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Biomedical subjects

V Hach-Wunderle

Publications and source records attributed to V Hach-Wunderle.

At least 19 recordsLinked to original sources
PubMed2001

Effects of a low-molecular-weight heparin on thrombus regression and recurrent thromboembolism in patients with deep-vein thrombosis.

BACKGROUND: Low-molecular-weight heparins are frequently used to treat venous thromboembolism, but optimal dosing regimens and clinical outcomes need further definition. METHODS: In this multicenter, open-label study with blinded adjudication of end points, we randomly assigned patients with acute deep-vein thrombosis to one of three treatment regimens: intravenous administration of unfractionated heparin; subcutaneous administration of a low-molecular-weight heparin, reviparin, twice a day for one week; or subcutaneous administration of reviparin once a day for four weeks. The primary end point was evidence of regression of the thrombus on venography on day 21; secondary end points were recurrent venous thromboembolism, major bleeding within 90 days after enrollment, and death. RESULTS: Of the patients receiving unfractionated heparin, 40.2 percent (129 of 321) had thrombus regression, as compared with 53.4 percent (175 of 328) of patients receiving reviparin twice daily and 53.5 percent (167 of 312) of the patients receiving reviparin once daily. With regard to thrombus regression, reviparin administered twice daily was significantly more effective than unfractionated heparin (relative likelihood of thrombus regression, 1.28; 97.5 percent confidence interval, 1.08 to 1.52), as was reviparin administered once daily (relative likelihood, 1.29; 97.5 percent confidence interval, 1.08 to 1.53). Mortality and the frequency of episodes of major bleeding were similar in the three groups. CONCLUSIONS: In acute deep-vein thrombosis, reviparin regimens are more effective than unfractionated heparin in reducing the size of the thrombus. Reviparin is also more effective than unfractionated heparin for the prevention of recurrent thromboembolism and equally safe.

Acute Disease↗
PubMed2000

The chronic venous compartment syndrome.

BACKGROUND: A chronic exertional compartment syndrome has only been observed in athletes and soldiers. In the vast majority, the disease affects the anterior compartment and the fibular muscle group, and only rarely the lateral and dorsal muscle compartments. Muscle tissue necrosis does not occur. In the course of venous diseases with a severe chronic venous stasis syndrome, a chronic venous compartment syndrome develops that differs considerably from the familiar functional syndrome. The predominant symptom is an uncurable cuff ulceration on the lower leg. PATIENTS AND METHODS: From 1993 to 1996 a total of 16 patients with a chronic fascial compression syndrome underwent surgery on 18 extremities. The crural fascia was resected and a mesh graft was applied. RESULTS: In the group of ten controls with healthy veins the average pressure in the deep compartment was 13.6 mmHg (range 9-17 mmHg) lying down and 29.9 mmHg (range 15-42 mmHg) standing up. In 14 patients with chronic fascial compression syndrome, the average pressure was higher, measuring 21.1 mmHg (range 8-47 mmHg) lying down and 62.5 mmHg (range 33-87) standing up. After surgery, the pressure dropped to 15.5 mmHg (range 5-24 mmHg) lying down and 34.5 mmHg (range 10-58 mmHg) standing up, but did not fall as low as the average values recorded in the control group or in the patient's healthy leg. The results from the standing up position were statistically significant (p = 0.003). Computed tomography showed major changes in the muscles indicating muscle atrophy and fatty degeneration. The crural fascia seemed to be incorporated in the scars of the subcutaneous tissue in large areas. After crural fasciectomy and healing of the ulceration, the tissue structure of the muscles recovered. CONCLUSIONS: In chronic fascial compression syndrome, the trellis arrangement of the collagen fibres becomes disordered. This results in a loss of flexibility during muscle contraction. Every step causes an increase of intracompartmental pressure and microstructural injury. The consequence is resection of the crural fascia.

Amputation, Surgical↗
PubMed2000

Postmenopausal hormone replacement therapy and the vascular wall: epidemiology and clinical studies.

The clinical relevance of estrogen's multiple acute and more delayed effects on vascular wall structure and function is incompletely understood. This review attempts to reevaluate epidemiological findings and clinical studies concerning the vascular actions of estrogens and gives implications for strategies in postmenopausal hormone replacement therapy (HRT). There is large evidence from observational studies that HRT reduces the risk of cardiovascular mortality and morbidity in postmenopausal women. However, according to the only large randomized, placebo-controlled, secondary prevention Heart and Estrogen/progestin Replacement Study (HERS), women with prevalent cardiovascular disease (CVD) have increased CVD events within the first year after onset of HRT. The net effects of HRT on atherosclerosis, coagulation, fibrinolysis or the inflammatory response are unproven. Randomized trials of intermediate outcomes reveal that HRT has favorable effects on isolated cardiovascular risk factors, e.g. lipoproteins, carbohydrate metabolism and vasodilatation, but the impact of this effects on clinical endpoints is still not clear. The basis of "evidenced based medicine" is currently not sufficient to provide exact recommendation who will benefit from HRT and who might not. Therefore, the decision about hormone use should consider individual benefit-risk profiles.

Adult↗
PubMed1999

Postmenopausal hormone replacement therapy and the vascular wall: mechanisms of 17 beta-estradiol's effects on vascular biology.

17 beta-estradiol (E2) protects against atherosclerosis independent of changes in plasma lipoproteins in a variety of animal models, which is explained by direct effects of E2 on the vascular wall. E2 improves vasomotion by modulation of vasoconstrictor and vasodilator systems through endothelium-dependent and endothelium-independent mechanisms. E2 affects the remodeling of the vascular wall by inhibiting smooth muscle cell proliferation and accelerating reendothelialization of injured blood vessels. E2 modulates the vascular inflammatory response by inhibiting cytokine production, cytokine-induced expression of cell adhesion molecules and platelet aggregation/adhesion. This review focuses on the cellular and molecular mechanisms underlying these vasculoprotective actions of E2. E2 can act through nongenomic stimulation of membrane/intracellular mediators and/or the classical genomic pathway of steroid actions, which is dependent on transcription and protein synthesis. The existence of at least two nuclear estrogen receptor (ER) subtypes alpha and beta and a putative membrane ER present the potential of tissue-specific as well as biologically different E2 actions. Nuclear ERs act as ligand-activated transcription factors and can affect gene regulation by interaction with the classical estrogen response element or other nonreceptor transcription factors. The molecular basis of genomic E2 actions by identifying transcription factors and regulatory elements involved in the induction and inhibition of E2 regulated gene expression is only at the beginning of being understood. The impact of E2-mediated increased NO availability on the hemodynamic and antiatherosclerotic actions of E2 is still a debate of controversy.

Cytokines↗
PubMed1999

Phlebography.

Explore the source record for details and available documents.

Humans↗
PubMed1999

[Predisposition and initiation of venous thrombosis].

The causes of thromboembolic disease are complex. In addition to acquired risks, thrombophilic diatheses in particular now play an important role. The combination of predisposing factors increases the risk of thrombosis. However, a precise prognosis cannot yet be made for an individual patient.

Humans↗
PubMed1997

Heparin-related thrombosis despite normal platelet counts in vascular surgery.

BACKGROUND: Acute graft thrombosis is a severe complication in vascular surgery that may require limb amputation or even cause death. Because nearly all patients undergoing vascular surgery have had previous exposure to heparin, the presence of heparin-related anti-platelet antibodies typical for heparin-associated thrombocytopenia (HAT) is one underlying possible mechanism of acute graft thrombosis. Although thrombocytopenia is a typical finding of HAT, it is not clear whether the occurrence of clinically important HAT is necessarily associated with thrombocytopenia. PATIENTS AND METHODS: Ten out of 246 patients undergoing vascular surgery were diagnosed with HAT because of otherwise unexplained acute graft thrombosis that required recurrent surgical interventions. RESULTS: In all of the 10 patients, heparin-related anti-platelet antibodies were detected although the platelet counts were within the normal range. When HAT was diagnosed, heparin administration was stopped and, after autoantibody cross-reactivity with the heparinoid Danaparoid had been excluded, anticoagulation was continued using this anticoagulant. After heparin therapy was discontinued none of the 10 patients developed further thrombotic complications. CONCLUSION: The data presented demonstrate clearly that a normal platelet count does not exclude the possibility of HAT. As a consequence of this, HAT should be suspected in patients who develop thrombotic complications during heparin treatment, regardless of the actual platelet counts.

Adult↗
PubMed1996

Intravenous somatic gene transfer with antisense tissue factor restores blood flow by reducing tumor necrosis factor-induced tissue factor expression and fibrin deposition in mouse meth-A sarcoma.

Fibrin is deposited on the endothelial cell surface in the vasculature of murine methylcholanthrene A-induced sarcomas after injection of tumor necrosis factor (TNF). Capillary endothelial cells of the tumor vascular bed become positive for tissue factor after TNF injection, based on immunocytochemistry and in situ hybridization. Intravascular clot formation was not dependent on tissue factor derived from tumor cells, since in vessels of tumors not expressing tissue factor, TNF also induced fibrin/fibrinogen deposition. However, the time course of fibrin/fibrinogen deposition after TNF differed in tumors expressing no, little, or greater amounts of tissue factor. Fibrin/fibrinogen deposition was more rapid in tumors in which the neoplastic cells expressed tissue factor than in tumors not expressing tissue factor. In the tumors not expressing tissue factor, activation of coagulation was dependent on TNF-induced synthesis of tissue factor by host cells, i.e., endothelium or monocytes/macrophages. Intravenous somatic gene transfer with tissue factor cDNA in the antisense orientation (but not sense or vector alone) reduced intravascular fibrin/fibrinogen deposition and restored blood flow to the tumor, showing that de novo tissue factor expression is central in TNF-induced activation of the coagulation mechanism.

Animals↗
PubMed1993

[Disorders of the liberation of tissue-type plasminogen activator (t-PA) from the venous wall as a cause for recurrent thromboses].

The release of tissue-type plasminogen activator (t-PA) after venous occlusion was tested in 290 patients with venous thrombosis, at earliest three months after the last thrombo-embolic episode. In 37 patients (12.8%) the t-PA-activity was decreased. In 14 patients (4.8%) the defect was confirmed by control. A reduced release of t-PA was found in 4 patients, while 10 out of 14 patients had comparatively higher levels of plasminogen-activator-inhibitor (PAI-I).

Adult↗
PubMed1989

[Prevention of venous thromboses with oral anticoagulants].

Oral anticoagulants are effective for prophylaxis of venous thromboembolism. The therapy is usually monitored by the one-stage prothrombin time (Quicktest). The aim of anticoagulant therapy is to reduce the coagulability of blood into a so called therapeutic range within which the patient is protected against thrombosis while being exposed to a minimal risk of bleeding. The standardization of methods for the prothrombin time assay by the International Normalized Ratio is of further benefit for monitoring the therapy in the individual patient.

Administration, Oral↗
PubMed1989

Anti-A in factor VIII concentrate: a cause of severe hemolysis in a patient with acquired factor VIII:C antibodies.

The authors report a case of acute macrohematuria in a patient with spontaneously acquired antibodies against factor VIII:C. Severe hemolysis was observed under factor VIII concentrate therapy. In 4 batches of the factor VIII concentrate high titers up to 1:512 of 'immune' anti-A were found. Clotting factor preparations used for replacement therapy, therefore, should be investigated for iso-antibodies, at least in situations where an intensive infusion therapy is required.

ABO Blood-Group System↗
PubMed1988

Congenital deficiency of plasminogen and its relationship to venous thrombosis.

In a patient with deep venous thrombosis, plasma concentrations of coagulant and inhibitor proteins were normal except for moderate deficiency of plasminogen. Family studies revealed a similar deficiency in the mother and sister of the propositus. Evaluation of purified plasminogen demonstrated that it functioned normally. The patient represents our only example of plasminogen deficiency in 435 German individuals evaluated with a history of thromboembolism.

Blood Coagulation Disorders↗