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Biomedical subjects

R Dechend

Publications and source records attributed to R Dechend.

23 records · Page 2Linked to original sources
PubMed1997

Sixty-minute alteplase protocol: a new accelerated recombinant tissue-type plasminogen activator regimen for thrombolysis in acute myocardial infarction.

OBJECTIVES: Our aim was to design and evaluate a new and easily administered recombinant tissue-type plasminogen activator (rt-PA) regimen for thrombolysis in acute myocardial infarction (AMI) based on established pharmacokinetic data that improve the reperfusion success rate. BACKGROUND: Rapid restoration of Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow is a primary predictor of mortality after thrombolysis in AMI. However, TIMI grade 3 patency rates 90 min into thrombolysis of only 50% to 60% indicate an obvious need for improved thrombolytic regimens. METHODS: Pharmacokinetic simulations were performed to design a new rt-PA regimen. We aimed for a plateau tissue-type plasminogen activator (t-PA) plasma level similar to that of the first plateau of the Neuhaus regimen. These aims were achieved with a 20-mg rt-PA intravenous (i.v.) bolus followed by an 80-mg i.v. infusion over 60 min (regimen A). This regimen was tested in a consecutive comparative trial in 80 patients versus 2.25 10(6) IU of streptokinase/60 min (B), and 70 mg (C) or 100 mg (D) of rt-PA over 90 min. Subsequently, a confirmation trial of regimen A in 254 consecutive patients was performed with angiographic assessment by independent investigators of patency at 90 min. RESULTS: The comparative phase of the trial yielded, respectively, TIMI grade 3 and total patency (TIMI grades 2 and 3) of 80% and 85% (regimen A), 35% and 50% (B), 50% and 55% (C) and 60% and 70% (D). In the confirmation phase of the trial, regimen A yielded 81.1% TIMI grade 3 and 87.0% total patency. At follow-up angiography 7 (4.1%) of 169 vessels had reoccluded. In-hospital mortality rate was 1.2%. Nadir levels of fibrinogen, plasminogen and alpha2-antiplasmin were 3.6 +/- 0.8 mg/ml, 60 +/- 21% and 42 +/- 16%, respectively (mean +/- SD). Fifty-seven patients (22.4%) suffered from bleeding; 3.5% needed blood transfusions. CONCLUSIONS: The 60-min alteplase thrombolysis in AMI protocol achieved a TIMI grade 3 patency rate of 81.1% at 90 min with no indication of an increased bleeding hazard; it was associated with a 1.2% overall mortality rate. These results are substantially better than those reported from all currently utilized regimens. Head to head comparison with established thrombolytic regimens in a large-scale randomized trial is warranted.

Blood Coagulation Tests↗
PubMed1997

Stent implantation in patients with superior vena cava syndrome.

OBJECTIVE: The purpose of this study was to determine the feasibility of using Wallstent implantation to treat superior vena cava syndrome due to malignant tumors. SUBJECTS AND METHODS: Digital subtraction angiography showed obstruction of the superior vena cava in 13 patients who then underwent transluminal dilatation and Wallstent implantation. The patients were treated with IV heparin and monitored in the emergency department. Thereafter, they were treated with a platelet inhibitor for 4 weeks. RESULTS: Because their signs and symptoms improved, patients were able to resume radiation therapy, chemotherapy, or both. One patient died of cardiac arrhythmia 1 day after stent placement. Although eight patients have subsequently died of their bronchial or thyroid gland tumors, superior vena cava syndrome did not recur in any patient. CONCLUSION: Percutaneous implantation of Wallstent endoprostheses provides excellent palliation for superior vena cava syndrome.

Aged↗
PubMed1994

Thrombolysis in thromboembolic diseases.

Thrombolysis in many manifestations of thromboembolic disease offers a valuable alternative to surgery. However, as thrombolysis is always associated with a bleeding hazard (though low) one should always weigh the risks against the expected benefits when the decision for or against this therapeutic option is made. Furthermore, in selecting the appropriate thrombolytic agent, one should be led by the urgency of reperfusion to maintain organ function. If one decides on an aggressive, high-dose, brief-duration regimen, reperfusion may be achieved more rapidly but may be incomplete in the majority of cases. On the other hand, by selecting an intermediate- or long-duration, low-dose regimen, reperfusion may happen too late to improve the patient's prognosis. Above all, one should keep in mind that the hazard of serious bleeding constantly increases with duration of thrombolysis. No matter which strategy is regarded as the best to resolve a clot in a particular patient with a particular type of thromboembolic disease, thrombolysis should be accompanied by high doses of i.v. heparin. Finally, if bleeding occurs in spite of all precautions taken, the new generation of fibrin-specific thrombolytic agents offers the advantage of short half-lives. In addition--in contrast to streptokinase--the hemostatic defect that they cause may be rapidly reversed by the infusion of antagonist drugs such as aprotinin, tranexamic acid, or epsilon-aminocaproic acid. This adds to the clinical safety profile of these thrombolytic agents.

Contraindications↗
PubMedDate not supplied

B-Myb, a repressed trans-activating protein.

B-Myb belongs to a family of related transcription factors which share a unique DNA binding domain. B-Myb plays an important role in regulation of the cell cycle. Its expression is upregulated by the human papilloma virus HPV16 E7 oncoprotein. Overexpression of B-Myb can bypass p53-mediated cell cycle arrest. The founding member of the myb gene family, c-Myb, and A-Myb are involved in hematopoiesis and neurogenesis, respectively, and are both activators of gene transcription. Whether B-Myb is a transactivator or a repressor, however, has remained a matter of discussion. We reviewed the transactivation potential of B-Myb in yeast, taking advantage of the fact that inducible gene activation is an evolutionarily conserved process. By mutational analysis we localized a conserved activation domain in B-Myb. In vertebrate cells the transactivation potential of B-Myb is concealed by the C-terminal part of the protein. We show that the cell cycle regulators cyclin A and cyclin E activate B-Myb by eradicating the inhibition mediated by its carboxy-terminus. Our data suggest that in vertebrates the trans-activating function of B-Myb is regulated during the cell cycle and link Myb functions to cell cycle progression.

Amino Acid Sequence↗