin function in vivo.

BACKGROUND: Adhesion molecules of the selectin family (mainly P- and L-selectin) have been suggested to mediate interactions between platelets, leukocytes and endothelial cells in thrombus formation. The polysaccharide fucoidan has anticoagulative properties, but is also able to bind and block the function of the selectins. Here, we investigated in vivo (i) if fucoidan can prevent microvascular thrombus formation, and (ii) whether this is potentially mediated by the inhibition of P-and/or L-selectin. MATERIALS AND METHODS: For this purpose, we used intravital microscopy in the mouse cremaster microcirculation in which thrombosis was induced photochemically by light exposure to individual arterioles and venules after intravenous (i.v.) injection of FITC-dextran. RESULTS: We found that intravenous administration of fucoidan significantly prolonged the time required for complete occlusion in arterioles and venules by almost seven- and nine-fold, respectively. In contrast, treatment with monoclonal antibodies against P- and L-selectin had no effect on the development of microvascular thrombosis. Fucoidan and also the anti-P-selectin antibody completely inhibited baseline venular leukocyte rolling in the cremaster muscle, indicating that these treatment regimes abolished P-selectin function. Importantly, fucoidan and the anti-P-selectin antibody had no effect on systemic platelet and leukocyte counts. On the other hand, we found that fucoidan treatment significantly altered coagulation parameters, including prothrombin time (Quick percentage), activated partial thromboplastin time (APTT) and thrombin clotting time (TCT), which may explain the potent in vivo anticoagulative effect of fucoidan observed here. CONCLUSIONS: Taken together, our novel findings suggest that fucoidan effectively prevents microvascular thrombus formation induced by endothelial damage in arterioles and venules in vivo. This protective effect of fucoidan is not attributable to inhibition of P- and L-selectin function but may instead be related to the anticoagulative capacity of fucoidan.

Animals↗
PubMed1999

[Heparin-induced thrombocytopenia (HIT). Importance for anesthesia and intensive care].

For many decades, heparins have been used successfully for prophylaxis and treatment of thromboembolic complications world-wide. Although heparin-induced thrombocytopenia (HIT Type II) is a well-known adverse effect of heparin therapy, thromboembolic complications during heparin therapy are rarely diagnosed exactly to be related to HIT. At present an immunologic etiology of HIT by generation of multimodal immune complexes against a neo antigen of heparin and platelet factor 4 is equivocally accepted. The incidence of HIT seems to be related to the type of heparin (unfractioned/low molecular weight) or other underlying risks such as peripheral occlusive vessel disease. Mortality and complications resulting from HIT is reported to be about 20-30% each. For diagnosis of HIT Type II, clinical observation and simultaneous laboratory testing are essential. Discontinuation of heparin is a simple and essential manoeuvre, and anticoagulation has to be continued by alternative drugs. The heparinoid danaparoid-sodium and the thrombin inhibitor recombinant hirudin have been used successfully world-wide for treatment in many patients with HIT Type II including cardiopulmonary bypass surgery or renal replacement procedures. Furthermore, other therapeutical alternatives (e.g. immunoglobulins, prostaglandines) exist. Randomised controlled studies have to evaluate which drug has to be preferred in the future including risk/benefit ratio. The need of supplementary surgical procedures (e.g. embolectomy) depends on the individual clinical status. The patients have to be informed in detail about their underlying disease and further deleterious consequences of re-exposition with heparin. HIT should be recorded in an emergency certificate and the national Committee on Drugs should be informed about this severe side effect of heparin therapy.

Anesthesia↗
PubMed1998

Diagnostic value of procalcitonin: the influence of cardiopulmonary bypass, aprotinin, SIRS, and sepsis.

BACKGROUND: The reasons for a systemic inflammatory response syndrome (SIRS) following ECC are not yet fully understood. Procalcitonin (PCT) blood levels may distinguish between bacterial infections and a non-bacterial systemic inflammation. We investigated the influence of ECC, ECC modified by application of aprotinin, systemic inflammation, and bacterial infection on the PCT values. METHODS: 20 CABG patients were randomized and divided in two groups. Group A served as the control group, while group B perioperatively received a high dose of aprotinin. Blood samples for measurement of PCT were taken 6 times perioperatively. Furthermore, blood samples were taken from 20 preoperatively comparable patients who suffered from bacterial infection (n = 10) (group C) or a SIRS (n = 10) (group D) after ECC; in these groups PCT was determined daily after the onset of inflammation. RESULTS: There was no significant elevation of PCT in group A or B at any time. In sepsis patients a significant elevation of PCT was seen, with the peak level of 18.6+/-6.3 ng/ml on the second day after diagnosis; the PCT level of SIRS patients remained constantly low (<0.9 ng/ml). CONCLUSIONS: In this study it was demonstrated that ECC and the use of aprotinin did not have any influence on the secretion of PCT. A systemic bacterial infection caused a significant increase of PCT, whereas PCT values remained normal in case of a SIRS. So it seems to be possible to distinguish between a primary SIRS and a bacterial sepsis by means of PCT.

Aged↗
PubMed1997

[A delayed hemolytic transfusion reaction due to irregular antibodies with an anti-Kidd(a) specificity].

HISTORY AND CLINICAL FINDINGS: A 56-year-old woman was admitted for replacement of a previously implanted right hip prosthesis which had become loose (no infection). She limped painfully on a shortened leg whose mobility was markedly impaired. At the site of the previous operation the pelvis was lower by about 2 cm; the scar looked well healed. INVESTIGATIONS: Routine laboratory tests were normal except for moderately raised erythrocyte sedimentation rate (18/ 27 mm). There was complete loosening of the prosthesis on X-ray. TREATMENT AND COURSE: Intraoperative bleeding from a branch of the inferior gluteal artery required blood transfusion and further erythrocyte infusions became necessary. Jaundice developed on the 4th postoperative day and 7 days later the direct Coombs test was positive with demonstrable agglutination. Free irregular erythrocytic anti-Kidd(a) (anti-jk[a]) antibodies were found in the serum. To counteract the delayed haemolytic transfusion reaction, exclusively jk(a)-negative erythrocytes were infused. The jaundice gradually disappeared and the bilirubin values became normal. CONCLUSION: Jaundice and signs of haemolysis after erythrocyte transfusion may be due to delayed transfusion reaction and should be investigated with the direct Coombs test.

Antibodies↗