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Biomedical subjects

F Asbeck

Publications and source records attributed to F Asbeck.

At least 19 recordsLinked to original sources
PubMed2002

[Use of heparin in acute myocardial infarction in routine clinical practice in Germany. Results of the MITRA and MIR registries].

OBJECTIVE: Among other adjunctive medication, heparin is widely used in the therapy of acute myocardial infarction (AMI) today. Large randomized trials, however, have shown inconclusive data on the benefit of adjunctive heparin therapy for patients with AMI. The aim of this study was to describe the use of heparin and complication rates in routine clinical practice today. METHODS: MITRA and MIR were multicenter registries of AMI patients in Germany. During the years 1994 to 1998, 22,697 patients were registered with MITRA and MIR. Of these patients 49.9% received reperfusion therapy. RESULTS: 21,004 patients (92%) received heparin during acute therapy of AMI. The following factors were associated with withholding heparin: Bleeding at admission (OR 4.7; CI 3.2-6.8), cardiogenic shock (OR 1.8; CI 1.4-2.3) and fibrinolytic therapy with streptokinase (OR 2.1; CI 1.8-2.3). Complication rates of patients with heparin were only slightly higher than among those without heparin: 1.7% strokes and 1.9% bleedings were reported among the patients with fibrinolysis and heparin compared to 1.3% strokes and 1.4% bleedings among patients without heparin (p = ns). Mortality rates were 14.1% for patients with and 27.3% for patients without heparin (p < 0.001). CONCLUSIONS: Of the patients in MITRA and MIR 92% received heparin during AMI. Patients with active bleeding or in critical condition received heparin significantly less often. The selection of critically ill patients may have contributed to the high mortality of patients without heparin for AMI. Bleeding complication rates of patients with adjunctive heparin were only slightly higher than reported in randomized trials.

Adult↗
PubMed2001

Characterization and clinical course of patients not receiving aspirin for acute myocardial infarction: results from the MITRA and MIR studies.

BACKGROUND: Clinical trials have shown the efficacy of aspirin for acute myocardial infarction (AMI). However, not all patients receive aspirin for AMI. The aim of this study was to provide information on characteristics and clinical course of patients not treated with aspirin for AMI. METHODS: We analyzed the data of the Myocardial Infarction Registry (MIR) and the Maximal Individual Therapy of Acute Myocardial Infarction (MITRA) registry. MITRA and MIR were prospective multicenter registries of patients with ST segment elevation myocardial infarction in Germany. RESULTS: Of 22,572 patients registered from 1994 to 1998, 1767 (7.8%) did not receive aspirin within the first 48 hours after admission. Multivariate analysis revealed two main factors associated with withholding aspirin for AMI: relative contraindications to aspirin (gastric ulcer [odds ratio (OR) 4.9, 95% confidence interval (CI) 3.7-5.7], renal insufficiency [OR 1.4, 95% CI 1.1-1.8]), and critical clinical state at admission (cardiogenic shock [OR 1.5, 95% CI 1.2-2.1] and prehospital resuscitation [OR 1.8, 95% CI 1.4-2.2]). In addition, these patients were significantly less likely to receive reperfusion therapy and adjunctive medical therapy such as beta-blockers and angiotensin-converting enzyme inhibitors. In-hospital mortality after adjustment for baseline characteristics was 27.2% in patients without aspirin compared with 11.1% in patients treated with aspirin. CONCLUSIONS: Only a minority of AMI patients (7.8%) did not receive aspirin. Relative contraindications to aspirin and a critical clinical state at admission were the main factors associated with withholding aspirin for AMI. Even after adjustment for patient characteristics, the mortality of patients without aspirin was almost three times higher.

Aged↗
PubMed1998

Endoscopic therapy of a pancreatic effusion caused by chronic pancreatitis.

A 36-year-old patient was hospitalized because of an extensive right pleural effusion. He complained of increasing dyspnea, moderate weight loss and night sweats. The pleural aspirate was hemorrhagic and, surprisingly, excessively elevated lipase activity (57,000 U/L) was measured. An ultrasound examination of the epigastric area revealed several cystic structures in the upper retroperitoneum, and CT scan additionally showed diffuse pancreatic calculi. After conservative treatment had failed, ERCP was performed. A pseudocyst and the indistinct outline of a stenosis of the pancreatic duct could be seen. A few fragments of calculi were removed and a pancreatic duct stent was positioned. Because of stent occlusion ERCP was repeated and some more calculi were extracted, after which the pleural effusion and the pseudocysts completely regressed. In cases of pleural effusion on unclear etiology, a pancreatic pleural effusion should be included in the differential diagnosis. In patients with this clinical picture ERCP can provide not only diagnostic information, but also opportunities for new modes of treatment.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1994

Detection of atrial fusion systole in patients with dual chamber pacemakers by 24-hour esophagus ECG.

We performed ambulatory 24-hour esophagus ECG in nine patients with dual chamber pacemakers suspect of transient arrhythmias in order to achieve correct and reliable P wave identification during daily life activities. In all patients episodes were observed with varying atrial artifact to left atrial depolarization sequences. These episodes probably reflected presence of atrial fusion systole, an ECG phenomenon which should be taken into account when analyzing ambulatory esophagus ECG. Thus, the ambulatory esophagus ECG revealed its ability to detect spontaneous atrial depolarization in the presence of pacemaker artifact in patients with DDD(R) pacemakers.

Activities of Daily Living↗
PubMed1986

[Cyclophosphamide stosstherapy synchronized with plasmapheresis in rapidly progressive glomerulonephritis].

High-dosage stosstherapy of cyclophosphamide was administered, as far as possible optimally synchronized with plasmapheresis, to 12 patients with rapidly progressive glomerulonephritis. The basis for such synchronization lies in experimental data pointing to an increased antibody production after plasmapheresis (antibody rebound). Initial large-volume plasmapheresis was followed by high-dose immunosuppression in the phase of likely maximal proliferation of antibody-producing cells. The serum creatinine level in the 12 patients was 7.7 +/- 3.3 mg/dl before treatment. Eight patients required dialysis. After a period of observation of one year, ten patients are still alive. In one patient treatment had to be discontinued because she did not tolerate it. In the other nine patients renal function stabilized on a dialysis-free level. After one year the serum creatinine level averaged 2.5 +/- 1.2 mg/dl. With one exception no maintenance immunosuppressive treatment is required after one year. These preliminary results suggest that this treatment concept further improves the prognosis of rapidly progressive glomerulonephritis.

Combined Modality Therapy↗
PubMed1985

Danazol in acquired amegakaryocytic thrombocytopenic purpura: a case report.

Acquired amegakaryocytic thrombocytopenic purpura is a rare disease. Most reported patients did not respond to any therapeutical approach. Recently we observed a striking improvement of this disorder in a female patient shortly after therapy with danazol had been initiated. This observation and its possible implication for the treatment of amegakaryocytic thrombocytopenia are reported herein.

Adult↗
PubMed1983

Systemic fibrinolytic activity and inhibitor levels during treatment of deep vein thrombosis with urokinase and streptokinase.

In a prospective, randomized trial 33 patients with deep vein thrombosis were treated either with 2,200 or 1,100 IU/kg/h urokinase or with 100,000 IU/h streptokinase for at least 6 days. While streptokinase was given continuously, urokinase was administered intermittently (12 hr urokinase alternating with 12 hr heparin). Urokinase treatment resulted in a dose-dependent fibrinolytic state with shortening of the euglobulin clot lysis time, easily demonstrable amidolytic activity and moderate decrease of plasminogen. At the end of each urokinase-free interval the fibrinolytic activity had mostly faded, but was reproducibly elicited again by each new urokinase administration. Streptokinase immediately evoked the customary, intense fibrinolytic state, which progressively tapered off as plasminogen fell to 1% of its pretreatment concentration. In all treatment groups alpha-2-antiplasmin dropped to approximately 40% of its initial value during the first 12 hr with a further decrease to about 20% after 6 days. alpha-2-macroglobulin fell only moderately with either urokinase regimen, whereas it decreased progressively to 45% under streptokinase. While the fibrinolytic activity decreased under streptokinase over the 6-day infusion period, it appeared to increase with each successive urokinase infusion particularly with 1100 IU/kg/h. Thus the final euglobulin clot lysis times and the final fibrinogen concentrations were similar in all three treatment groups on the sixth day.

Blood Coagulation Tests↗
PubMed1983

Controlled multicenter pilot study of urokinase- heparin and streptokinase in deep vein thrombosis.

Thirty-three patients with acute iliofemoral thrombosis were randomly assigned to three treatment groups in a pilot dose-ranging study of thrombolytic therapy in deep vein thrombosis. One group received tissue culture urokinase in a dose of 2,200 I.U./kg/hr, and a second group in a dose of 1,100 I.U./kg/hr following a loading dose of 4,400 I.U./kg given in ten min. Urokinase was administered for 12 hr periods, alternating with 12 hr periods of heparin. A third group received an initial dose of 250,000 I.U. of streptokinase in 20 min, followed by 100,000 I.U./hr. Treatment of all patients continued for three days. At the end of this period little improvement, evaluated by "blinded" interpretation of pre- and post-treatment phlebograms, was found in five out of ten of the higher-dose urokinase patients, seven out of eleven of lower-dosage urokinase patients, and six out of ten of streptokinase patients. Optional treatment for another three days showed little further improvement of urokinase-patients and moderate further improvement in the streptokinase-patients. Neither of the 2 dosage schemes at intermittent application of urokinase appeared to be advantageous. Urokinase treated patients experienced fewer adverse reactions.

Adolescent↗
PubMed1981

In vivo studies on the inhibition of coagulation by fractionated heparin and by a heparin analogue. II. Effects of a heparin analogue.

SSHA, a semi-synthetic heparin analogue, and sodium heparin from porcine intestinal mucosa were injected subcutaneously into six healthy volunteers over a period of three days in a cross-over trial. Before injection and 2, 4, 6, 8 hrs afterwards, the heparin-like activity was measured with the APTT, the anti-Xa clotting test and two chromogenic substrate assays. The results show that SSHA mediates both anti-Xa and antithrombin activities in vivo. A comparison between the effects of SSHA and heparin is problematical due to the heterogeneity of different heparin preparations. Low doses of the analogue (45 mg s.c.) induced proportionally higher and longer lasting anti-Xa activities than higher doses (90 mg s.c.). Repeated injections of SSHA twice daily led to increasing effects on two tests for heparin-like activity, whereas two other tests remained unchanged. Both drugs were tolerated equally well, side effects were not detected. Clinical studies are required to demonstrate whether SSHA is similar or superior to low-dose heparin for use in thrombosis prophylaxis.

Adult↗
PubMed1981

In vivo studies on the inhibition of coagulation by fractionated heparin and by a heparin analogue. I. Effects of heparin fractions.

High and low molecular weight heparin fractions obtained by gel filtration chromatography of sodium mucosal heparin were injected subcutaneously into six healthy volunteers and compared with the unfractionated substance in a cross-over trial. Equal doses of 5,000 U were administered twice daily over a period of three days and heparin activity was repeatedly controlled before and 2, 4, 8 hrs after injection by means of the APTT, the anti-Xa clotting test and a chromogenic substrate assay. In addition, the in vivo effect of subcutaneously administered fractionated heparin on platelet function was examined on three of the volunteers. The results show that s.c. injections of the low molecular weight fraction induced markedly higher anti-Xa activity than injections of the other preparations. At the same time, APTT results did not significantly differ. Unfractionated heparin and the high molecular weight fraction enhanced ADP-induced platelet aggregation and collagen-mediated MDA production, while the low molecular weight fraction hardly affected these assays, but potently inhibited thrombin-induced MDA production. All heparin preparations stimulated the release of platelet Factor 4 in plasma. During the three-day treatment periods, no side-effects and no significant changes in the response to heparin injections were detected.

Adult↗
PubMed1980

The determination of antithrombin III, alpha 2-macroglobulin and alpha 2-antiplasmin in plasma by laser nephelometry.

Specific assay procedures were developed to determine antithrombin III, alpha 2-macroglobulin, and alpha 2-antiplasmin in plasma with the aid of a Laser nephelometer. About 100 normal and pathological plasmas were examined and the results compared with those obtained by conventional immunological methods, such as radial immunodiffusion or rocket electrophoresis. Nephelometry proved to be a very rapid, precise, and reproducible method for the determination of antithrombin III and alpha 2-macroglobulin. The reproducibility of the alpha 2-antiplasmin assay was poor, probably as a consequence of the low concentration of this inhibitor in normal plasma.

Antithrombin III↗