Literature DB >> 3148788

[Persistent changes in tissue-type plasminogen activator and plasminogen activator inhibitor fibrinolytic parameters in patients following juvenile ischemic cerebral infarct].

C Baumgartner1, K Huber, F Holzner, K Zeiler, E Auff, B R Binder.   

Abstract

In diseases associated with thrombotic or thromboembolic complications, a reduction in the fibrinolytic potential may contribute to the risk to develop thrombosis. To investigate whether juvenile cerebral infarction is associated with a permanent defect of the fibrinolytic system we measured the main components of the fibrinolytic system, tissue plasminogen activator (t-PA) and its fast acting inhibitor (PAI) in plasma samples of 21 patients (aged 21-44 years) 3-24 months after the acute event. The data obtained were compared to those from thirteen healthy young volunteers (22-46 years). A direct effect of known risk factors on the fibrinolytic system could be excluded because patients avoided their risk factors immediately after the ischemic cerebral attack. Hypertension and the combination of oral contraceptives and smoking had been the most striking original risk factors. Levels of t-PA antigen and t-PA activity before and after venous occlusion, or PAI activity were not different between patients and controls suggesting that at least a permanent decrease in the activity of the fibrinolytic system does not exist in these patients. However, our findings do not exclude that a temporary defect in fibrinolysis might have contributed to the acute onset of the thrombotic cerebral event possibly induced by the risk factors originally present.

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Year:  1988        PMID: 3148788     DOI: 10.1007/bf01727845

Source DB:  PubMed          Journal:  Klin Wochenschr        ISSN: 0023-2173


  41 in total

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Authors:  J G Vermylen; D A Chamone
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Authors:  W T Longstreth; P D Swanson
Journal:  Stroke       Date:  1984 Jul-Aug       Impact factor: 7.914

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Authors:  S E Johnson; H Skre
Journal:  Stroke       Date:  1986 Jul-Aug       Impact factor: 7.914

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Authors:  L J Dorfman; W H Marshall; D R Enzmann
Journal:  Neurology       Date:  1979-03       Impact factor: 9.910

Review 6.  The decline of stroke.

Authors:  J P Whisnant
Journal:  Stroke       Date:  1984 Jan-Feb       Impact factor: 7.914

7.  A study of hemostasis in ischemic cerebrovascular disease. III. Abnormalities in vascular plasminogen activators, antiactivators and alpha 2-antiplasmin.

Authors:  K L Mettinger; N Egberg
Journal:  Thromb Res       Date:  1982-05-01       Impact factor: 3.944

8.  Circadian fluctuations of plasminogen activator inhibitor and tissue plasminogen activator levels in plasma of patients with unstable coronary artery disease and acute myocardial infarction.

Authors:  K Huber; D Rosc; I Resch; E Schuster; D H Glogar; F Kaindl; B R Binder
Journal:  Thromb Haemost       Date:  1988-12-22       Impact factor: 5.249

9.  Platelet aggregation and fibrinolytic activity in transient cerebral ischemia.

Authors:  L A Andersen; J Gormsen
Journal:  Acta Neurol Scand       Date:  1977-01       Impact factor: 3.209

10.  [Status of oral contraceptives as a risk factor in cerebrovascular diseases].

Authors:  E Auff; K Zeiler; F Holzner; S Wimmer; L Deecke
Journal:  Wien Klin Wochenschr       Date:  1986-05-16       Impact factor: 1.704

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  2 in total

1.  Effect of garlic on platelet aggregation in patients with increased risk of juvenile ischaemic attack.

Authors:  H Kiesewetter; F Jung; E M Jung; C Mroweitz; J Koscielny; E Wenzel
Journal:  Eur J Clin Pharmacol       Date:  1993       Impact factor: 2.953

Review 2.  Plasminogen activator inhibitor type-1 (part one): basic mechanisms, regulation, and role for thromboembolic disease.

Authors:  K Huber
Journal:  J Thromb Thrombolysis       Date:  2001-05       Impact factor: 2.300

  2 in total

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